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The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has resulted in thousands of deaths in the world. Information about prediction model of prognosis of SARS-CoV-2 infection is scarce. We used machine learning for processing laboratory findings of 110 patients with SARS-CoV-2 pneumonia (including 51 non-survivors and 59 discharged patients). The maximum relevance minimum redundancy (mRMR) algorithm and the least absolute shrinkage and selection operator logistic regression model were used for selection of laboratory features. Seven laboratory features selected in the model were: prothrombin activity, urea, white blood cell, interleukin-2 receptor, indirect bilirubin, myoglobin, and fibrinogen degradation products. The signature constructed using the seven features had 98% [93%, 100%] sensitivity and 91% [84%, 99%] specificity in predicting outcome of SARS-CoV-2 pneumonia. Thus it is feasible to establish an accurate prediction model of outcome of SARS-CoV-2 pneumonia based on laboratory findings.

Bart Haagmans (Erasmus MC) concludes: "The observations made in this study provide definite proof that SARS-CoV-2 can multiply in cells of the gastrointestinal tract. However, we don't yet know whether SARS-CoV-2, present in the intestines of COVID-19 patients, plays a significant role in transmission. Our findings indicate that we should look into this possibility more closely." The current study is in line with other recent studies that identified gastrointestinal symptoms in a large fraction of COVID-19 patients and virus in the stool of patients free of respiratory symptoms. Special attention may be needed for those patients with gastrointestinal symptoms. More extensive testing using not only nose and throat swabs, but also rectal swabs or stool samples may thus be needed.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) detection platforms currently report qualitative results. However, technology based on RT-PCR allows for calculation of viral load, which is associated with transmission risk and disease severity in other viral illnesses.1 Viral load in COVID-19 might correlate with infectivity, disease phenotype, morbidity, and mortality. To date, no studies have assessed the association between viral load and mortality in a large patient cohort.2, 3, 4 To our knowledge, we are the first to report on SARS-CoV-2 viral load at diagnosis as an independent predictor of mortality in a large hospitalised cohort (n=1145).

Clinical suspicion and indicated SARS-CoV-2 testing, including antibody testing, might be needed to recognize and treat adults with MIS-A. Further research is needed to understand the pathogenesis and long-term effects of this condition. Ultimately, the recognition of MIS-A reinforces the need for prevention efforts to limit spread of SARS-CoV-2. COVID-19

In December 2019, the Coronavirus disease 2019 (COVID-19), caused by a novel coronavirus SARS-CoV-2, emerged in Wuhan, Hubei province, China1 and soon spread across the world. In this ongoing pandemic, public health concerns and the urgent need for effective therapeutic measures require a deep understanding of its epidemiology, transmissibility and pathogenesis. Here we analyzed the clinical, molecular and immunological data from 326 confirmed cases of COVID-19 in Shanghai. Genomic sequences of SARS-CoV-2 assembled from 112 quality samples together with sequences in the Global Initiative on Sharing All Influenza Data (GISAID) showed a stable evolution and suggested two major lineages with differential exposure history during the early phase of the outbreak in Wuhan. Nevertheless, they exhibited similar virulence and clinical outcomes. Lymphocytopenia, especially the reduced CD4+ and CD8+ T cell counts upon admission, was predictive of disease progression. High levels of IL-6 and IL-8 during treatment were observed in patients with severe or critical disease and correlated with decreased lymphocyte count. The determinants of disease severity seemed to stem mostly from host factors such as age, lymphocytopenia, and its associated cytokine storm, whereas viral genetic variation did not significantly affect the outcomes.

