A genetic mutation is marginal in the coronavirus that causes COVID-19 significantly increased the ability of the virus to infect cells, according to laboratory experiments conducted by Scripps Research. The coronaviruses take their name from the spikes on the virus surface, giving an appearance of the crown and allowing them to bind to and infect host cells. The mutation found by Scripps greatly increases the number of peaks, which makes it much more easy for the virus to attach to cells. “The virus with this mutation were much more infectious than those who did not have the mutation in the cell culture system that we used,” explained hyeryun Choe, ph.d., ph.d., lead author of the study. “The number – or density – peaks functional on the virus is four or five times higher because of this mutation. “In a report published on the website of pre-publication bioRxiv, Choe and his colleagues the authors state that the mutation, labeled D614G, is the reason for which certain regions such as New York and Italy have seen a surge in rapid disease, overwhelming local health systems, while other regions such as California have experienced a spreading rate more manageable. The report is currently the subject of a peer review. All of the virus develop tiny mutations in their genetic code as they replicate and spread, although these changes seldom affect the physical condition of the virus – it is the ability to flourish in an environment – positively or negatively. Yet, the virus of SARS-CoV-2, which causes COVIDE-19, did not have the mutation D614G in the early stages of the spread. The variant with the mutation is now the dominant strain in the world – in February, none of the virus sample genetically sequenced by scientists in the world have shown the mutation; in march, a quarter of the samples showed the change. In may, the number had risen to 70 %. Was the question before the scientists was whether this finding was due to “founder effect” seen when a small number of variants were prevalent simultaneously in a large population. “At least a dozen scientific articles have talked about the prevalence of this mutation,” said co-author Michael Farzan, Ph.D., co-chair of the department of the Scripps research immunology and microbiology. “Are we on track to a” founder effect ” ? Our data on the hammer. This is not the founder effect. On the contrary, the authors believe that the mutation provides greater flexibility to the tips, making them less susceptible to rupture. “Our data are very clear, the virus becomes much more stable with the mutation,” explains Choe. The results are based on research using a harmless virus designed to recreate the key protein of the coronavirus. After studying a coronavirus for nearly 20 years, Choe and Farzan have noted a structural difference key between the virus of SARS-CoV-2, and a coronavirus earlier, the outbreak of SARS. The two men were the first to discover that SARS binds to the receptor ACE2 on the cell, and the SARS-CoV-2 is no different. However, while the protein peak on the SARS virus will have a form of tripod when they are seen under an electron microscope, the tripod of the new virus is divided into two separate sections. This product spikes inherently unstable, with only about a quarter of the spikes on each virus maintain their structure long enough to bind a host cell. But the mutation changes the properties of the pic, which makes it more flexible and so less likely to break. “Over time, he found how best to hang in there and not collapse until he needs it,” said Farzan. “The virus is made, under the selection pressure, the more stable. “It is not known whether the mutation has an effect on the severity of the symptoms experienced by persons infected with the SARS-CoV-2, or if it increases the mortality. To find out much more data, ideally from controlled studies, should be collected, Choe said. However, the team noted that the immunity transmitted by the serum of people infected seems to work equally well on both variants of the virus, although they have added that studies of the real world are necessary to fully understand how the mutation affects the transmission.