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I’m feeling run down. Why am I more likely to get sick? And how can I boost my immune system?

<div class="theconversation-article-body"> <a href="https://theconversation.com/profiles/sathana-dushyanthen-1169328">Sathana Dushyanthen</a>, <a href="https://theconversation.com/institutions/the-university-of-melbourne-722">The University of Melbourne</a> It has been a long winter, filled with many viruses and cost-of-living pressures, on top of the usual mix of work, study, life admin and caring responsibilities. Stress is an inevitable part of life. In short bursts, our stress response has evolved as a survival mechanism to help us be more alert in <a href="https://theconversation.com/no-you-cant-blame-all-your-health-issues-on-high-cortisol-heres-how-the-hormone-works-203162">fight or flight situations</a>. But when stress is chronic, it weakens the immune system and makes us more vulnerable to illnesses such as the <a href="https://www.healthline.com/health/can-stress-make-you-sick#:%7E:text=The%20common%20cold&text=Inflammation%20has%20been%20linked%20to,to%20the%20cold%2Dcausing%20germs.">common cold</a>, <a href="https://journals.lww.com/psychosomaticmedicine/abstract/1999/03000/psychological_stress,_cytokine_production,_and.9.aspx">flu</a> and <a href="https://onlinelibrary.wiley.com/doi/abs/10.1002/smi.3017">COVID</a>. <h2>Stress makes it harder to fight off viruses</h2> When the immune system starts to break down, a virus that would normally have been under control starts to flourish. Once you begin to feel sick, the <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4465119/">stress response</a> rises, making it harder for the immune system to fight off the disease. You may be sick more often and for longer periods of time, without enough immune cells primed and ready to <a href="https://link.springer.com/chapter/10.1007/978-3-030-16996-1_6">fight</a>. In the 1990s, American psychology professor Sheldon Cohen and his colleagues conducted a number of <a href="https://www.cmu.edu/common-cold-project/">studies</a> where healthy people were exposed to an upper respiratory infection, through drops of virus placed directly into their <a href="https://www.nejm.org/doi/full/10.1056/NEJM199108293250903">nose</a>. These participants were then quarantined in a hotel and monitored closely to determine who became <a href="https://theconversation.com/stress-less-it-might-protect-you-from-covid-153361">ill</a>. One of the most important factors predicting who got sick was prolonged psychological <a href="https://journals.sagepub.com/doi/full/10.1177/1745691620942516">stress</a>. <h2>Cortisol suppresses immunity</h2> “Short-term stress” is stress that lasts for a period of minutes to hours, while “chronic stress” persists for several hours per day for <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5964013/#:%7E:text=Therefore%2C%20a%20major%20distinguishing%20characteristic,weeks%20or%20months%20%5B9%5D.">weeks or months</a>. When faced with a perceived threat, psychological or physical, the hypothalamus region of the brain sets off an alarm system. This signals the release of a surge of hormones, including adrenaline and <a href="https://www.embopress.org/doi/full/10.15252/msb.20209510">cortisol</a>. <figure class="align-center "><img src="https://images.theconversation.com/files/616892/original/file-20240903-18-blrqoz.png?ixlib=rb-4.1.0&q=45&auto=format&w=754&fit=clip" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px" srcset="https://images.theconversation.com/files/616892/original/file-20240903-18-blrqoz.png?ixlib=rb-4.1.0&q=45&auto=format&w=600&h=472&fit=crop&dpr=1 600w, https://images.theconversation.com/files/616892/original/file-20240903-18-blrqoz.png?ixlib=rb-4.1.0&q=30&auto=format&w=600&h=472&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/616892/original/file-20240903-18-blrqoz.png?ixlib=rb-4.1.0&q=15&auto=format&w=600&h=472&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/616892/original/file-20240903-18-blrqoz.png?ixlib=rb-4.1.0&q=45&auto=format&w=754&h=593&fit=crop&dpr=1 754w, https://images.theconversation.com/files/616892/original/file-20240903-18-blrqoz.png?ixlib=rb-4.1.0&q=30&auto=format&w=754&h=593&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/616892/original/file-20240903-18-blrqoz.png?ixlib=rb-4.1.0&q=15&auto=format&w=754&h=593&fit=crop&dpr=3 2262w" alt="Human brain illustration" /><figcaption>The hypothalamus sets off an alarm system in response to a real or perceived threat. <a class="source" href="https://www.shutterstock.com/image-illustration/hypothalamus-causes-vasoconstriction-illustration-medical-brain-435142264">stefan3andrei/Shutterstock</a></figcaption></figure> In a typical stress response, <a href="https://www.sciencedirect.com/science/article/abs/pii/S147149060300173X">cortisol levels</a> quickly increase when stress occurs, and then rapidly drop back to normal once the stress has subsided. In the short term, cortisol suppresses inflammation, to ensure the body has enough energy available to respond to an <a href="https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2019.00245/full">immediate threat</a>. But in the longer term, chronic stress can be harmful. A Harvard University study <a href="https://jamanetwork.com/journals/jamapsychiatry/fullarticle/2796097">from 2022</a> showed that people suffering from psychological distress in the lead up to their COVID infection had a greater chance of experiencing long COVID. They <a href="https://jamanetwork.com/journals/jamapsychiatry/fullarticle/2796097">classified</a> this distress as depression, probable anxiety, perceived stress, worry about COVID and loneliness. Those suffering distress had close to a <a href="https://jamanetwork.com/journals/jamapsychiatry/fullarticle/2796097">50% greater risk</a> of long COVID compared to other <a href="https://theconversation.com/being-stressed-out-before-you-get-covid-increases-your-chances-of-long-covid-heres-why-190649">participants</a>. Cortisol has been shown to be high in the most severe cases of <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7102614/">COVID</a>. <h2>Stress causes inflammation</h2> <a href="https://stories.uq.edu.au/imb/the-edge/inflammation/what-is-inflammation/index.html">Inflammation</a> is a short-term reaction to an injury or infection. It is responsible for trafficking immune cells in your body so the right cells are present in the right locations at the right times and at the right <a href="https://link.springer.com/article/10.1007/s12026-014-8517-0">levels</a>. The immune cells also store a memory of that threat to respond faster and more effectively the next <a href="https://theconversation.com/being-stressed-out-before-you-get-covid-increases-your-chances-of-long-covid-heres-why-190649">time</a>. Initially, circulating immune cells detect and flock to the site of <a href="https://www.nature.com/articles/ni1275">infection</a>. Messenger proteins, known as pro-inflammatory cytokines, are released by immune cells, to signal the danger and recruit help, and our immune system responds to neutralise the <a href="https://stories.uq.edu.au/imb/the-edge/inflammation/what-is-inflammation/index.html">threat</a>. During this response to the infection, if the immune system produces too much of these inflammatory chemicals, it can trigger symptoms such as nasal congestion and runny <a href="https://journals.sagepub.com/doi/full/10.1177/1745691620942516">nose</a>. <h2>What about chronic stress?</h2> Chronic stress causes persistently high cortisol secretion, which remains high even in the absence of an immediate <a href="https://theconversation.com/no-you-cant-blame-all-your-health-issues-on-high-cortisol-heres-how-the-hormone-works-203162">stressor</a>. The immune system becomes desensitised and unresponsive to this <a href="https://www.sciencedirect.com/science/article/abs/pii/S1043661816307435">cortisol suppression</a>, increasing low-grade “silent” inflammation and the production of pro-inflammatory cytokines (the messenger proteins). Immune cells become exhausted and start to <a href="https://www.fxmedicine.com.au/blog-post/adrenal-immune-connection">malfunction</a>. The body loses the ability to turn down the inflammatory <a href="https://journals.sagepub.com/doi/full/10.1177/1745691620942516">response</a>. Over time, the immune system changes the way it responds by reprogramming to a “<a href="https://www.unimelb.edu.au/newsroom/news/2021/april/how-stress-can-stop-immune-cells-in-their-tracks">low surveillance mode</a>”. The immune system misses early opportunities to destroy threats, and the process of recovery can take <a href="https://theconversation.com/being-stressed-out-before-you-get-covid-increases-your-chances-of-long-covid-heres-why-190649">longer</a>. <h2>So how can you manage your stress?</h2> We can actively strengthen our immunity and natural defences by managing our <a href="https://theconversation.com/stuck-in-fight-or-flight-mode-5-ways-to-complete-the-stress-cycle-and-avoid-burnout-or-depression-218599">stress levels</a>. Rather than letting stress build up, try to address it early and frequently by: 1) Getting enough sleep Getting enough sleep reduces <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3132857/">cortisol levels</a> and inflammation. During sleep, the immune system <a href="https://link.springer.com/chapter/10.1007/978-1-4939-6578-6_12">releases</a> <a href="https://theconversation.com/sleep-wont-cure-the-coronavirus-but-it-can-help-our-bodies-fight-it-134674">cytokines</a>, which help fight infections and inflammation. 2) Taking regular exercise Exercising helps the lymphatic system (which balances bodily fluids as part of the immune system) circulate and allows immune cells to monitor for threats, while sweating flushes <a href="https://www.healthline.com/nutrition/does-exercise-boost-immune-system">toxins</a>. Physical activity also lowers stress hormone levels through the release of positive brain <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7387807/">signals</a>. 3) Eating a healthy diet Ensuring your diet contains enough nutrients – such as the B vitamins, and the full breadth of minerals like magnesium, iron and zinc – during times of stress has a positive impact on overall stress <a href="https://www.ncbi.nlm.nih.gov/pubmed/22782571">levels</a>. Staying hydrated helps the body to flush out <a href="https://theconversation.com/a-strong-immune-system-helps-ward-off-colds-and-flus-but-its-not-the-only-factor-99512">toxins</a>. 4) Socialising and practising meditation or mindfulness These activities increase endorphins and serotonin, which improve mood and have <a href="https://www.sciencedirect.com/science/article/pii/S2949834123000351">anti-inflammatory effects</a>. Breathing exercises and meditation stimulate the parasympathetic nervous system, which calms down our stress responses so we can “reset” and reduce <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4940234/">cortisol levels</a>.<img style="border: none !important; box-shadow: none !important; margin: 0 !important; max-height: 1px !important; max-width: 1px !important; min-height: 1px !important; min-width: 1px !important; opacity: 0 !important; outline: none !important; padding: 0 !important;" src="https://counter.theconversation.com/content/237456/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /> <a href="https://theconversation.com/profiles/sathana-dushyanthen-1169328">Sathana Dushyanthen</a>, Academic Specialist & Lecturer in Cancer Sciences & Digital Health| Superstar of STEM| Science Communicator, <a href="https://theconversation.com/institutions/the-university-of-melbourne-722">The University of Melbourne</a> Image credits: Shutterstock This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/im-feeling-run-down-why-am-i-more-likely-to-get-sick-and-how-can-i-boost-my-immune-system-237456">original article</a>. </div>

