1. Smoking worsens COVID-19 severity, warn researchers  News-Medical.Net
  2. The virus that causes COVID-19 has been silently brewing in bats for decades  Popular Science
  3. Wuhan coronavirus hunter Shi Zhengli speaks out  Science
  4. Looking beyond COVID-19's spike protein for the next wave of vaccines  FierceBiotech
  5. Covid-19: Infectious coronaviruses 'circulating in bats for decades'  BBC News
  6. View Full coverage on Google News
A study conducted by researchers at the University of California, Los Angeles, suggests that smoking increases the risk of more severe lung disease in cases of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.A study conducted by researchers at the University of California, Los Angeles, suggests that smoking increases the risk of more severe lung disease in cases of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection.

Smoking worsens COVID-19 severity, warn researchers

The decline seen in some studies is normal, experts say. But scientists must wait to see whether infection confers long-term protectionThe decline seen in some studies is normal, experts say. But scientists must wait to see whether infection confers long-term protection

Concerns about Waning COVID-19 Immunity Are Likely Overblown - Scientific American

In late January, when hospitals in the United States confirmed the presence of the novel coronavirus, health workers knew to watch for precisely three symptoms: fever, cough, and shortness of breath. ...

We thought COVID-19 was just a respiratory virus—we were wrong

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Dropping antibody counts aren’t a sign that our immune system is failing against the coronavirus, nor an omen that we can’t develop a viable vaccine.Dropping antibody counts aren’t a sign that our immune system is failing against the coronavirus, nor an omen that we can’t develop a viable vaccine.

Here are the COVID-19 vaccine prospects that have made it to phase three trials and beyond.Here are the COVID-19 vaccine prospects that have made it to phase three trials and beyond.

Dozens of COVID-19 vaccines are in development. Here are the ones to follow.

The mounting evidence suggests that SARS-CoV-2 can infect immune privileged sites and, from there, result in chronic persistent — but not latent — infectionsThe mounting evidence suggests that SARS-CoV-2 can infect immune privileged sites and, from there, result in chronic persistent — but not latent — infections

Does coronavirus linger in the body? What we know about how viruses in general hang on in the brain and testicles

The SARS-CoV-2 lineage circulated in bats for 50 or 60 years before jumping to humans at the end of last year, a new study finds.Dozens of other unknown bat coronavirus could be capable of infecting humans.

Ancestors of coronavirus have been hiding out in bats for decades, ready to infect humans | Live Science

Two new studies from different parts of the world arrived at the same conclusion: that young children not only transmit SARS-CoV-2 efficiently, but may be major drivers of the pandemic as well. Two new studies from different parts of the world arrived at the same conclusion: that young children not only transmit SARS-CoV-2 efficiently, but may be major drivers of the pandemic as well.

New Evidence Suggests Young Children Spread Covid-19 More Efficiently Than Adults

One of the greatest struggles of the COVID-19 pandemic has been the fact that the entire world has to watch the normal scientific process happen in realtime. Scientists don’t have the space t…

The most comprehensive and accessible explanation of how COVID-19 works (so far) / Boing Boing

A study published yesterday in Nature Microbiology suggests the viral lineage leading to the novel coronavirus—SARS-CoV-2—might have been “circulating unnoticed in bats for decades.”A study published yesterday in Nature Microbiology suggests the viral lineage leading to the novel coronavirus—SARS-CoV-2—might have been “circulating unnoticed in bats for decades.”

The virus that causes COVID-19 has been silently brewing in bats for decades | Popular Science

Most viruses produce a long-lasting memory in a person’s immune system, but this is not always the case, says an observer.Most viruses produce a long-lasting memory in a person’s immune system, but this is not always the case, says an observer.

