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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.

Given constant emergence of new infectious threats, Infectious Diseases (ID) should be one of the most attractive medical specialties to students and trainees. Yet, ID Fellowship programs continue to not fill in the match, and ID remains among the lowest paid specialties. Nearly 35 years after Dr. Petersdorf first asked the question, we find ourselves once again wondering, "Whither Infectious Diseases?" To answer this question, and align with predominant US market forces, ID experts should push for: 1) restrictions regarding utilization of ID diagnostics and antimicrobial agents; 2) pay-for-performance measures regarding antimicrobial prescribing rates; and 3) healthcare reform as called for by the American College of Physicians to move away from fee-for-service medicine. Einstein said, "Continuing to do the same thing over and over and expecting a different result is the definition of insanity." We must move towards alignment with market forces, to benefit our patients, society, and our colleagues.

A Purdue University-led team of scientists has evidence that tomatoes may be more sensitive to these types of diseases because they've lost the protection offered by certain soil microbes. The researchers found that wild relatives and wild-type tomatoes that associate more strongly with a positive soil fungus grew larger, resisted disease onset and fought disease much better than modern plants.

Now, a research group under the leadership of professor and virologist Søren Riis Paludan from the Department of Biomedicine at Aarhus University, Denmark, has identified a mechanism which is activated in the cells of the immune system when they are attacked by disease. The discovery involves the protein STING, which sends signals to the nucleus of the cell when an infection threatens.

Land use change-for example, the conversion of natural habitats to agricultural or urban ecosystems-is widely recognized to influence the risk and emergence of zoonotic disease in humans1,2. However, whether such changes in risk are underpinned by predictable ecological changes remains unclear. It has been suggested that habitat disturbance might cause predictable changes in the local diversity and taxonomic composition of potential reservoir hosts, owing to systematic, trait-mediated differences in species resilience to human pressures3,4. Here we analyse 6,801 ecological assemblages and 376 host species worldwide, controlling for research effort, and show that land use has global and systematic effects on local zoonotic host communities. Known wildlife hosts of human-shared pathogens and parasites overall comprise a greater proportion of local species richness (18-72% higher) and total abundance (21-144% higher) in sites under substantial human use (secondary, agricultural and urban ecosystems) compared with nearby undisturbed habitats. The magnitude of this effect varies taxonomically and is strongest for rodent, bat and passerine bird zoonotic host species, which may be one factor that underpins the global importance of these taxa as zoonotic reservoirs. We further show that mammal species that harbour more pathogens overall (either human-shared or non-human-shared) are more likely to occur in human-managed ecosystems, suggesting that these trends may be mediated by ecological or life-history traits that influence both host status and tolerance to human disturbance5,6. Our results suggest that global changes in the mode and the intensity of land use are creating expanding hazardous interfaces between people, livestock and wildlife reservoirs of zoonotic disease.

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).

While scientists still don't fully understand the diverse nature of RNA molecules, it is believed that the proteins binding to them, called RNA-binding proteins, are associated with many types of disease formation. Research led by biomedical scientists from City University of Hong Kong (CityU) has led to a novel detection method, called CARPID, to identify binding proteins of specific RNAs in living cells. It is expected that the innovation can be applied in various types of cell research, from identifying biomarkers of cancer diagnosis to detecting potential drug targets for treating viral diseases.

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.

The "Perturb-Seq" method, published in the journal Science, is an efficient way to identify potential biological mechanisms underlying autism spectrum disorder, which is an important first step toward developing treatments for the complex disease. The method is also broadly applicable to other organs, enabling scientists to better understand a wide range of disease and normal processes.