Body

We finally know why some people got COVID while others didn’t

<div class="theconversation-article-body"><a href="https://theconversation.com/profiles/marko-nikolic-1543289">Marko Nikolic</a>, <a href="https://theconversation.com/institutions/ucl-1885">UCL</a> and <a href="https://theconversation.com/profiles/kaylee-worlock-1543639">Kaylee Worlock</a>, <a href="https://theconversation.com/institutions/ucl-1885">UCL</a> Throughout the pandemic, one of the key questions on everyone’s mind was why some people avoided getting COVID, while others caught the virus multiple times. Through a collaboration between University College London, the Wellcome Sanger Institute and Imperial College London in the UK, we set out to answer this question using the world’s first controlled <a href="https://www.nature.com/articles/s41591-022-01780-9">“challenge trial” for COVID</a> – where volunteers were deliberately exposed to SARS-CoV-2, the virus that causes COVID, so that it could be studied in great detail. Unvaccinated healthy volunteers with no prior history of COVID were exposed – via a nasal spray – to an extremely low dose of the original strain of SARS-CoV-2. The volunteers were then closely monitored in a quarantine unit, with regular tests and samples taken to study their response to the virus in a highly controlled and safe environment. For our <a href="https://www.nature.com/articles/s41586-024-07575-x">recent study</a>, published in Nature, we collected samples from tissue located midway between the nose and the throat as well as blood samples from 16 volunteers. These samples were taken before the participants were exposed to the virus, to give us a baseline measurement, and afterwards at regular intervals. The samples were then processed and analysed using single-cell sequencing technology, which allowed us to extract and sequence the genetic material of individual cells. Using this cutting-edge technology, we could track the evolution of the disease in unprecedented detail, from pre-infection to recovery. To our surprise, we found that, despite all the volunteers being carefully exposed to the exact same dose of the virus in the same manner, not everyone ended up testing positive for COVID. In fact, we were able to divide the volunteers into three distinct infection groups (see illustration). Six out of the 16 volunteers developed typical mild COVID, testing positive for several days with cold-like symptoms. We referred to this group as the “sustained infection group”. Out of the ten volunteers who did not develop a sustained infection, suggesting that they were able to fight off the virus early on, three went on to develop an “intermediate” infection with intermittent single positive viral tests and limited symptoms. We called them the “transient infection group”. The final seven volunteers remained negative on testing and did not develop any symptoms. This was the “abortive infection group”. This is the first confirmation of abortive infections, which were previously <a href="https://www.nature.com/articles/s41586-021-04186-8">unproven</a>. Despite differences in infection outcomes, participants in all groups shared some specific novel immune responses, including in those whose immune systems prevented the infection. When we compared the timings of the cellular response between the three infection groups, we saw distinct patterns. For example, in the transiently infected volunteers where the virus was only briefly detected, we saw a strong and immediate accumulation of immune cells in the nose one day after infection. This contrasted with the sustained infection group, where a more delayed response was seen, starting five days after infection and potentially enabling the virus to take hold in these volunteers. In these people, we were able to identify cells stimulated by a key antiviral defence response in both the nose and the blood. This response, called the “interferon” response, is one of the ways our bodies signal to our immune system to help fight off viruses and other infections. We were surprised to find that this response was detected in the blood before it was detected in the nose, suggesting that the immune response spreads from the nose very quickly. <h2>Protective gene</h2> Lastly, we identified a specific gene called HLA-DQA2, which was expressed (activated to produce a protein) at a much higher level in the volunteers who did not go on to develop a sustained infection and could hence be used as a marker of protection. Therefore, we might be able to use this information and identify those who are probably going to be protected from severe COVID. These findings help us fill in some gaps in our knowledge, painting a much more detailed picture regarding how our bodies react to a new virus, particularly in the first couple of days of an infection, which is crucial. We can use this information to compare our data to other data we are currently generating, specifically where we are “challenging” volunteers to other viruses and more recent strains of COVID. In contrast to our current study, these will mostly include volunteers who have been vaccinated or naturally infected – that is, people who already have immunity. Our study has significant implications for future treatments and vaccine development. By comparing our data to volunteers who have never been exposed to the virus with those who already have immunity, we may be able to identify new ways of inducing protection, while also helping the development of more effective vaccines for future pandemics. In essence, our research is a step towards better preparedness for the next pandemic.<img style="border: none !important; box-shadow: none !important; margin: 0 !important; max-height: 1px !important; max-width: 1px !important; min-height: 1px !important; min-width: 1px !important; opacity: 0 !important; outline: none !important; padding: 0 !important;" src="https://counter.theconversation.com/content/233063/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /> <a href="https://theconversation.com/profiles/marko-nikolic-1543289">Marko Nikolic</a>, Principal Research Fellow/Honorary consultant Respiratory Medicine, <a href="https://theconversation.com/institutions/ucl-1885">UCL</a> and <a href="https://theconversation.com/profiles/kaylee-worlock-1543639">Kaylee Worlock</a>, Postdoc Research Fellow, Molecular and Cellular Biology, <a href="https://theconversation.com/institutions/ucl-1885">UCL</a> Image credits: Shutterstock This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/we-finally-know-why-some-people-got-covid-while-others-didnt-233063">original article</a>. </div>

Body

What happens in our body when we encounter and fight off a virus like the flu, SARS-CoV-2 or RSV?

<a href="https://theconversation.com/profiles/lara-herrero-1166059">Lara Herrero</a>, <a href="https://theconversation.com/institutions/griffith-university-828">Griffith University</a> and <a href="https://theconversation.com/profiles/wesley-freppel-1408971">Wesley Freppel</a>, <a href="https://theconversation.com/institutions/griffith-university-828">Griffith University</a> <a href="https://www.labcorp.com/coronavirus-disease-covid-19/covid-news-education/covid-19-vs-flu-vs-rsv-how-tell-difference">Respiratory viruses</a> like influenza virus (flu), SARS-CoV-2 (which causes COVID) and respiratory syncytial virus (RSV) can make us sick by infecting our respiratory system, including the nose, upper airways and lungs. They spread from person to person through respiratory droplets when someone coughs, sneezes, or talks and can cause death in serious cases. But what happens in our body when we first encounter these viruses? Our immune system uses a number of strategies to fight off viral infections. Let’s look at how it does this. <h2>First line of defence</h2> When we encounter respiratory viruses, the <a href="https://www.sciencedirect.com/science/article/pii/S193131281600038X?via%3Dihub/">first line of defence</a> is the physical and chemical barriers in our nose, upper airways, and lungs. Barriers like the mucus lining and hair-like structures on the surface of cells, work together to trap and remove viruses before they can reach deeper into our respiratory system. Our defence also includes our behaviours such as coughing or sneezing. When we blow our nose, the mucus, viruses, and any other pathogens that are caught within it are expelled. But sometimes, viruses manage to evade these initial barriers and sneak into our respiratory system. This activates the cells of our innate immune system. <h2>Patrolling for potential invaders</h2> While our acquired immune system develops over time, our innate immune system is present at birth. It generates “non-specific” immunity by identifying what’s foreign. The cells of innate immunity act like a patrol system, searching for any invaders. These innate cells patrol almost every part of our body, from our skin to our nose, lungs and even internal organs. Our respiratory system has different type of innate cells such – as macrophages, neutrophils and natural killer cells – which patrol in our body looking for intruders. If they recognise anything foreign, in this case a virus, they will initiate an attack response. Each cell type plays a slightly different role. Macrophages, for example, will not only engulf and digest viruses (phagocytosis) but also release a cocktail of different molecules (cytokines) that will warn and recruit other cells to <a href="https://onlinelibrary.wiley.com/doi/full/10.1111/cmi.12580">fight against the danger</a>. In the meantime, natural killer cells, aptly named, attack infected cells, and stop viruses from multiplying and <a href="https://www.nature.com/articles/s41577-021-00558-3">invading our body further</a>. Natural killer cells also promote inflammation, a <a href="https://www.hindawi.com/journals/jir/2018/1467538/">crucial part of the immune response</a>. It helps to recruit more immune cells to the site of infection, enhances blood flow, and increases the permeability of blood vessels, allowing immune cells to reach the infected tissues. At this stage, our immune system is fighting a war against viruses and the result can cause inflammation, fevers, coughs and congestion. <h2>Launching a specific attack</h2> As the innate immune response begins, another branch of the immune system called the adaptive immune system is <a href="https://www.ncbi.nlm.nih.gov/books/NBK21070/">activated</a>. The adaptive immune system is more specific than the innate immune system, and it decides on the correct tools and strategy to fight off the viral invaders. This system plays a vital role in eliminating the virus and providing long-term protection against future infections. Specialised cells called T cells and B cells are key players in acquired immunity. T cells (specifically, helper T cells and cytotoxic T cells) recognise viral proteins on the surface of infected cells: <ul> <li> helper T cells release molecules that <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3764486/">further activate immune cells</a> </li> <li> cytotoxic T cells directly kill infected cells with a very great precision, <a href="https://www.frontiersin.org/articles/10.3389/fimmu.2018.00678/full">avoiding any healthy cells around</a>. </li> </ul> B cells produce antibodies, which are proteins that can bind to viruses, neutralise them, and mark them for <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7247032/">destruction by other immune cells</a>. B cells are a critical part of memory in our immune system. They will remember what happened and won’t forget for years. When the same virus attacks again, B cells will be ready to fight it off and will neutralise it faster and better. Thanks to the adaptive immune system, vaccines for respiratory viruses such as the COVID mRNA vaccine keep us protected from <a href="https://www.health.gov.au/our-work/covid-19-vaccines/our-vaccines/how-they-work">being sick or severely ill</a>. However, if the same virus became mutated, our immune system will act as if it was a new virus and will have to fight in a war again. <h2>Neutralising the threat</h2> As the immune response progresses, the combined efforts of the innate and adaptive immune systems helps control the virus. Infected cells are cleared, and the virus is neutralised and eliminated from the body. As the infection subsides, symptoms gradually improve, and we begin to feel better and to recover. But recovery varies depending on the specific virus and us as individuals. Some respiratory viruses, like rhinoviruses which cause the common cold, may cause relatively mild symptoms and a quick recovery. Others, like the flu, SARS-CoV-2 or severe cases of RSV, may lead to more severe symptoms and a longer recovery time. Some viruses are very strong and too fast sometimes so that our immune system does not have the time to develop a proper immune response to fight them off. <img style="border: none !important; box-shadow: none !important; margin: 0 !important; max-height: 1px !important; max-width: 1px !important; min-height: 1px !important; min-width: 1px !important; opacity: 0 !important; outline: none !important; padding: 0 !important;" src="https://counter.theconversation.com/content/207023/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /> <a href="https://theconversation.com/profiles/lara-herrero-1166059">Lara Herrero</a>, Research Leader in Virology and Infectious Disease, <a href="https://theconversation.com/institutions/griffith-university-828">Griffith University</a> and <a href="https://theconversation.com/profiles/wesley-freppel-1408971">Wesley Freppel</a>, Research Fellow, Institute for Glycomics, <a href="https://theconversation.com/institutions/griffith-university-828">Griffith University</a> Image credits: Getty Images This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/what-happens-in-our-body-when-we-encounter-and-fight-off-a-virus-like-the-flu-sars-cov-2-or-rsv-207023">original article</a>.