Commentary: Booster shots will likely be needed even if a COVID-19 vaccine is ready - CNA

Viruses enter cells and initiate infection by binding to their cognate cell surface receptors. The expression and distribution of viral entry receptors therefore regulates their tropism, determining the tissues that are infected and thus disease pathogenesis. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the third human coronavirus known to co-opt the peptidase angiotensin-converting enzyme 2 (ACE2) for cell entry ([ 1 ][1]). The interaction between SARS-CoV-2 and ACE2 is critical to determining both tissue tropism and progression from early SARS-CoV-2 infection to severe coronavirus disease 2019 (COVID-19). Understanding the cellular basis of SARS-CoV-2 infection could reveal treatments that prevent the development of severe disease, and thus reduce mortality. As with all coronaviruses, SARS-CoV-2 cell entry is dependent on its 180-kDa spike (S) protein, which mediates two essential events: binding to ACE2 by the amino-terminal region, and fusion of viral and cellular membranes through the carboxyl-terminal region ([ 2 ][2]). Infection of lung cells requires host proteolytic activation of spike at a polybasic furin cleavage site ([ 3 ][3]). To date, this cleavage site is found in all spike proteins from clinical SARS-CoV-2 isolates, as well as some other highly pathogenic viruses (e.g., avian influenza A), but it is absent from SARS-CoV and is likely to have been acquired by recombination between coronaviruses in bats. Cleavage by the furin protease therefore expands SARS-CoV-2 cell tropism and may have facilitated transmission from bats to humans ([ 1 ][1]). Membrane fusion also requires cleavage by additional proteases, particularly transmembrane protease serine 2 (TMPRSS2), a host cell surface protease that cleaves spike shortly after binding ACE2 ([ 3 ][3]). SARS-CoV-2 tropism is therefore dependent on expression of cellular proteases, as well as ACE2. Other proteins that enable SARS-CoV-2 cell entry are also emerging, including neuropilin 1 (NRP1), a receptor that binds the carboxyl-terminal RXXR motif in spike that is exposed after furin cleavage. How NRP1 promotes cell entry is unclear, but it may further increase the cell types infected ([ 4 ][4]). Of the seven known human coronaviruses, three are highly pathogenic [SARS-CoV, SARS-CoV-2, and Middle East respiratory syndrome (MERS)-CoV], and the remaining four (HCoV-NL63, HCoV-229E. HCoV-OC43, and HCOV-HKU1) are less virulent, causing “common colds.” SARS-CoV, SARS-CoV-2, and HCoV-NL63 use ACE2 as their cell entry receptor. MERS-CoV binds DPP4 (dipeptidyl peptidase 4) and HCoV-229E uses CD13 (aminopeptidase N) ([ 2 ][2]). No host protein receptors have been identified for the other two viruses. It seems a notable coincidence that all known human coronavirus receptors are cell surface peptidases, particularly because the interactions do not involve the endopeptidase active site ([ 2 ][2]). The presence of a specific region within ACE2, targeted by three coronaviruses, is particularly noteworthy ([ 1 ][1]). Conversely, the receptor-binding domain of spike is encoded by the most variable part of the coronavirus genome ([ 1 ][1]). This implies that diversification of these viruses generated different sequences that converged on the same region of the same protein using alternative structural solutions. What, then, is so special about ACE2? ACE2 is a transmembrane protein best characterized for its homeostatic role in counterbalancing the effects of ACE on the cardiovascular system ([ 5 ][5]). ACE converts angiotensin I to angiotensin II, a highly active octapeptide that exhibits both vasopressor (vascular contraction to increase blood pressure) and proinflammatory activities. The carboxypeptidase activity of ACE2 converts angiotensin II to the heptapeptide angiotensin-(1-7), a functional antagonist of angiotensin II. Because ACE is highly expressed in vascular endothelial cells of the lungs, angiotensin II is also likely to be high in the pulmonary vasculature. Indeed, Ace2 deletion in mouse models of acute lung injury results in more severe disease, suggesting a protective role for ACE2 in lung tissue ([ 5 ][5]). In many host-virus interactions, expression of the viral receptor is down-regulated in infected cells, and expression of ACE2 in the lungs of mice was reduced by SARS-CoV infection. Depletion of ACE2 may thus play a causative role in the lung injury caused by SARS-CoV and SARS-CoV-2, and high plasma angiotensin II is reported in patients with COVID-19. However, MERS-CoV causes a similar lung disease without targeting ACE2, so other factors must also be important. As a respiratory virus, SARS-CoV-2 must initially enter cells lining the respiratory tract. Single-cell sequencing and RNA in situ mapping of the human respiratory tract show ACE2 and TMPRSS2 expression to be highest in ciliated nasal epithelial cells, with