Nature wades through the literature on the new coronavirus — and summarizes key papers as they appear.
29 May — The nose could be the body’s entry point to infection
The nose is the probable starting point for COVID-19 infections.
Richard Boucher and Ralph Baric at the University of North Carolina at Chapel Hill and their colleagues tracked the ease with which the new coronavirus infects various cell types in the respiratory tract. The researchers found a gradient of infectivity that decreases from the upper to the lower respiratory tract: the most easily infected cells are in the nasal cavity, and the least easily infected deep in the lungs. (Y. J. Hou et al. Cell http://doi.org/dw2j; 2020). That gradient mapped neatly onto the distribution of cells that express ACE2, a protein that SARS-CoV-2 uses to enter cells.
The authors speculate that the virus gets a foothold in the nose, then sneaks down the respiratory tract when breathed into the airways. They say the results support the use of masks and preventative measures such as nasal cleansing.
28 May — A lost opportunity to stop viral spread in the United States
Genomic analysis has contradicted a high-profile finding about the origins of the first community spread of the new coronavirus in the United States.Machine learning can help get COVID-19 aid to those who need it most
In late February, a widely publicized genomic analysis suggested that SARS-CoV-2 had been silently spreading for weeks in Washington state. The analysis traced the outbreak’s origin to a traveller designated WA1 — even though officials had quickly detected WA1’s infection after his arrival from China on 15 January and had done extensive contact tracing to stop transmission.
But modelling by Michael Worobey at the University of Arizona, Tucson, and his colleagues suggests that WA1 did not trigger a wider outbreak. Instead, the team found evidence that the virus that spread in Washington reached the state from China in mid-February (M. Worobey et al. Preprint at bioRxiv http://doi.org/dwx3; 2020). The findings have not yet been peer-reviewed.
The four weeks between WA1’s arrival and the arrival of the actual source were a “missed opportunity” to stop the virus from taking hold in the United States, the authors say.
27 May — Superspread in Israel caused a high portion of infections
An “extremely high level” of viral superspread helped to seed the new coronavirus across Israel, according to the authors of a genomic analysis.Withholding funding from the World Health Organization is wrong and dangerous, and must be reversed
Adi Stern at Tel Aviv University in Israel and her colleagues sequenced and analysed more than 200 SARS-CoV-2 genomes from people across Israel (D. Miller et al. Preprint at medRxiv http://doi.org/dwvb; 2020). The results, which have not yet been peer-reviewed, show that only 1–10% of infected people caused 80% of the next wave of cases, illustrating the power of superspreaders in viral transmission.
The analysis also found that travelers from the United States and Europe carried the virus to Israel, but US travelers were responsible for a disproportionate share of viral spread. One possible explanation: Israel began restricting entry of people arriving from Europe before it banned US arrivals.
26 May — Exposed children escape infection more often than adults
Children and adolescents under the age of 20 are much less likely than adults to become infected by the new coronavirus, finds a large systematic review of journal articles, preprints and reports.
Russell Viner at University College London and his colleagues screened more than 6,000 studies, of which 18 provided data that met the authors’ criteria for inclusion. The 18 included 7 that had been peer reviewed (R. M. Viner et al. Preprint at medRxiv http://doi.org/dwp6; 2020).Coronavirus tests: researchers chase new diagnostics to fight the pandemic
Studies that traced the contacts of infected individuals show that children are 56% less likely to get infected than adults when in contact with an infected person. The analysis suggests that children have played a smaller part than adults in spreading the virus in the population, but the evidence for this finding is weak. There has not been enough research to determine whether infected children are less likely than adults to pass on the infection, the authors conclude.