Body

Long COVID could be caused by the virus lingering in the body. Here’s what the science says

<a href="https://theconversation.com/profiles/stephen-kent-1283387">Stephen Kent</a>, <a href="https://theconversation.com/institutions/the-university-of-melbourne-722">The University of Melbourne</a> and <a href="https://theconversation.com/profiles/chansavath-phetsouphanh-1436741">Chansavath Phetsouphanh</a>, <a href="https://theconversation.com/institutions/unsw-sydney-1414">UNSW Sydney</a> While most people survive and recover from COVID, for some people symptoms can <a href="https://www.nature.com/articles/s41586-021-03553-9">persist for months</a> or years. When symptoms last longer than 12 weeks, the condition is known as <a href="https://www.cdc.gov/coronavirus/2019-ncov/long-term-effects/index.html">long COVID</a>. Long COVID encompasses up to <a href="https://www.nature.com/articles/s41579-022-00846-2?utm_source=substack&utm_medium=email">200 different symptoms</a>. To determine evidence-based treatments for these symptoms, we need to understand the causes. One factor that may be associated with long COVID is that the virus hasn’t fully cleared from the body after the initial infection. We know from other viruses that viral fragments can remain in different tissues for months or even years. This could be the case with SARS-CoV-2, the virus that causes COVID. Here’s what the science says so far. <h2>Other viruses lurk in the body</h2> Herpesviruses (such as Epstein-Barr virus, the cause of glandular fever), as well as HIV (human immunodeficiency virus) can exist in a “latency state” for life. This means the virus conceals itself within cells and remains dormant. HIV, in particular, can remain dormant in infected cells throughout the body. Even though it’s inactive, it can still promote immune activation and inflammation. Other viruses such as <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7728251/">Zika</a>, <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7492426/">measles</a> and <a href="https://bmjopen.bmj.com/content/6/1/e008859">Ebola</a> have been found in tissues of infected people months or years after initial infection. This viral persistence can <a href="https://www.ahajournals.org/doi/10.1161/circulationaha.105.548156">cause chronic illness</a>. Several studies have shown COVID can also reactivate the Epstein-Barr virus, which has remained in the body in a latent state. Research shows this has been <a href="https://www.jci.org/articles/view/163669">linked to</a> fatigue and problems with thinking and reasoning in <a href="https://www.mdpi.com/2076-0817/10/6/763">people with long COVID</a>. <figure class="align-center "><img src="https://images.theconversation.com/files/530287/original/file-20230606-15-u0ykc8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px" srcset="https://images.theconversation.com/files/530287/original/file-20230606-15-u0ykc8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/530287/original/file-20230606-15-u0ykc8.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/530287/original/file-20230606-15-u0ykc8.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/530287/original/file-20230606-15-u0ykc8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/530287/original/file-20230606-15-u0ykc8.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/530287/original/file-20230606-15-u0ykc8.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" alt="Man looks at laptop, confused" /><figcaption>Latent viruses can cause fatigue and problems with thinking and reasoning. <a class="source" href="https://unsplash.com/photos/4-EeTnaC1S4">Wes Hicks/Unsplash</a></figcaption></figure> <h2>How do we know COVID stays in the body?</h2> Several studies have identified the genetic sequences of SARS-CoV-2 (RNA) as well as SARS-CoV-2 proteins in tissues and stool (poo) samples months following infection. These studies include multiple autopsy reports that <a href="https://www.nature.com/articles/s41586-022-05542-y">found viral RNA and protein in a variety of tissues</a> from people who died up to seven months after infection. SARS-CoV-2 RNA was detected in at least half the samples of heart, lymph glands, eye, nerve, brain and lung tissue tested. In people who survived, <a href="https://www.nature.com/articles/s41586-021-03207-w">viral RNA was found</a> four months after infection within intestinal tissues obtained through colonoscopy, when a thin tube is used to take tissue from the large intestine. These patients had asymptomatic COVID and were PCR-negative from swabs of the nose and throat at four months. A 2022 study found SARS-CoV-2 in the stool of about half of the participants in the first week after infection. At four months, there was no virus present in the respiratory tract but <a href="https://doi.org/10.1016/j.medj.2022.04.001">12.7% of stool samples were RNA positive</a>. A further 3.8% of faecal samples remained positive for RNA at seven months. <a href="https://doi.org/10.1016/S2213-2600(21)00240-X">Initial studies</a> did not always suggest a strong relationship between the long-term detection of SARS-CoV-2 and long COVID symptoms. But more recently, the presence of SARS-CoV-2 RNA (or protein translated from RNA) in the <a href="https://academic.oup.com/cid/article/76/3/e487/6686531">blood</a> and gut tissue was found to <a href="https://doi.org/10.1053/j.gastro.2022.04.037">increase the likelihood</a> of developing long COVID symptoms. <figure class="align-center "><img src="https://images.theconversation.com/files/530289/original/file-20230606-27-p7vgd8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px" srcset="https://images.theconversation.com/files/530289/original/file-20230606-27-p7vgd8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=335&fit=crop&dpr=1 600w, https://images.theconversation.com/files/530289/original/file-20230606-27-p7vgd8.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=335&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/530289/original/file-20230606-27-p7vgd8.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=335&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/530289/original/file-20230606-27-p7vgd8.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=421&fit=crop&dpr=1 754w, https://images.theconversation.com/files/530289/original/file-20230606-27-p7vgd8.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=421&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/530289/original/file-20230606-27-p7vgd8.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=421&fit=crop&dpr=3 2262w" alt="Person gets a blood test" /><figcaption>The presence of SARS-CoV-2 in the blood increases the likelihood of developing long COVID symptoms. <a class="source" href="https://unsplash.com/photos/ufwC2cmbaaI">Nguyễn Hiệp/Unsplash</a></figcaption></figure> <h2>How might the delay in clearing the virus impact people with long COVID?</h2> Delayed clearance of SARS-CoV-2 particles in different parts of the body could drive illness through several potential processes: 1) Inflammation. The continued immune stimulation by viral proteins causes inflammation, makes our immune system tired, and alters how our immune cells work as time goes on. <a href="https://www.nature.com/articles/s41590-021-01113-x">We have previously shown</a> immune dysfunction and inflammation persist up to eight months in people with long COVID that initially had mild to moderate disease. 2) Activation of other dormant viruses. The continued immune response to persistent SARS-CoV-2 can cause reactivation of latent viruses. Antibodies reactive to Epstein-Barr virus are elevated in people with long COVID suggesting Epstein-Barr virus <a href="https://doi.org/10.1101/2022.08.09.22278592">reactivation</a>, likely through activating the immune system. Other latent viruses, such as human endogenous retroviruses (HERVs; ancient viruses that have become a part of our DNA, like a genetic fossil) have recently been shown to become reactivated after infection. HERV proteins <a href="https://www.sciencedirect.com/science/article/pii/S2589004223006818">were detected</a> in blood cells and tissues of COVID patients. These proteins could potentially drive inflammatory processes in long COVID. <figure class="align-center "><img src="https://images.theconversation.com/files/530290/original/file-20230606-27-6s4g00.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px" srcset="https://images.theconversation.com/files/530290/original/file-20230606-27-6s4g00.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=400&fit=crop&dpr=1 600w, https://images.theconversation.com/files/530290/original/file-20230606-27-6s4g00.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=400&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/530290/original/file-20230606-27-6s4g00.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=400&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/530290/original/file-20230606-27-6s4g00.jpg?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=503&fit=crop&dpr=1 754w, https://images.theconversation.com/files/530290/original/file-20230606-27-6s4g00.jpg?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=503&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/530290/original/file-20230606-27-6s4g00.jpg?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=503&fit=crop&dpr=3 2262w" alt="3D illustration of the Epstein-Barr virus in green and red" /><figcaption>Reactivation of the Epstein-Barr virus could drive inflammation in long COVID. <a class="source" href="https://www.shutterstock.com/image-illustration/epsteinbarr-virus-ebv-herpes-which-causes-556379407">Shutterstock</a></figcaption></figure> 3) Antibodies made by combating SARS-CoV-2 could become “self” reactive. These autoantibodies (antibodies produced by our immune system that mistakenly target and attack our own body’s tissues or organs) might cross-react with host receptors or proteins and <a href="https://www.nature.com/articles/s41577-020-00458-y">drive autoimmune</a> disease. Importantly, recent studies have shown new onset of autoimmune diseases (such as type 1 diabetes, inflammatory bowel disease and psoriasis) are significantly associated with SARS-CoV-2 infection and <a href="https://www.nature.com/articles/s41584-023-00964-y">a link between autoimmunity and long COVID</a> is plausible. This suggests COVID not only has immediate health impacts but could also potentially trigger long-term changes in the immune system. While the studies mentioned above provide initial evidence of persistence of SARS-CoV-2 long after initial infection, more studies are needed to show a convincing link between lingering virus and long COVID. This should include examination of viral RNA and protein in both blood and tissues in people with long COVID independent of disease severity. And it must involve well-developed cohort studies that track large groups of people internationally. <a href="https://clinicaltrials.gov/ct2/show/NCT05668091">Several</a> <a href="https://clinicaltrials.gov/ct2/show/NCT05576662">trials are underway</a> to assess whether treating long COVID with antivirals such as Paxlovid may reduce viral antigens and improve symptoms, although this remains experimental.<img style="border: none !important; box-shadow: none !important; margin: 0 !important; max-height: 1px !important; max-width: 1px !important; min-height: 1px !important; min-width: 1px !important; opacity: 0 !important; outline: none !important; padding: 0 !important;" src="https://counter.theconversation.com/content/205025/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /> <a href="https://theconversation.com/profiles/stephen-kent-1283387">Stephen Kent</a>, Professor and Laboratory Head, <a href="https://theconversation.com/institutions/the-university-of-melbourne-722">The University of Melbourne</a> and <a href="https://theconversation.com/profiles/chansavath-phetsouphanh-1436741">Chansavath Phetsouphanh</a>, Senior Research Associate, Kirby Institute, <a href="https://theconversation.com/institutions/unsw-sydney-1414">UNSW Sydney</a> This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/long-covid-could-be-caused-by-the-virus-lingering-in-the-body-heres-what-the-science-says-205025">original article</a>. Images: Getty