lesser amounts in ciliated bronchial epithelial cells and type II alveolar epithelial cells ([ 6 ][6]). This translates to greater permissivity of upper versus lower respiratory tract epithelial cells for SARS-CoV-2 infection in vitro and fits disease pathology: Upper respiratory tract symptoms are common early in disease, with nasopharyngeal and throat swabs positive for SARS-CoV-2 at clinical presentation ([ 7 ][7]). In contrast to SARS-CoV, infectivity of patients with SARS-CoV-2 peaks before symptom onset ([ 8 ][8]). Indeed, presymptomatic transmission makes SARS-CoV-2 impossible to contain through case isolation alone and is a key driver of the pandemic ([ 8 ][8]). This alteration in the pattern of disease may relate to the acquisition of the furin cleavage site in spike or increased binding affinity for ACE2 in SARS-CoV-2, compared with SARS-CoV ([ 9 ][9]). If the main role of ACE2 is to cleave angiotensin II, it is unclear why expression in lung tissue is more prominent in epithelial than in endothelial cells. Furthermore, the Human Cell Atlas highlights ACE2 expression in intestinal enterocytes, rather than in the lungs. This distribution may reflect nonenzymatic roles of ACE2, such as chaperoning amino acid transporters. Indeed, SARS-CoV-2 infection of the gastrointestinal (GI) tract is common, with viral RNA detectable in stool in up to 30% of COVID-19 patients. This likely contributes to the frequency of GI symptoms. Conversely, whereas fecal-oral transmission of coronaviruses is thought to be prominent among bats, it appears to be a minor transmission route for SARS-CoV-2 in humans, perhaps because colonic fluid inactivates the virus. Whether extrapulmonary ACE2 expression and concomitant viral infection account for other clinical manifestations of SARS-CoV-2 is unclear. The association between SARS-CoV-2 infection and anosmia (loss of smell) may reflect ACE2 and TMPRSS2 expression in sustentacular cells, which maintain the integrity of olfactory sensory neurons. Olfactory epithelial cells also express NRP1 and could provide a direct route to the brain ([ 4 ][4]). Although a substantial proportion of SARS-CoV-2–infected individuals report few, if any, symptoms and recover completely, chest computed tomography (CT) evidence of viral pneumonitis is present in >90% of symptomatic cases within 3 to 5 days of onset ([ 10 ][10]). This presumably reflects viral replication in the lower respiratory tract, with infection of type II pneumocytes and accompanying inflammation (see the figure). Lung pathology in this early phase is poorly reported because most patients recover. Histopathology from cynomolgus monkeys, 4 days after inoculation with SARS-CoV-2, shows a viral pneumonitis with alveolar edema, capillary leakage, inflammatory cell infiltration, interstitial thickening, and cell fusion (a feature of coronavirus infection), with viral spike expression on alveolar epithelial cells ([ 11 ][11]). ![Figure][12]</img> Key phases of disease progression Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) binds to angiotensin-converting enzyme 2 (ACE2). Initial infection of cells in the upper respiratory tract may be asymptomatic, but these patients can still transmit the virus. For those who develop symptoms, up to 90% will have pneumonitis, caused by infection of cells in the lower respiratory tract. Some of these patients will progress to severe disease, with disruption of the epithelial-endothelial barrier, and multi-organ involvement. GRAPHIC: V. ALTOUNIAN/ SCIENCE Around 80% of patients with COVID-19 pneumonitis recover without specific treatment ([ 12 ][13]). However, ∼20% of patients deteriorate, often rapidly, ∼7 to 10 days after symptom onset. This is when patients are most frequently admitted to hospital, with worsening fever, hypoxia, lymphopenia, rising inflammatory markers [C reactive protein (CRP), interleukin-1 (IL-1), and IL-6], coagulopathy, and cardiovascular involvement. About 25% of these patients will require mechanical ventilation, which is associated with high mortality (50 to 80%). The demographic of this “at risk” group is reproduced across many countries: older men with hypertension, diabetes, and obesity, as well as a less well defined contribution of ethnicity ([ 12 ][13]). Similar factors regulate ACE2 expression, which may therefore contribute to disease severity. Nonetheless, the amount and distribution of ACE2 expression cannot be the only factor affecting disease progression, because the three human coronaviruses that use ACE2 for cell entry exhibit markedly different pathogenicity. What causes the sharp deterioration that leads to severe systemic COVID-19? The lung pathology in severe disease is different from the earlier pneumonitis, with progressive loss of epithelial-endothelial integrity, septal capillary injury, and a marked neutrophil infiltration, with complement deposition, intravascular viral antigen deposition, and localized