Ehre, a member of the UNC Marsico Lung Institute and the UNC Children's Research Institute, captured these images to illustrate how intense the SARS-CoV-2 infection of the airways can be in very graphic and easily understood images. Her lab conducted this research in collaboration with the labs of Ralph Baric, Ph.D., the William R. Kenan Distinguished Professor of Epidemiology at the UNC Gillings School of Public Health, who holds a joint faculty appointment at the UNC Department of Microbiology and Immunology, and Richard Boucher, MD, the James C. Moeser Eminent Distinguished Professor of Medicine and Director of the Marsico Lung Institute at the UNC School of Medicine Covid-19

The emergence of three lethal coronaviruses in <20 years and the urgency of the COVID-19 pandemic have prompted efforts to develop new therapeutic strategies, including by repurposing existing agents. After performing a comparative analysis of the three pathogenic human coronaviruses severe acute respiratory syndrome coronavirus 1 (SARS-CoV-1), SARS-CoV-2, and Middle East respiratory syndrome coronavirus (MERS-CoV), we identified shared biology and host-directed drug targets to prioritize therapeutics with potential for rapid deployment against current and future coronavirus outbreaks.

A study of nearly 2,000 Marine recruits who went through supervised quarantine before starting basic training revealed several instances of asymptomatic transmission of SARS-CoV-2, the virus that causes COVID-19, despite the quarantine measures.

Aerosol transmission of viruses must be acknowledged as a key factor leading to the spread of infectious respiratory diseases. Evidence suggests that SARS-CoV-2 is silently spreading in aerosols exhaled by highly contagious infected individuals with no symptoms. Owing to their smaller size, aerosols may lead to higher severity of COVID-19 because virus-containing aerosols penetrate more deeply into the lungs (10). It is essential that control measures be introduced to reduce aerosol transmission. A multidisciplinary approach is needed to address a wide range of factors that lead to the production and airborne transmission of respiratory viruses, including the minimum virus titer required to cause COVID-19; viral load emitted as a function of droplet size before, during, and after infection; viability of the virus indoors and outdoors; mechanisms of transmission; airborne concentrations; and spatial patterns. More studies of the filtering efficiency of different types of masks are also needed. COVID-19 has inspired research that is already leading to a better understanding of the importance of airborne transmission of respiratory disease.

Among the many uncertainties that remain about Covid-19 is how the human immune system responds to infection and what that means for the spread of the disease. Immunity after any infection can range from lifelong and complete to nearly nonexistent. So far, however, only the first glimmers of data are available about immunity to SARS-CoV-2, the coronavirus that causes Covid-19.

Efforts to track SARS-CoV-2 sequences have helped identify worrying variants - but researchers are blind to emerging mutations in some regions.

More than a year after COVID-19 emerged, many mysteries persist about the disease: why do some people get so much sicker than others? Why does lung damage sometimes continue to worsen well after the body seems to have cleared the SARS-CoV-2 virus? And what is behind the extended, multi-organ illness that lasts for months in people with 'long COVID'? A growing number of studies suggest that some of these questions might be explained by the immune system mistakenly turning against the body - a phenomenon known as autoimmunity.

This virus wasn't something we knew nothing about. There was so much we knew, from day one, including because of SARS, the previous almost-pandemic that was also a similar coronavirus. We could have used that vital pre-information better if we had matched the requisite epistemic humility that a pandemic requires-an acknowledgement that we aren't certain of anything-with an insistence that this situation wasn't a blank slate. We could have utilized our prior knowledge to plan ahead, while not letting go of the uncertainty-taking thoughtful steps but without overstating our confidence.

There is a need to better understand the contribution of asymptomatic SARS-CoV-2 infections (those with no symptoms at all throughout the infection) in driving the current pandemic. However, there are caveats that in our opinion are pertinent when interpreting the reported findings of this review, including the lack of a clear definition of asymptomatic infection and selective inclusion of cross-sectional studies. In addition, there is a problematic interpretation of a narrative review containing a dearth of poor-quality evidence resulting in an overestimate of asymptomatic infections, which might misinform policy response.

Converging lines of evidence indicate that SARS-CoV-2, the coronavirus responsible for the COVID-19 pandemic, can pass from person to person in tiny droplets called aerosols that waft through the air and accumulate over time. After months of debate about whether people can transmit the virus through exhaled air, there is growing concern among scientists about this transmission route.

team of researchers concludes that a game-theory approach may offer new insights into both the spread and disruption of viruses, such as SARS-CoV-2. Its work, described in the Journal of the Royal Society Interface, applies a "signaling game" to an analysis of cellular processes in illuminating molecular behavior.