Body

COVID nasal sprays may one day prevent and treat infection

We have vaccines to boost our immune response to SARS-CoV-2, the virus that causes COVID. We have medicines you can take at home (and in hospital) to treat COVID. Now researchers are trialling something new. They want to develop drugs that stop the virus getting into the body in the first place. That includes nasal sprays that stop the virus attaching to cells in the nose. Other researchers are looking at the potential for nasal sprays to stop the virus replicating in the nose, or to make the nose a hostile place to enter the body. Here’s where the science is up to and what we can expect next. <h2>How could we block the virus?</h2> “Viral blockade”, as the name suggests, is a simple premise based on blocking SARS-CoV-2. In other words, if something gets in its way, the virus cannot attach to a cell and it can’t infect you. As SARS-CoV-2 is a respiratory virus, it makes sense to deliver this type of medicine where the virus mainly enters the body – via the nose, in a nasal spray. There are various groups around the world working on this concept. Some research is still being conducted in the lab. Some agents have progressed to preliminary human trials. None are yet available for widespread use. Heparin Heparin is a common medicine that’s been used for decades to thin the blood. Studies in mice show that when heparin is delivered via the nose, <a href="https://link.springer.com/article/10.1007/s11095-022-03191-4" target="_blank" rel="noopener">it’s safe</a> and <a href="https://journals.asm.org/doi/10.1128/JVI.01987-20" target="_blank" rel="noopener">effective</a> in preventing the virus binding to nose cells. Researchers believe heparin binds to the virus itself and stops the virus attaching to the cells it’s trying to infect. A <a href="https://clinicaltrials.gov/ct2/show/NCT05204550" target="_blank" rel="noopener">clinical trial</a> is being <a href="https://www.premier.vic.gov.au/covid-nasal-spray-treatment-clinical-trials-begin" target="_blank" rel="noopener">conducted in Victoria</a> in collaboration between multiple Melbourne-based research centres and the University of Oxford. Covixyl-V Covixyl-V (ethyl lauroyl arginine hydrochloride) is another nasal spray <a href="https://assets.researchsquare.com/files/rs-911449/v1/0577f1f1-56f8-476f-97f6-d27d332ea9ca.pdf?c=1643375660" target="_blank" rel="noopener">under development</a>. It aims to prevent COVID by blocking or modifying the cell surface to prevent the virus from infecting. This compound has been explored for use in various viral infections, and <a href="https://assets.researchsquare.com/files/rs-911449/v1/0577f1f1-56f8-476f-97f6-d27d332ea9ca.pdf?c=1643375660" target="_blank" rel="noopener">early studies</a> in cells and small animals has shown it can prevent attachment of SARS-CoV-2 and reduce the overall viral load. Iota-carrageenan This molecule, which is extracted from seaweed, acts by blocking virus entry into <a href="https://www.frontiersin.org/articles/10.3389/fviro.2021.746824/full" target="_blank" rel="noopener">airway cells</a>. One study of about 400 health-care workers suggests a nasal spray may reduce the incidence of COVID <a href="https://www.dovepress.com/efficacy-of-a-nasal-spray-containing-iota-carrageenan-in-the-postexpos-peer-reviewed-fulltext-article-IJGM" target="_blank" rel="noopener">by up to 80%</a>. IGM-6268 This is <a href="https://www.nature.com/articles/s41586-021-03673-2" target="_blank" rel="noopener">an engineered antibody</a> that binds to SARS-CoV-2, <a href="https://www.sciencedaily.com/releases/2021/06/210603171306.htm" target="_blank" rel="noopener">blocking</a> the virus from attaching to cells in the nose. A nasal and oral (mouth) spray are in a clinical trial <a href="https://clinicaltrials.gov/ct2/show/NCT05184218?term=IGM-6268&draw=2&rank=2" target="_blank" rel="noopener">to assess safety</a>. Cold atmospheric plasma This is a gas that contains charged particles. At cold temperatures, it can <a href="https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0165322" target="_blank" rel="noopener">alter the surface</a> of a cell. A <a href="https://www.thno.org/v12p2811.htm" target="_blank" rel="noopener">lab-based study</a> shows the gas changes expression of receptors on the skin that would normally allow the virus to attach. This results in less SARS-CoV-2 attachment and infection. Scientists now think this technology could be adapted to a nasal spray to prevent SARS-CoV-2 infection. <h2>How could we stop the virus replicating?</h2> Another tactic is to develop nasal sprays that stop the virus replicating in the nose. Researchers are designing genetic fragments that bind to the viral RNA. These fragments – known as “<a href="https://www.nature.com/articles/s41467-022-32216-0" target="_blank" rel="noopener">locked nucleic acid antisense oligonucleotides</a>” (or LNA ASOs for short) – put a proverbial spanner in the works and stop the virus from replicating. A spray of these genetic fragments delivered into the nose <a href="https://www.nature.com/articles/s41467-022-32216-0" target="_blank" rel="noopener">reduced virus replication in the nose</a> and prevented disease in small animals. <h2>How could we change the nose?</h2> A third strategy is to change the nose environment to make it less hospitable for the virus. That could be by using a nasal spray to change moisture levels (with saline), alter the pH (making the nose more acidic or alkaline), or adding a virus-killing agent (iodine). Saline can reduce the amount of <a href="https://jamanetwork.com/journals/jamaotolaryngology/fullarticle/2768627" target="_blank" rel="noopener">SARS-CoV-2 in the nose</a> by simply washing away the virus. One study has even found that saline nasal irrigation <a href="https://journals.sagepub.com/doi/10.1177/01455613221123737" target="_blank" rel="noopener">can lessen COVID disease</a> severity. But we would need further research into saline sprays. An Australian-led study has found that an iodine-based nasal spray <a href="https://www.theajo.com/article/view/4466/html" target="_blank" rel="noopener">reduced the viral load</a> in the nose. Further <a href="https://www.uwa.edu.au/news/Article/2022/February/Study-finds-nasal-spray-could-aid-battle-against-COVID" target="_blank" rel="noopener">clinical trials</a> are planned. <a href="https://www.sciencedirect.com/science/article/pii/S1386653222001809#!" target="_blank" rel="noopener">One study</a> used a test spray – containing ingredients including eucalyptus and clove oils, potassium chloride and glycerol. The aim was to kill the virus and change the acidity of the nose to prevent the virus attaching. This novel formulation has been tested in the lab and in a <a href="https://www.sciencedirect.com/science/article/pii/S1386653222001809#!" target="_blank" rel="noopener">clinical trial</a> showing it to be safe and to reduce infection rate from about 34% to 13% when compared to placebo controls. <h2>Barriers ahead</h2> Despite promising data so far on nasal sprays for COVID, one of the <a href="https://www.nature.com/articles/d41586-022-03341-z" target="_blank" rel="noopener">major barriers</a> is keeping the sprays in the nose. To overcome this, most sprays need multiple applications a day, sometimes every few hours. So based on what we know so far, nasal sprays will not singlehandedly beat COVID. But if they are shown to be safe and effective in clinical trials, and receive regulatory approval, they might be another tool to help prevent it. This article originally appeared on <a href="https://theconversation.com/covid-nasal-sprays-may-one-day-prevent-and-treat-infection-heres-where-the-science-is-up-to-193840" target="_blank" rel="noopener">The Conversation</a>. Image: Shutterstock

Body

Why has my cold dragged on so long, and how do I know when it’s morphed into something more serious?