intravascular coagulation ([ 13 ][14]). If the earlier viral pneumonitis reflects direct ACE2-mediated infection of type II pneumocytes, what drives this next, potentially deadly phase of acute lung injury, with the concomitant breakdown of the respiratory epithelial barrier, endothelial damage, and patient deterioration ([ 14 ][15])? Most importantly—how can it be stopped? The timing of deterioration suggests a role for the adaptive immune system, either antibodies or T cells, and has many hallmarks of immune-driven inflammation. Endothelial injury may result from immune-mediated damage, through complement activation, antibody-dependent enhancement, and/or cytokine release. Attention has therefore focused on the use of immunomodulatory therapies in patients with severe disease. Nonetheless, the most obvious culprit for severe disease is the virus itself, either alone or with immune pathology. Breakdown of the lung epithelial-endothelial barrier might trigger endothelial damage and viral dissemination, with more widespread infection ([ 14 ][15]). Studies documenting the time course of SARS-CoV-2 RNA shedding are mainly limited to mild disease ([ 7 ][7]) and typically show a progressive decline after a peak around symptom onset. However, viral load from lung swabs may correlate with disease severity ([ 15 ][16]), and patients with severe lung disease remain RNA-positive for longer. It is critical to determine how long active viral replication really persists in the lungs of patients with severe disease, and how frequently viral replication occurs at extrapulmonary sites where ACE2 (or other receptors) is expressed, such as vascular endothelium. Although there are huge efforts to understand and treat severe COVID-19, it would be preferable to prevent the development and progression of clinical disease. How might this be achieved? Vaccine candidates are mainly aimed at eliciting neutralizing antibodies, to prevent the binding of spike to ACE2. The same rationale underpins the use of passive immunization, with convalescent plasma or monoclonal antibodies, or the administration of recombinant, soluble ACE2. Alternatively, antiviral drugs may be used to target essential viral enzymes such as the RNA-dependent RNA polymerase. Experience from other infections, such as influenza, emphasizes that treatment with antiviral agents is most effective when administered as early as possible in infection. Therefore, it is essential to identify individuals with early SARS-CoV-2 infection who are at high risk of progression to severe disease, and test antiviral therapies to prevent viral entry and replication. It should not be too difficult to identify these “at risk” patients who are in danger of progressing to severe disease through contact tracing and testing, even prior to symptom onset. Conversely, delaying candidate antiviral treatment until patients are hospitalized with severe lung injury may be too late, and combination with immune modulation is likely to be required. 1. [↵][17]1. K. G. Andersen et al ., Nat. Med. 26, 450 (2020). [OpenUrl][18][CrossRef][19][PubMed][20] 2. [↵][21]1. F. Li , J. Virol. 89, 1954 (2015). [OpenUrl][22][Abstract/FREE Full Text][23] 3. [↵][24]1. M. Hoffmann et al ., Mol. Cell 78, 779 (2020). [OpenUrl][25] 4. [↵][26]1. L. Cantuti-Castelvetri et al ., bioRxiv 2020.06.07.137802 (2020). 5. [↵][27]1. K. Kuba et al ., J. Mol. Med. 84, 814 (2006). [OpenUrl][28][CrossRef][29][PubMed][30][Web of Science][31] 6. [↵][32]1. Y. J. Hou et al ., Cell 10.1016/j.cell.2020.05.042 (2020). 7. [↵][33]1. R. Wölfel et al ., Nature 581, 465 (2020). [OpenUrl][34][CrossRef][35][PubMed][20] 8. [↵][36]1. X. He et al ., Nat. Med. 26, 672 (2020). [OpenUrl][37][PubMed][20] 9. [↵][38]1. D. Wrapp et al ., Science 367, 1260 (2020). [OpenUrl][39][Abstract/FREE Full Text][40] 10. [↵][41]1. A. Bernheim et al ., Radiology 295, 200463 (2020). [OpenUrl][42][PubMed][20] 11. [↵][43]1. B. Rockx et al ., Science 368, 1012 (2020). [OpenUrl][44][Abstract/FREE Full Text][45] 12. [↵][46]1. Z. Wu, 2. J. M. McGoogan , JAMA 323, 1239 (2020). [OpenUrl][47][CrossRef][48][PubMed][20] 13. [↵][49]1. C. Magro et al ., Transl. Res. 220, 1 (2020). [OpenUrl][50] 14. [↵][51]1. L. A. Teuwen et al ., Nat. Rev. Immunol. 20, 389 (2020). [OpenUrl][52] 15. [↵][53]1. J. Chen et al ., J. Infect. 10.1016/j.jinf.2020.03.004 (2020). Acknowledgments: The authors are supported by the Medical Research Council (CSF MR/P008801/1 to N.J.M.), NHS Blood and Transplant (WPA15-02 to N.J.M.), and the Wellcome Trust (PRF 210688/Z/18/Z to P.J.L.). 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{openurl}?query=rft.jtitle%253DNat.%2BRev.%2BImmunol.%26rft.volume%253D20%26rft.spage%253D389%26rft.genre%253Darticle%26rft_val_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Ajournal%26ctx_ver%253DZ39.88-2004%26url_ver%253DZ39.88-2004%26url_ctx_fmt%253Dinfo%253Aofi%252Ffmt%253Akev%253Amtx%253Actx [53]: #xref-ref-15-1 "View reference 15 in text"

