Virus World

A tiny genetic mutation in the SARS coronavirus 2 variant circulating throughout Europe and the United States significantly increases the virus’ ability to infect cells, lab experiments performed at Scripps Research show. “Viruses with this mutation were much more infectious than those without the mutation in the cell culture system we used,” says Scripps Research virologist Hyeryun Choe, PhD, senior author of the study. The mutation had the effect of markedly increasing the number of functional spikes on the viral surface, she adds. Those spikes are what allow the virus to bind to and infect cells. “The number—or density—of functional spikes on the virus is 4 or 5 times greater due to this mutation,” Choe says.

The spikes give the coronavirus its crown-like appearance and enable it to latch onto target cell receptors called ACE2. The mutation, called D614G, provides greater flexibility to the spike’s “backbone,” explains co-author Michael Farzan, PhD, co-chairman of the Scripps Research Department of Immunology and Microbiology. More flexible spikes allow newly made viral particles to navigate the journey from producer cell to target cell fully intact, with less tendency to fall apart prematurely, he explains.  “Our data are very clear, the virus becomes much more stable with the mutation,” Choe says.

There has been much debate about why COVID-19 outbreaks in Italy and New York have so quickly overwhelmed health systems, while early outbreaks in places like San Francisco and Washington state proved more readily managed, at least initially. Was it something about those communities and their response, or had the virus somehow changed? All viruses acquire minute genetic changes as they reproduce and spread. Those changes rarely impact fitness or ability to compete. The SARS-CoV-2 variant that circulated in the earliest regional outbreaks lacked the D614G mutation now dominating in much of the world. But was that because of the so-called “founder effect,” seen when a small number of variants fan out into a wide population, by chance? Choe and Farzan believe their biochemical experiments settle the question. “There have been at least a dozen scientific papers talking about the predominance of this mutation,” Farzan says. “Are we just seeing a ‘founder effect?’ Our data nails it. It is not the founder effect.”

Preprint Available at bioRxiv (June 12, 2020):

https://doi.org/10.1101/2020.06.12.148726

A new report, sent to the White House science adviser, says the country should not rely on warm weather to stop contagion. The homebound and virus-wary across the Northern Hemisphere, from President Trump to cooped-up schoolchildren, have clung to the possibility that the coronavirus pandemic will fade in hot weather, as some viral diseases do.

But the National Academies of Sciences, Engineering and Medicine, in a public report sent to the White House, has said, in effect: Don’t get your hopes up. After reviewing a variety of research reports, a panel concluded that the studies, of varying quality of evidence, do not offer a basis to believe that summer weather will interfere with the spread of the coronavirus. The pandemic may lessen because of social distancing and other measures, but the evidence so far does not inspire confidence in the benefits of sun and humidity.

The report, sent to Kelvin Droegemeier, director of the Office of Science and Technology Policy at the White House and acting director of the National Science Foundation, was a brief nine-page communication known as a rapid expert consultation. Kristian Andersen, an immunologist at the Scripps Research Translational Institute in California and a member of the Standing Committee on Emerging Infectious Diseases and 21st Century Health Threats at the National Academies, said: “Given current data, we believe that the pandemic likely will not diminish because of summer, and we should be careful not to base policies and strategies around the hope that it will.”

“We might very well see a reduction in spread in the beginning of the summer,” he added, “but we have to be careful not to put that down to a changing climate — it is plausible that such a reduction could be due to other measures put in place.”

Original Report (April 7, 2020):

https://www.nap.edu/read/25771/chapter/1

The coronavirus that causes COVID-19, SARS-CoV-2, can survive for several hours in an aerosolized form and for up to three days on plastic and steel surfaces, researchers reported Tuesday (March 10) on medRxiv. While the detection of viable virus means it’s theoretically possible to transmit the disease from contaminated surfaces or from the air—in addition to the typical route of having larger droplets land directly on a new host after an infected person, say, coughs in their proximity—“We’re not by any way saying there is aerosolized transmission of the virus,” coauthor Neeltje van Doremalen of the National Institute of Allergy and Infectious Diseases tells the Associated Press.

The authors applied SARS-CoV-2 and SARS-CoV, the virus that caused the SARS outbreak of 2003, to plastic, stainless steel, copper, and cardboard in the lab and created aerosolized viruses using a nebulizer. They found viable SARS-CoV-2 three hours after the virus was aerosolized and suspended in the air within a drum, and on surfaces four hours, 24 hours, and 2–3 days after it was deposited to copper, cardboard, and steel or plastic, respectively. SARS-CoV lasted about as long, although it lost viability sooner on cardboard and more slowly on copper. The median half-life for SARS-CoV-2 was 13 hours on steel and 16 hours on plastic. “It’s a solid piece of work that answers questions people have been asking,” Julie Fischer, a microbiologist at Georgetown University who was not involved in the study, tells the AP. “What we need to be doing is washing our hands, being aware that people who are infected may be contaminating surfaces,” and not touching our faces....

Published in medRxiv (March 13, 2020):

https://doi.org/10.1101/2020.03.09.20033217 

The new  coronavirus can survive long exposure to high temperatures, according to an experiment by a team of French scientists. Professor Remi Charrel and colleagues at the Aix-Marseille University in southern 

This paper investigates how air temperature and humidity influence the transmission of COVID-19. After estimating the serial interval of COVID-19 from 105 pairs of the virus carrier and the infected, we calculate the daily effective reproductive number, R, for each of all 100 Chinese cities with more than 40 cases. Using the daily R values from January 21 to 23, 2020 as proxies of non-intervened transmission intensity, we find, under a linear regression framework for 100 Chinese cities, high temperature and high relative humidity significantly reduce the transmission of COVID-19, respectively, even after controlling for population density and GDP per capita of cities. One degree Celsius increase in temperature and one percent increase in relative humidity lower R by 0.0383 and 0.0224, respectively.

This result is consistent with the fact that the high temperature and high humidity significantly reduce the transmission of influenza. It indicates that the arrival of summer and rainy season in the northern hemisphere can effectively reduce the transmission of the COVID-19.

Published on arXIV (March 9, 2020):

https://arxiv.org/ftp/arxiv/papers/2003/2003.05003.pdf