Common colds are caused by viruses. There are no effective cures, and antibiotics do not work on viruses, so treatment is targeted at managing the symptoms until your immune system has cleared the cold. So why might someone go to a doctor at all for a cold? Well, occasionally a cold might turn into something more serious requiring assessment and specific treatment, and a GP visit could be warranted. Or you may just want reassurance and advice. <h2>Don’t rush to the GP for something totally normal</h2> Problems arise when there too many unwarranted visits to GPs for cold symptoms. Studies have shown <a href="https://www.annfammed.org/content/11/1/5" target="_blank" rel="noopener">antibiotics</a> are <a href="https://onlinelibrary.wiley.com/doi/abs/10.5694/mja16.01042" target="_blank" rel="noopener">still prescribed widely</a> for viral colds, even though they don’t help, and this contributes to antibiotic resistance. It hastens the arrival of an era when many antibiotics simply don’t work at all. On average, children have <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7152362/" target="_blank" rel="noopener">four to six colds</a> per year, while in adults the average is <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7152362/" target="_blank" rel="noopener">two to three</a>. Some people are more <a href="https://www.sciencedirect.com/science/article/abs/pii/S1530156705601189?via%3Dihub" target="_blank" rel="noopener">prone</a> to colds, but we don’t know exactly why. The usual cold persists about one week, although 25% last two weeks. In one <a href="https://journals.asm.org/doi/10.1128/jcm.35.11.2864-2868.1997" target="_blank" rel="noopener">study</a> with 346 adults, the infection lasted 9.5 to 11 days. Cold symptoms may last longer in younger children. One <a href="https://publications.aap.org/pediatrics/article-abstract/87/2/129/56810/Upper-Respiratory-Tract-Infections-in-Young?redirectedFrom=fulltext" target="_blank" rel="noopener">study</a> showed an average duration of colds ranged from 6.6 to 9 days. But symptoms lasted more than 15 days in 6.5% of 1-3 year old children in home care, and 13.1% of 2-3 year old children in day care. A cough tends to last longer than other symptoms, and often beyond the actual viral infection. The average <a href="https://www.annfammed.org/content/11/1/5" target="_blank" rel="noopener">duration</a> of a cough is about 17.8 days. <h2>Discoloured sputum, cough or snot</h2> Discoloured mucus in snot or cough is a common trigger for requesting antibiotics from a GP. But as we know, antibiotics are useless against a virus. They only work against bacterial infection. In fact, thick or coloured nasal mucus secretion is common following colds. Only a tiny proportion <a href="https://europepmc.org/article/pmc/pmc7151789" target="_blank" rel="noopener">involve</a> bacterial infection. When it happens, this is termed <a href="https://www.nps.org.au/australian-prescriber/articles/treating-acute-sinusitis-3" target="_blank" rel="noopener">acute rhinosinusitis</a>. But antibiotics are not recommended unless it lasts more than ten to 14 days and there are <a href="https://europepmc.org/article/pmc/pmc7151789" target="_blank" rel="noopener">signs</a> of bacterial sinusitis infection, such as: <ul> <li>symptoms worsening after improvement in the original cold</li> <li>return of fever and</li> <li>strong facial pain.</li> </ul> A prolonged cough after colds is usually caused by an irritated throat or the clearing of sticky mucus coming down from the nose. The cough may sound moist (so wrongly called “chesty”) due to the phlegm, but only small amounts of phlegm are coughed up. Yellow or green coloured mucus is often interpreted as a <a href="http://theconversation.com/health-check-what-you-need-to-know-about-mucus-and-phlegm-33192" target="_blank" rel="noopener">sign</a> of bacterial infection. But yellow or green sputum alone <a href="https://www.tandfonline.com/doi/full/10.1080/02813430902759663" target="_blank" rel="noopener">does not</a> mean you have a serious bacterial infection. One study found being prescribed antibiotics under these circumstances <a href="https://erj.ersjournals.com/content/38/1/119" target="_blank" rel="noopener">failed</a> to shorten recovery time. Nasal saline sprays and washes can be used to rinse out the nose and sinuses and possibly <a href="https://dtb.bmj.com/content/57/4/56" target="_blank" rel="noopener">shorten</a> rhinosinusitis and cough after colds. <h2>Could it just be hayfever, or another underlying issue?</h2> Hayfever or allergic rhinitis is a common cause for prolonged symptoms after a cold, especially cough and nasal congestion and maybe also sneezing. The damage in the upper airways following a viral infection may allow airborne allergens to trigger hayfever. Self-medicating with antihistamines, nasal saline spray or intranasal steroids is worthwhile if <a href="https://theconversation.com/health-check-why-do-i-have-a-cough-and-what-can-i-do-about-it-119172" target="_blank" rel="noopener">allergic rhinitis</a> is suspected. There may be other reasons for persistence of cough, such as exacerbation of underlying asthma or chronic lung disease. If so, this may require a visit to your GP. <h2>What about bronchitis or pneumonia?</h2> Many people worry about developing a chest infection after a cold. Acute bronchitis is a self-limiting infectious disease characterised by acute cough with or without sputum but without <a href="https://www.nhs.uk/conditions/pneumonia/" target="_blank" rel="noopener">signs of pneumonia</a> (such as high temperatures and feeling breathless). Most acute bronchitis cases are caused by viruses. Antibiotics are often prescribed, but produce <a href="https://www.tandfonline.com/doi/full/10.1080/14787210.2016.1193435" target="_blank" rel="noopener">no significant clinical improvement</a> compared with placebo, so are not recommended. Pneumonia is a potentially serious secondary disease that <a href="https://pubmed.ncbi.nlm.nih.gov/28159155/" target="_blank" rel="noopener">may follow</a> an episode of flu in a small number of cases, but is <a href="https://www.ncbi.nlm.nih.gov/books/NBK532961/" target="_blank" rel="noopener">relatively rare</a> following a cold. Symptoms and signs of pneumonia feature heavily in the list of warning signs that signal the need for a medical assessment. <h2>When should I seek medical help for a cough or a cold?</h2> Contact a GP if you experience: <ul> <li>shortness of breath or trouble breathing</li> <li>feeling faint or dizzy</li> <li>chest pain</li> <li>dehydration</li> <li>fever or cough symptoms that improve but then return or worsen</li> <li>worsening of chronic medical conditions such as asthma.</li> </ul> This is not a complete list, but may guide you on what to expect and what to watch out for. You might also contact your GP (perhaps for a telehealth consult) if you are finding your symptoms very unpleasant, or are concerned your condition is more serious or prolonged than expected. You might just need reassurance and education about self care options. This article originally appeared on <a href="https://theconversation.com/why-has-my-cold-dragged-on-so-long-and-how-do-i-know-when-its-morphed-into-something-more-serious-190429" target="_blank" rel="noopener">The Conversation</a>. Image: Shutterstock

Body

COVID-19 virus-detecting mask can alert of exposure via your smartphone

Move over <a href="https://cosmosmagazine.com/health/covid/rise-of-rapid-antigen-testing/" target="_blank" rel="noreferrer noopener">inaccurate RATs</a>. Get out of my nose and throat PCR swab tests. There’s a new method of COVID-19 detection and it’s wearable. A research team from Tongji University in China, has created a face mask that can detect COVID-19 (as well as other common respiratory viruses such as colds and influenza) and send an alert to your smartphone. The mask is highly sensitive, with the inbuilt sensor able to detect the virus <a href="https://cosmosmagazine.com/health/lets-clear-the-air-on-ventilation-cosmos-weekly-taster/" target="_blank" rel="noreferrer noopener">in the air</a> after only ten minute’s exposure at extremely low concentrations – far less than produced by sneezing, coughing or talking. “Previous research has shown face mask wearing can reduce the risk of spreading and contracting the disease. So, we wanted to create a mask that can detect the presence of virus in the air and alert the wearer,” says Yin Fang, an author of the study and a material scientist at Shanghai Tongji University. <div class="newsletter-box"> <div id="wpcf7-f6-p214217-o1" class="wpcf7" dir="ltr" lang="en-US" role="form"> <form class="wpcf7-form mailchimp-ext-0.5.62 spai-bg-prepared init" action="/science/covid-19-detecting-mask-smartphone/#wpcf7-f6-p214217-o1" method="post" novalidate="novalidate" data-status="init"> <input class="wpcf7-form-control wpcf7-text referer-page" name="referer-page" type="hidden" value="https://cosmosmagazine.com/people/" data-value="https://cosmosmagazine.com/people/" aria-invalid="false" /> </form> </div> </div> The sensor on the mask has tiny synthetic molecules – called ‘aptamers’ – which are able to be tweaked to detect proteins unique to specific pathogens, such as SARS-Cov-2, H5N1 (colloquially known as ‘bird flu’) and H1N1 (‘swine flu’). Once the aptamer detects the virus, the sensor amplifies the signal via a specialised component known as an <a href="https://www.researchgate.net/publication/344400852_Ion-Gated_Transistor_An_Enabler_for_Sensing_and_Computing_Integration" target="_blank" rel="noreferrer noopener">ion-gate transistor</a> (which is highly sensitive and able to detect very low voltage signals) and sends an alert to the user’s phone. “Our mask would work really well in spaces with poor ventilation, such as elevators or enclosed rooms, where the <a href="https://cosmosmagazine.com/health/covid-ventilation-standards/" target="_blank" rel="noreferrer noopener">risk of getting infected is high</a>,” Fang says. The device is also highly customisable and can be swiftly modified to detect new and emerging threats. This is not the first time <a href="https://cosmosmagazine.com/health/smart-masks-to-detect-covid-19/" target="_blank" rel="noreferrer noopener">‘smart masks’ have been created</a> to detect COVID-19, but what sets these devices apart is their sensitivity and ‘tunability’ to different viruses. The team is working on reducing the detection time and increasing the sensitivity of their devices. In the future, they hope the technology could be expanded to further applications and wearables for other conditions such as cancers and heart diseases. “Currently, doctors have been relying heavily on their experiences in diagnosing and treating diseases. But with richer data collected by wearable devices, disease diagnosis and treatment can become more precise,” Fang says.  <img id="cosmos-post-tracker" style="opacity: 0; height: 1px!important; width: 1px!important; border: 0!important; position: absolute!important; z-index: -1!important;" src="https://syndication.cosmosmagazine.com/?id=214217&title=COVID-19+virus-detecting+mask+can+alert+of+exposure+via+your+smartphone" width="1" height="1" />  <div id="contributors"> <a href="https://cosmosmagazine.com/science/covid-19-detecting-mask-smartphone/" target="_blank" rel="noopener">This article</a> was originally published on <a href="https://cosmosmagazine.com" target="_blank" rel="noopener">Cosmos Magazine</a> and was written by <a href="https://cosmosmagazine.com/contributor/clare-kenyon" target="_blank" rel="noopener">Clare Kenyon</a>. Clare Kenyon is a science journalist for Cosmos. An ex-high school teacher, she is currently wrangling the death throes of her PhD in astrophysics, has a Masters in astronomy and another in education. Clare also has diplomas in music and criminology and a graduate certificate of leadership and learning. Image: Getty Images </div>

Technology

Why it's important to install updates on your device

Ever wondered if installing updates is worth the bother? Here's what you need to know. Whether you use an iPad, tablet, laptop or desktop computer, you have probably been prompted at one point to update your device. While these pop-up boxes may look like the spam you see on websites, they’re far from it. The device you use will have an operating system built into it, so iPads or Mac laptops will operate on Apple’s iOS system while tablets and laptops not made by Apple will run on Windows. Whichever system your device uses, it will eventually need an update. While it can be easy to dismiss the update notifications when they pop up on your screen, here’s why you shouldn’t. What’s the point? When a software program is developed, it is put through tests and quality checks and only once that has been satisfied is it released to the general public. However, once the software is out there in the world, and being used in real-life environments, it can come across little issues which get reported back to the developer. These companies then fix the issues and release the solutions as software updates. For electronic devices, especially laptops and desktop computers, security issues can be a big problem. Software updates include security solutions to malware or hackers, as well as fixes to bugs and any other issues that have occurred since the software was released. Is it different to an upgrade? While they may sound similar, a software update and an upgrade provide two different functions. An update will install a current version of your software to your device, so basically updating your existing version of iOS or Windows. On the other side of the coin is an upgrade, which allows you to upgrade a program to its next major version. Generally, there will be a cost for a software upgrade. How do I get updates? If your device is connected to the internet and it detects an update is available, it will prompt you with a notification message. This will alert you to the fact that an update is available and advise you of the next steps to step, such as clicking on a button on the notification message which will start the process for you. In System Settings on Apple devices and Control Panel for Windows devices, there’s an option where you can turn on automatic updating. This can provide significant benefits, such as improved security and reliability. Ultimately, software updates exist for a reason. While they may take a little while to download and install on your device, they are worth it. So, the next time that grey box pops up on your screen saying there’s an update available, click on it. It’ll keep your tablet or laptop secure and up-to-date with your software’s latest features. Image credits: Getty Images