How does SARS-CoV-2 cause COVID-19? | Science

T cells could be valuable allies in pandemic control Protective and enduring immune responses to viral infections or vaccines usually arise from the combined actions of lymphocytes: B cells (responsible for humoral antibody immunity) and T cells (responsible for cellular immunity and helping B cell responses). B cells produce detectable antibodies in classes IgM, IgG, and IgA along with lesser amounts of IgD and IgE. For SARS-CoV-2, the causative agent of covid-19, the focus is mainly on IgM, IgG, and IgA antibodies that can neutralise the virus by binding to the spike and other membrane proteins and thus preventing infection.1 Understanding the lesser known roles of T cells and cellular immunity will deepen our insights into covid-19 pathogenesis and help inform both vaccine development and pandemic containment strategies. An effective immune response to SARS-CoV-2 involves four types or subsets of T cells: T helper cells (CD4) are responsible for cellular immunity and for helping B cells to produce neutralising antibodies; cytotoxic or killer T cells (CD8) directly kill infected cells—aided by helper T cells2; …

Cellular immune responses to covid-19 | The BMJ

Dealers in Kenya’s popular second-hand clothes market are pushing the government to lift a ban on imports. Do they have their facts right?Dealers in Kenya’s popular second-hand clothes market are pushing the government to lift a ban on imports. Do they have their facts right?