Technology

First local monkeypox case recorded in NSW

The first case of locally-acquired monkeypox has been recorded in New South Wales, with authorities confirming that 42 people have been infected with the virus to date. Although most contracted monkeypox overseas, two people were infected in other parts of Australia. The announcement, made by NSW Health on Sunday, comes as a first for NSW a week after the JYNNEOS vaccination program was launched for those most at risk from the virus. “NSW Health is urging the community, particularly gay, bisexual and other men who have sex with men (GBMSM), to continue to be vigilant for the symptoms of monkeypox following local transmission of the virus in NSW,” NSW Health said. Symptoms - which include a rash or lesions around the genital area, headache, body aches and fever - commonly appear between seven to 14 days after prolonged skin-to-skin contact with an infected person. Illness generally lasts for two to four weeks, with most experiencing mild symptoms that can be lessened with regular over-the-counter pain medicines and oral fluids and monitored by their GP, according to <a href="https://www.health.nsw.gov.au/Infectious/factsheets/Pages/monkeypox.aspx" target="_blank" rel="noopener">NSW Health</a>. For those with severe illness, antiviral medications are also available. “It is important that people with these symptoms avoid close contact with others, including sexual activity, as condoms are not effective at preventing the transmission of monkeypox,” NSW Health Executive Director of Health Protection Richard Broome said in a <a href="https://www.health.nsw.gov.au/news/Pages/20220821_00.aspx" target="_blank" rel="noopener">statement</a>. NSW Health also warns that monkeypox can also be transmitted by respiratory droplets during the initial infectious period and from contact with contaminated clothing, linen and other items. The news comes after Victorian authorities reported monkeypox was spreading in Melbourne last week, which was the first widespread example of local transmission in Australia since the global outbreak began. Prior to the 2022 outbreak, cases of monkeypox have mostly been reported in Central and Western African countries, with the <a href="https://doi.org/10.1136/bmjgh-2022-009838" target="_blank" rel="noopener">first human case reported</a> in the Democratic Republic of Congo in 1970. According to the <a href="https://www.cdc.gov/poxvirus/monkeypox/response/2022/world-map.html" target="_blank" rel="noopener">CDC</a>, 41,358 confirmed cases of monkeypox have been recorded as of publication, with 40,971 reported in locations without any historical cases of the virus, with a total of 89 in Australia and four in New Zealand. Image: Getty Images

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Poxy McPoxface, TRUMP-22, Mpox: Public called on to rename monkeypox virus

The World Health Organisation has called on the expertise of the public to help them rename the monkeypox virus after claiming the name is "misleading". Names for viruses are usually chosen by a committee behind closed doors, but the WHO has decided to open up the process to allow submissions from all over the world. Names such as Poxy McPoxface, TRUMP-22 or Mpox have been put forward so far, prompting the WHO to say they will choosing a serious name. WHO spokesperson Fadela Chaib said, "I am sure we will not come up with a ridiculous name." Dozens of submissions have now been made from a range of contributors including academics, doctors, and a gay community activist. One more technical submission came from Harvard Medical School emergency physician Jeremy Faust, who said the virus should simply be called OPOXID-22. Another proposal, TRUMP-22, appeared to be refer to former US President Donald Trump who used the controversial term "Chinese virus" for the new coronavirus, although its author said it stood for "Toxic Rash of Unrecognized Mysterious Provenance of 2022". Pressure is growing for a new name for the disease, largely because critics say it is misleading, since the virus did not originate in monkeys. A group of leading scientists wrote a position paper in June calling for a name that was "neutral, non-discriminatory and non-stigmatizing" amid fears the name can be used in a racist way. "It's very important we find a new name for monkeypox because this is best practice not to create any offence to an ethical group, a region, a country, an animal etc," Miss Chaib said. "The WHO is very concerned by this issue and we want to find a name that is not stigmatising," she added without giving a timeline of when the new name may be decided. Monkeypox was first discovered in 1958 and named after the first animal to show symptoms. The WHO declared the current outbreak a public health emergency in July having reported more than 32,000 cases from over 80 countries. Image credits: Getty Images

Caring

Another booster recommended to Aussies

A fourth Covid vaccine will be made available to more Australians as infections continue to soar across the country. The Australian Technical Advisory Group on Immunisation (ATAGI) met with health officials agreeing to expand the booster program to those aged over 50 as well as some eligibility for those in their 30s. Health Minister Mark Butler is expected to make the announcement on Friday and is urging Aussies to pull up their sleeves. “I’m very confident that, if there’s an expansion of the fourth doses by ATAGI over the next couple of days, we’ve got more than enough vaccine in the warehouses and more than enough capacity in our pharmacies in our GP surgeries to deliver that as soon as people want it,” he said. “The real challenge is to get people lining up to get it. There’s more than five million people who are overdue their third dose, so it’s more than six months since they had their second dose. “They’re still overdue their third dose and I encourage them to go out and get it.” The fourth shot is currently only available for vulnerable people and Aussies aged 65 and over. Australia is on average recording 33,000 Covid-19 cases every day. Image: Shutterstock

Body

Can your mobile phone get a virus?

With nearly <a href="https://www.bankmycell.com/blog/how-many-phones-are-in-the-world" target="_blank" rel="noopener">84%</a> of the world’s population now owning a smartphone, and our dependence on them growing all the time, these devices have become an attractive avenue for scammers. Last year, cyber security company Kaspersky detected nearly <a href="https://securelist.com/mobile-malware-evolution-2021/105876/" target="_blank" rel="noopener">3.5 million</a> malicious attacks on mobile phone users. The spam messages we get on our phones via text message or email will often contain links to viruses, which are a type of malicious software (malware). There’s a decent chance that at some point you’ve installed <a href="https://ieeexplore.ieee.org/stamp/stamp.jsp?arnumber=6138859" target="_blank" rel="noopener">malware</a> that infected your phone and worked (without you noticing) in the background. According to a global report commissioned by private company Zimperium, more than <a href="https://www.zimperium.com/global-mobile-threat-report/" target="_blank" rel="noopener">one-fifth</a> of mobile devices have encountered malware. And four in ten mobiles worldwide are <a href="https://blog.checkpoint.com/2020/08/06/achilles-small-chip-big-peril/" target="_blank" rel="noopener">vulnerable</a> to cyber attacks. But how do you know if your phone has been targeted? And what can you do? How does a phone get infected? Like personal computers, phones can be compromised by malware. For example, the Hummingbad virus infected <a href="https://www.wired.co.uk/article/hummingbad-malware-10-million-android-devices" target="_blank" rel="noopener">ten million</a> Android devices within a few months of its creation in 2016, and put as many as <a href="https://www.theguardian.com/technology/2016/jul/06/what-is-hummingbad-malware-android-devices-checkpoint" target="_blank" rel="noopener">85 million</a> devices at risk. Typically, a phone virus works the same way as a computer virus: a malicious code infects your device, replicates itself and spreads to other devices by auto-messaging others in your contact list or auto-forwarding itself as an email. A virus can limit your phone’s functionality, send your personal information to hackers, send your contacts spam messages linking to malware, and even allow the virus’s operator to “spy” on you by capturing your screen and keyboard inputs, and tracking your geographical location. In Australia, Scamwatch received <a href="https://www.scamwatch.gov.au/news-alerts/missed-delivery-call-or-voicemail-flubot-scams" target="_blank" rel="noopener">16,000 reports</a> of the Flubot virus over just eight weeks in 2021. This <a href="https://suretyit.com.au/blog/what-is-the-flubot-virus/" target="_blank" rel="noopener">virus</a> sends text messages to Android and iPhone users with links to malware. Clicking on the links can lead to a malicious app being downloaded on your phone, giving scammers access to your personal information. Flubot scammers regularly change their <a href="https://www.bitdefender.com/blog/labs/new-flubot-and-teabot-global-malware-campaigns-discovered" target="_blank" rel="noopener">target countries</a>. According to cyber security firm Bitdefender, FluBot operators targeted Australia, Germany, Poland, Spain, Austria and other European countries between December 1 2021 and January 2 of this year. Is either Apple or Android more secure? While Apple devices are generally considered more secure than Android, and <a href="https://ieeexplore.ieee.org/stamp/stamp.jsp?arnumber=6637558" target="_blank" rel="noopener">less prone</a> to virus attacks, iPhone users who “jailbreak” or modify their phone open themselves up to security vulnerabilities. Similarly, Android users who install apps from outside the Google Play store increase their risk of installing malware. It’s recommended all phone users stay on guard, as both Apple and Android are <a href="https://www.forbes.com/sites/zakdoffman/2021/03/16/iphone-12-pro-max-and-iphone-13-not-more-secure-than-google-and-samsung-android-warns-cyber-billionaire/?sh=596442d623f8" target="_blank" rel="noopener">vulnerable</a> to security risks. That said, phones are generally better protected against viruses than personal computers. This is because software is usually installed through authorised app stores that vet each app (although some malicious apps can occasionally slip through <a href="https://blog.pradeo.com/spyware-facestealer-google-play" target="_blank" rel="noopener">the cracks</a>). Also, in comparison to computers, phones are more secure as the apps are usually “<a href="https://source.android.com/security/app-sandbox" target="_blank" rel="noopener">sandboxed</a>” in their own isolated environment – unable to access or interfere with other apps. This reduces the risk of infection or cross contamination from malware. However, no device is entirely immune. <figure class="align-center zoomable"><a href="https://images.theconversation.com/files/459712/original/file-20220426-12-4550kz.png?ixlib=rb-1.1.0&q=45&auto=format&w=1000&fit=clip"><img src="https://images.theconversation.com/files/459712/original/file-20220426-12-4550kz.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&fit=clip" sizes="(min-width: 1466px) 754px, (max-width: 599px) 100vw, (min-width: 600px) 600px, 237px" srcset="https://images.theconversation.com/files/459712/original/file-20220426-12-4550kz.png?ixlib=rb-1.1.0&q=45&auto=format&w=600&h=338&fit=crop&dpr=1 600w, https://images.theconversation.com/files/459712/original/file-20220426-12-4550kz.png?ixlib=rb-1.1.0&q=30&auto=format&w=600&h=338&fit=crop&dpr=2 1200w, https://images.theconversation.com/files/459712/original/file-20220426-12-4550kz.png?ixlib=rb-1.1.0&q=15&auto=format&w=600&h=338&fit=crop&dpr=3 1800w, https://images.theconversation.com/files/459712/original/file-20220426-12-4550kz.png?ixlib=rb-1.1.0&q=45&auto=format&w=754&h=424&fit=crop&dpr=1 754w, https://images.theconversation.com/files/459712/original/file-20220426-12-4550kz.png?ixlib=rb-1.1.0&q=30&auto=format&w=754&h=424&fit=crop&dpr=2 1508w, https://images.theconversation.com/files/459712/original/file-20220426-12-4550kz.png?ixlib=rb-1.1.0&q=15&auto=format&w=754&h=424&fit=crop&dpr=3 2262w" alt="A smartphone with a virus alert warning is held up by a hand in front of a dark background." /></a><figcaption>Apple devices are generally considered more secure against malware than Android devices, but they’re still at risk. Pixabay/Pexels.com (edited), <a class="license" href="http://creativecommons.org/licenses/by/4.0/" target="_blank" rel="noopener">CC BY</a></figcaption></figure> Watch out for the signs While it’s not always easy to tell whether your phone is infected, it will exhibit some abnormal behaviours if it is. Some signs to watch out for include: <ul> <li> poor performance, such as apps taking longer than usual to open, or crashing randomly </li> <li> excessive battery drain (due to the malware constantly working in the background) </li> <li> increased mobile data consumption </li> <li> unexplained billing charges (which may include increased data usage charges as a result of the malware chewing up your data) </li> <li> unusual pop-ups, and </li> <li> the device overheating unexpectedly. </li> </ul> If you do suspect a virus has infected your device, there are some steps you can take. First, to prevent further damage you’ll need to remove the malware. Here are some simple troubleshooting steps: <ol> <li> Use a reliable antivirus app to scan your phone for infections. Some reputable vendors offering paid and free protection services include <a href="https://apps.apple.com/us/app/avast-security-privacy/id1276551855" target="_blank" rel="noopener">Avast</a>, <a href="https://www.avg.com/en-au/antivirus-for-android#pc" target="_blank" rel="noopener">AVG</a>, <a href="https://www.bitdefender.com/solutions/mobile-security-android.html" target="_blank" rel="noopener">Bitdefender</a>, <a href="https://www.mcafee.com/en-us/antivirus/mobile.html" target="_blank" rel="noopener">McAfee</a> or <a href="https://us.norton.com/products/mobile-security-for-android" target="_blank" rel="noopener">Norton</a>. </li> <li> Clear your phone’s storage and cache (in Android devices), or browsing history and website data (in Apple devices). </li> <li> Restart your iPhone, or restart your Android phone to <a href="https://www.digitaltrends.com/mobile/how-to-turn-safe-mode-on-and-off-in-android/" target="_blank" rel="noopener">go into safe mode</a> – which is a feature on Android that prevents third-party apps from operating for as long as it’s enabled. </li> <li> Delete any suspicious or unfamiliar apps from your downloaded apps list and, if you’re an Android user, turn safe mode off once the apps are deleted. </li> </ol> As a last resort, you can back up all your data and perform a factory reset on your phone. Resetting a phone to its original settings will eliminate any malware. Protecting your phone from infection Now you’ve fixed your phone, it’s important to safeguard it against future viruses and other security risks. The mobile security apps mentioned above will help with this. But you can also: <ul> <li> avoid clicking unusual pop-ups, or links in unusual text messages, social media posts or emails </li> <li> only install apps from authorised app stores, such as Google Play or Apple’s App Store </li> <li> avoid jailbreaking or modifying your phone </li> <li> check app permissions before installing, so you’re aware of what the app will access (rather than blindly trusting it) </li> <li> back up your data regularly, and </li> <li> keep your phone software updated to the latest version (which will have the latest security patches). </li> </ul> Continually monitor your phone for suspicious activity and trust your gut instincts. If something sounds too good to be true, it probably is.<img style="border: none !important; box-shadow: none !important; margin: 0 !important; max-height: 1px !important; max-width: 1px !important; min-height: 1px !important; min-width: 1px !important; opacity: 0 !important; outline: none !important; padding: 0 !important;" src="https://counter.theconversation.com/content/181720/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1" /> <figure><iframe src="https://www.youtube.com/embed/nvIXGeB1WgE?wmode=transparent&start=38" width="440" height="260" frameborder="0" allowfullscreen="allowfullscreen"></iframe><figcaption>Google’s tips on how to spot malware.</figcaption></figure> <a href="https://theconversation.com/profiles/ritesh-chugh-162770" target="_blank" rel="noopener">Ritesh Chugh</a>, Associate Professor - Information and Communications Technology, <a href="https://theconversation.com/institutions/cquniversity-australia-2140" target="_blank" rel="noopener">CQUniversity Australia</a> This article is republished from <a href="https://theconversation.com" target="_blank" rel="noopener">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/can-your-mobile-phone-get-a-virus-yes-and-youll-have-to-look-carefully-to-see-the-signs-181720" target="_blank" rel="noopener">original article</a>. Image: Getty Images

Technology

Japanese encephalitis virus contracted in Victoria claims its first victim

Victorians are being warned to protect themselves from mosquito bites after Japanese encephalitis virus (JEV) was <a href="https://www.oversixty.com.au/health/body/fresh-warnings-after-spread-of-mosquito-born-disease">contracted locally for the first time</a>. A Victorian man has died from the virus, the Victorian Department of Health announced yesterday after Australia’s acting chief medical officer declared a national alert about the spread of JEV. The Victorian man, who was from the state's north and aged in his 60s, died on 28th of February. An autopsy has since revealed JEV was the cause of his death, with investigations into how he contracted the virus now underway. The man's death is the first JEV death in the state, while seven cases have been found in the same state this year. Victoria Deputy Chief Health Officer Associate Professor Deborah Friedman said before now JEV had only ever been acquired overseas. "This is the first time that Victoria has ever had locally acquired cases of Japanese encephalitis virus," she said. Associate Professor Friedman called on people to protect themselves against mosquitos, with JEV spread through the bite of an infected insects. Health Minister Martin Foley echoed the same advice, saying "if you're around mosquitos, please cover up". Associate Professor Friedman said mosquito levels were high across the state, particularly in northern Victoria, increasing the risk of infection. Most humans who contract the virus do not experience any symptoms, or only mild symptoms like headaches or fever.

Body

Fresh warnings after spread of mosquito-born disease

Two NSW residents have fallen seriously ill and are currently being hospitalised with a mosquito-borne disease that can result in potentially severe neurological impacts, sparking warnings about avoiding bites. NSW Health on Monday evening said the patients were a man from Corowa and a child from Wentworth, both in the NSW-Victoria border region. The department said the man was in intensive care and the child had been discharged from the ICU but was staying in hospital because of the seriousness of their illness. Authorities are expecting more cases to be confirmed in the future and several people are undergoing further testing. Acting Chief Health Officer Marianne Gale urged NSW residents to take steps to avoid being bitten by mosquitos. "We are working closely with the NSW Department of Primary Industries and other states and territories to determine the extent to which the virus is circulating," Dr Gale said. "Unfortunately, our recent wet weather has led to very high mosquito numbers, so we need the community to be particularly vigilant and take steps to avoid mosquito bites. "We know mosquitoes are most active between dusk and dawn, and we need people planning activities near waterways or where mosquitoes are present to be especially cautious, particularly those in the vicinity of the Murray River and its branches." Australia's acting Chief Medical Officer Dr Sonya Bennett last week declared a national alert over the virus, which is spread through the bite of an infected mosquito. Fortunately, this disease cannot move directly from person to person. The virus is common in a wide swathe of Asia and the Western Pacific, including India, most of China, Indonesia, Papua New Guinea and Japan. Recent cases are the first time it's been identified in NSW in humans or animals, according to NSW Health. Most humans who contract the virus do not experience any symptoms or only experience mild symptoms like headaches or fever. But the worst affected may suffer inflammation of the brain, a sudden onset of vomiting, high fever and chills, severe headaches, sensitivity to light, neck stiffness and nausea. Image: Getty

Body

New vaccine trial targets 2000-year-old virus

The researchers behind the AstraZeneca COVID-19 vaccine have started a new trial to treat a much older disease: the plague. In the phase-one trial, scientists at the University of Oxford will be testing a new vaccine for the ancient virus on at least 40 healthy volunteers aged between 18 and 55. The new vaccine, which uses the same technology as the AstraZeneca jab, is being trialled to check how well the body recognises and learns how to fight the plague after vaccination. Though the virus hasn’t been seen in most of the world since the Black Death swept through Europe in the 14th century, there are still cases in some rural areas of Africa, Asia and America. Between 2010 and 2015, 3,248 cases of the plague were reported globally, including 584 deaths. <blockquote style="background: #FFF; border: 0; border-radius: 3px; box-shadow: 0 0 1px 0 rgba(0,0,0,0.5),0 1px 10px 0 rgba(0,0,0,0.15); margin: 1px; max-width: 540px; min-width: 326px; padding: 0; width: calc(100% - 2px);" class="instagram-media" data-instgrm-captioned="" data-instgrm-permalink="https://www.instagram.com/p/CSJQK9CLXF5/?utm_source=ig_embed&utm_campaign=loading" data-instgrm-version="13"> <div style="padding: 16px;"> <div style="display: flex; flex-direction: row; align-items: center;"> <div style="background-color: #f4f4f4; border-radius: 50%; flex-grow: 0; height: 40px; margin-right: 14px; width: 40px;"></div> <div style="display: flex; flex-direction: column; flex-grow: 1; justify-content: center;"> <div style="background-color: #f4f4f4; border-radius: 4px; flex-grow: 0; height: 14px; margin-bottom: 6px; width: 100px;"></div> <div style="background-color: #f4f4f4; border-radius: 4px; flex-grow: 0; height: 14px; width: 60px;"></div> </div> </div> <div style="padding: 19% 0;"></div> <div style="display: block; height: 50px; margin: 0 auto 12px; width: 50px;"></div> <div style="padding-top: 8px;"> <div style="color: #3897f0; font-family: Arial,sans-serif; font-size: 14px; font-style: normal; font-weight: 550; line-height: 18px;">View this post on Instagram</div> </div> <p style="color: #c9c8cd; font-family: Arial,sans-serif; font-size: 14px; line-height: 17px; margin-bottom: 0; margin-top: 8px; overflow: hidden; padding: 8px 0 7px; text-align: center; text-overflow: ellipsis; white-space: nowrap;"><a style="color: #c9c8cd; font-family: Arial,sans-serif; font-size: 14px; font-style: normal; font-weight: normal; line-height: 17px; text-decoration: none;" rel="noopener" href="https://www.instagram.com/p/CSJQK9CLXF5/?utm_source=ig_embed&utm_campaign=loading" target="_blank">A post shared by Oxford Vaccine Group (@oxford_vaccinegroup)</a> </div> </blockquote> Just two years later, <a rel="noopener" href="https://www.ox.ac.uk/news/2021-07-26-phase-i-trial-begins-new-vaccine-against-plague" target="_blank">an epidemic</a> in Madagascar saw 2,119 suspected cases and 171 deaths over several months. With many of the regions at risk of outbreaks being in remote locations, a vaccine could be a new way to protect these communities. Larissa, 26, studies genetics at the University of Oxford and is one of the participants who hopes she can help save lives by getting the jab. <img style="width: 500px; height:281.25px;" src="https://oversixtydev.blob.core.windows.net/media/7843432/_119964702_capture.png" alt="" data-udi="umb://media/faa0b5599bbf49738fdbc2a4e0278892" /> Image: Oxford University “I’m lucky enough to live in a time where vaccines are being developed,” Larissa said. “And so, when I saw that there was a study aiming at developing a vaccine against a disease that’s been around for 2000 years and has killed millions and millions of people, I didn’t hesitate, I just wanted to do my bit.” When asked if she was worried about side effects, Larissa said she wasn’t “too concerned”. “The vaccine that’s being assessed today is using the same platform as the Covid vaccine, which has literally been administered to millions of people around the world.” Like the Oxford-AstraZeneca Covid vaccine, the plague vaccine uses a weakened version of adenovirus - a common-cold virus from chimpanzees - that has been genetically altered so people do not get infected. The vaccine does not contain plague bacterium, meaning recipients of the jab cannot contract the plague. Instead, the adenovirus has additional genes that make proteins from Yersinia pestis, the plague bacterium. With these added genes, the vaccine should be able to teach the immune systems of recipients how to fend off a real infection of the plague if it needs to. This technique could also be used against other diseases, according to the researchers. “We’ve already done clinical trials using similar technology against a bacterium, meningitis B, and a virus, Zika,” Dr Maheshi Ramasamy, the senior clinical researcher of the Oxford Vaccine Group, said. “But we’re also looking to develop vaccines against new and emerging diseases such as Lassa fever or the Marburg virus.” The plague vaccine trial is expected to run for at least a year.