Can coronavirus only live up to 9 days on objects, as Kenyan traders claim? | Africa Check

A new study by Penn State scientists claims the pandemic-causing coronavirus may have first evolved in bats way back in 1948.A new study by Penn State scientists claims the pandemic-causing coronavirus may have first evolved in bats way back in 1948.

Study Claims Coronavirus May Have First Evolved In Bats In 1948

Scientists think they know why some people seem to be able to brush off coronavirus while others end up in intensive care.Scientists think they know why some people seem to be able to brush off coronavirus while others end up in intensive care.

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COVID-19’s effects on the body are much more complex (and potentially destructive) than that, UCSF doctors say.COVID-19’s effects on the body are much more complex (and potentially destructive) than that, UCSF doctors say.

We thought it was just a respiratory virus. We were wrong. | University of California

Scientists have made a significant breakthrough in discovering how the SARS-CoV-2 virus infiltrates human cells, and provokes them into producing proteins that enable it to spread through the human body.Scientists have made a significant breakthrough in discovering how the SARS-CoV-2 virus infiltrates human cells, and provokes them into producing proteins that enable it to spread through the human body.

A new study published in the journal Nature finds some people could have immunity to novel coronavirus even though they may have never been exposed to the virus. Researchers in Berlin, Germany examined T cells in blood donors, honing in on the CD4 T cells which react in response to the virus. These T cells were found in 83% of patients who had tested positive for COVID-19 but they were also found in 35% of patients who had not been found positive.A new study published in the journal Nature finds some people could have immunity to novel coronavirus even though they may have never been exposed to the virus. Researchers in Berlin, Germany examined T cells in blood donors, honing in on the CD4 T cells which react in response to the virus. These T cells were found in 83% of patients who had tested positive for COVID-19 but they were also found in 35% of patients who had not been found positive.

Some people who haven't had COVID-19 could have immunity study finds | WZTV

Some people who haven't had COVID-19 could have immunity study finds

Our experts answer: Can an air conditioning unit spread COVID-19? What is a superspreader? How do we achieve herd immunity?

COVID questions: AC, superspreaders, herd immunity

One in three people with no prior exposure to SARS-CoV-2 have T-helper cells that recognize the virus, which may be due to prior coronavirus infections.One in three people with no prior exposure to SARS-CoV-2 have T-helper cells that recognize the virus, which may be due to prior coronavirus infections.

Past Coronavirus Infections May Leave behind T Cells That Recognize SARS-CoV-2

The researchers from National Institute of Allergy and Infectious Diseases in the US and the Oxford University found that the ChAdOx1 nCoV-19 vaccine protects the macaques from COVID-19 pneumonia.The researchers from National Institute of Allergy and Infectious Diseases in the US and the Oxford University found that the ChAdOx1 nCoV-19 vaccine protects the macaques from COVID-19 pneumonia.

Oxford Vaccine Shows Protection Against Covid-19 in Monkeys: Study

When SARS-CoV-2 infects us, the infected body cells release messenger substances known as type 1 interferons. These attract our killer cells, which kill the infected cells.When SARS-CoV-2 infects us, the infected body cells release messenger substances known as type 1 interferons. These attract our killer cells, which kill the infected cells.

New Research: Protein identified as potential Achilles’ heel of coronavirus | Explained News,The Indian Express

Todd Castoe, associate professor of biology at The University of Texas at Arlington, has co-authored two papers regarding the COVID-19 virus and its...Todd Castoe, associate professor of biology at The University of Texas at Arlington, has co-authored two papers regarding the COVID-19 virus and its...

UTA biologists: COVID-19 virus originated in bats, not dogs | Mirage News

Research has reported troubling news that the virus that causes COVID-19 may have mutated in such a way to make it more transmissible.Research has reported troubling news that the virus that causes COVID-19 may have mutated in such a way to make it more transmissible.