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"Shouting doesn't work against this virus": Dan Andrews responds to gatecrasher

Victoria's COVID-19 press conference was met with a gatecrasher on Wednesday, after a man yelled at Premier Dan Andrews for more than half an hour. During the announcement of further lockdown restrictions, the man started shouting for “Premier Daniel Andrews” from the floor above where the conference was taking place. The said he had a letter for the Victorian Premier and claimed he called to try and speak to him the day before. Police eventually stepped in to arrest the man, as reporters asked Andrews to address the man's obvious frustrations about continuing COVID-19 restrictions. The Premier said in response, "Whether you support me or not I will do everything I can to protect you from this virus." “Shouting doesn’t work against this virus. Like I said the other day, if frustration and anger was effective against coronavirus, we’d all be double dosed vaccinated by now." The Victorian Premier has received a lot of scrutiny over the many lockdowns Victoria has endured, as he continues to say he will do whatever is necessary to protect Victorians from the deadly Delta strain of coronavirus. Melbourne went into another snap lockdown last Thursday evening and was said to only last a week. However, as cases continue to rise, Andrews said authorities needed more time and extended it to now last until midnight on Thursday August 19.

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“Fit” Sydney mum details battle with COVID Virus: “This virus is hell”

A Sydney woman diagnosed with COVID has shared her hellish battle in a series of heartbreaking posts. Melissa Green knew something was very, very wrong when she was admitted to hospital on 19 July after her oxygen levels dropped. She described that she and her partner Dion were both “fit and healthy” when they were struck down with the virus. Eventually, it also infected their three-year-old daughter Lola. Melissa told 7NEWS.com.au that she and her family had been “shocked” to receive positive results for COVID, after taking all the necessary precautions. She said in a detailed post that her family were “all OK”, aside from Dion who lost his sense of smell and taste. However just a day later, Melissa reported that fingertip oxygen monitors showed her oxygen level was “lower than it should be” and her heart rate higher than normal. “Nothing to worry about, just body aches, chills and headaches,” the mum wrote at the time. “Dion is just feeling really fatigued like he has run a marathon but just been in bed. We will get through this,” she said. <img style="width: 500px; height: 281.25px;" src="https://oversixtydev.blob.core.windows.net/media/7842787/melissa-covid-4.jpg" alt="" data-udi="umb://media/2c992b894da841749ea3ca49f7b5576c" /> Sadly just 48 hours later, the mum explained her partner was rushed to the hospital when he began to suffer from “severe chest pains” and had “difficulty breathing”. “He is one of the strongest and fittest people I know so this has been a total shock,” Melissa wrote on July 18. Dion was able to return home a day later, but Melissa’s oxygen levels were plummeting and she was taken to Emergency. Sharing a devastating image of herself in a hospital bed on July 20, Melissa urged people to “take this seriously.” “Vaccinate or not it’s everyone’s choice. But if you think our hospital system can deal with the virus by opening up, you have another thing coming,” Melissa wrote. “This variant is attacking the young, old, fit and healthy as well as those with health issues. Please take this seriously.” Melissa reported the next day she was still in hospital and facing her “hardest day yet”. “I’ve been fighting temps of 40C all day. I am still on oxygen and tomorrow I will start on tocilizumab and remdesivir and hopefully that will give me some relief,” she said. “I found out today that there are another 14 people here in the hospital and a good few in ICU. “Dion is still at home with Lola managing on his asthma plan but severely fatigued and short of breath but doing a great job taking care of our baby. “Hopefully tomorrow is a better day. One thing about this virus is you are up and down but when you hit the deck it’s worse than the time before. “The nurse tells me the next few days could be even harder.” Melissa came to Facebook the next day to share that her symptoms were on the up, noting that while she no longer had as much pain, she’d “lost control of things no one would wish to experience”. “This virus has torn me apart,” she wrote. “I am away from my baby and my partner all alone in a fishbowl of a room trying to fight to get back home to the two people I love with all my heart. “All I want is to get home and hold my baby tight. <img style="width: 0px; height: 0px;" src="https://oversixtydev.blob.core.windows.net/media/7842786/melissa-covid-3.jpg" alt="" data-udi="umb://media/936b9a61bd014462b423c6568451dc61" /> “Fingers crossed I’m on the way up.” On July 23 Melissa told family and friends in another post how she was likely to remain in hospital for another five days. “That’s another five days of no hugs with my baby, no hugs with my partner. “I cried and cried today all alone in a room fighting the hardest fight. “They tried to get me up and walking and I lasted 40 seconds before I collapsed on the bed - this is insane! “For someone who plays numerous games or netball and umpires weekly and now I can’t even walk for 40 seconds. What has this virus done to me? How long will I take to recover? Who knows? “I know everyone is doing it tough but trust me this place is the toughest both mentally and physically. Stay home everyone and stay safe.” On July 24, Melissa revealed it was her “hardest day yet”. “I woke this morning with the lowest levels of oxygen I have had since being here and had to fight with the doctors to leave me on the ward as I didn’t want to go to ICU,” she wrote. “At least where I am I have a window to the outside world.” Melissa said watching the Sydney lockdown protests left her “saddened”. “I believe in freedom and people’s rights but ... those out protesting have cost us all more time under lockdown so you only have yourselves to blame,” she wrote. After a week in hospital, Melissa admitted her heart was “breaking”. “This virus is hell,” she wrote. “It separates people from loved ones, rips your health apart and challenges you mentally. “Can people not see how contagious it is? Seriously, stay home so we can all see an end in sight.” Melissa told Facebook after eight days in hospital, she was finally home. “Recovering slowly, but I’ll get there,” she said. “Stay home and stay safe.” Images: Supplied

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"Like India": Epidemiologists warn about Delta outbreak

Australian infectious disease experts are warning that the country "could end up with a situation like India" if the Delta variant of COVID-19 is allowed to run throughout the community. This comes after NSW Health Minister Brad Hazzard suggested that the state might never control its current outbreak and will have to live with the virus "for good". Mr Hazzard said if people don’t do the right thing over the coming days, “then at some point we’re going to move to a stage where we’re going to have to accept that the virus has a life which will continue in the community”. Raina Macintyre from the Kirby Institute said that letting the virus continue would be "really risky". “I think for Australia, for NSW, that’s a different proposition to countries that have high vaccination rates and high levels of disease. We’ve got virtually no immunity in the community because very few people have been fully vaccinated, and very few people have been infected,” she said to ABC Breakfast. “So we are absolutely susceptible. If we let it spread in Sydney, it could impact the whole country and we could end up with a situation like we saw in India in March and April. “We can’t afford to relax until we’ve got the vaccination rates high.” Ms Macintyre said there would be at least a three-month wait until vaccine supplies in Australia became “adequate”. “It would be really risky to throw it all away without waiting that three months and doing everything that we can to crush this outbreak and to prevent further leaks from hotel quarantine and the international borders by mitigating airborne transmission more comprehensively than we have done,” she said.

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Alarming new way the Vic outbreak is spreading

Victorian authorities say people are becoming infected with COVID after just "brushing past" strangers with the virus. Testing Commander Jeroen Weimar said at least four of the state's 54 locally transmitted cases have come from "fleeting" contact between Victorians, “What we’re seeing now is people are brushing past each other in a small shop, they are going to a display home, they are looking at photos in a Telstra shop,” he said. “This is relatively speaking, relatively fleeting. They do not know each other’s names, and that is very different from what we have been before. “This is stranger to stranger transmission.” He said the ease with which the virus is spreading may be a feature of the Indian variant. “We are used with previous variants, we are more used to transmission roccurring in the home, in the workplace, where people know each other already, not all of those big social settings,” he said. “These are quite different.” “We have seen transmission in these places with very fleeting contact. We have transmission in places like the Telstra store in South Melbourne, JMD Grocers, the display home we talked about a few days ago, I’d add Craigieburn Central shopping centre. “They are all examples of transmission with very limited contact. With previous variants, we are more used to transmission occurring in the home, in the workplace, where people know each other already, not at all of those big social settings. These are quite different.” If anyone has been to any of the following sites in the past two weeks, they should come forward and get tested: • Craigieburn Central • Bay Street shops in Port Melbourne • Clarendon Street in the South Melbourne • Pacific Epping, also known as the Epping Plaza • The Epping North shopping centre • Broadway Reservoir

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