How many COVID-19 virus mutations are there? - AOL Lifestyle

Now the idea of &#39;cross immunity&#39; among the broader population is gaining some groundNow the idea of &#39;cross immunity&#39; among the broader population is gaining some ground

Covid-19: Could it be burning out after 20% of a population is infected? | Dhaka Tribune

Inside his laboratory at Washington State University, Michael Letko is determined to give the world a leg up on the next pandemic.

Bracing for the next pandemic | WSU Insider | Washington State University

More viruses with the potential to infect humans are circulating in the mammalsMore viruses with the potential to infect humans are circulating in the mammals

Coronaviruses had circulated in bats for decades- The New Indian Express

Some people might have T-cells that are able to recognize and fight the coronavirus.

Study: Memory of disease-fighting cells could explain partial immunity to COVID-19 - silive.com

People infected with Covid-19 do show an immune response to the virus, but the bad news is we don&#x27;t know how long that response lastsPeople infected with Covid-19 do show an immune response to the virus, but the bad news is we don&#x27;t know how long that response lasts

Here's everything we know about coronavirus immunity so far | WIRED UK

In a recent research, scientists have found that people who have been infected with the strains of coronaviruses that cause the common cold may have immunity against the novel coronavirus.

A Recent Bout of Common Cold May Have Provided You COVID-19 Immunity: Study

New research has discovered T cells in people not yet exposed to the coronavirus, indicating that some people may have preexisting COVID immunity.New research has discovered T cells in people not yet exposed to the coronavirus, indicating that some people may have preexisting COVID immunity.

Why You May Actually Already Be Safe From COVID, New Study Says

Can prior exposure to random coronaviruses help protect against the more lethal novel coronavirus that causes COVID-19? A new study out of Germany points to the tantalizing possibility.Can prior exposure to random coronaviruses help protect against the more lethal novel coronavirus that causes COVID-19? A new study out of Germany points to the tantalizing possibility.

'Common cold' coronavirus exposure could help in COVID-19: study - New York Daily News

Research suggests a close ancestor of the coronavirus emerged in bats more than 40 years ago.Research suggests a close ancestor of the coronavirus emerged in bats more than 40 years ago.

Covid-19: Infectious coronaviruses 'circulating in bats for decades' - BBC News

Universitätsmedizin Berlin and the Max Planck Institute for Molecular Genetics (MPIMG) show that some healthy individuals possess immune cells capable of recognizing the novel coronavirus, SARS-CoV-2. ...

Could prior exposure to common cold viruses affect the severity of SARS-CoV-2 symptoms?

The immune systems of some people who have not been exposed to the novel coronavirus could have some familiarity with the pathogen — possibly helping to reduce the severity of illness if that…

Why some people who haven't had Covid-19 might already have some immunity

The immune systems of some people who have not been exposed to the novel coronavirus could have some familiarity with the pathogen — possibly helping to reduce the severity of illness if that person does get Covid-19, a new study suggests. The study, published in the journal Nature on Wednesday, found that among a sample […]The immune systems of some people who have not been exposed to the novel coronavirus could have some familiarity with the pathogen — possibly helping to reduce the severity of illness if that…

Some people who haven’t had COVID-19 could already have some immunity; here’s why | KTLA

The immune systems of some people who have not been exposed to the novel coronavirus could have some familiarity with the pathogen — possibly helping to reduce the severity of illness if that…

Some people who haven’t had COVID-19 could already have some immunity; here’s why | KTLA

The immune systems of some people who have not been exposed to the novel coronavirus could have some familiarity with the pathogen -- possibly helping to reduce the severity of illness if that person does get Covid-19, a new study suggests.The immune systems of some people who have not been exposed to the novel coronavirus could have some familiarity with the pathogen -- possibly helping to reduce the severity of illness if that person does get Covid-19, a new study suggests.

Why some people who haven't had COVID-19 might already have some immunity - Citizentv.co.ke