SARS-CoV-2 replicates 10 times faster than 2003 SARS

The new Covid-19 coronavirus reproduces at lightning speed and produces three times more pathogens than the virus that caused the SARS epidemic in 2003. However, it can go unnoticed by the immune system. which explains why people with very high viral loads remain asymptomatic.

In 2003, it had taken six months to contain the SARS epidemic, mainly confined to China and a few Asian countries. It had affected a total of 8,098 people worldwide and caused 774 deaths. In less than three months, the new coronavirus SARS-CoV-2 has already affected more than 2.4 million people in 193 countries with 165,000 deaths. And this, despite a much lower mortality rate (between 0.25% and 5% according to estimates against 10% for the SARS).

SARS-CoV-2 replicates up to 100 times in 48 hours

One of the possible explanations for this surge may lie in the formidable effectiveness of the new virus, reports a study published in the journal Clinical Infectious Diseases by a prominent virologist from Hong Kong University, Yuen Kwok-yung. The researcher and his team conducted an unprecedented procedure for compare the two viruses, by infecting samples of lung tissue donated by patients. The results are enough to thrill. " In some cases, the SARS-CoV-2 replicates up to 100 times in 48 hours, compared to 10 to 20 times with SARS-CoV "Reports Chu Hin, an assistant to the professor and co-author of the study, in the South China Morning Post. Not only does the virus infect cells much faster, but it also produces 3.2 times more viral particles in 48 hours, the researcher says. Suddenly, while the viral load maximum within secretions Nasal is observed after 10 days in patients with SARS-CoV, those with SARS-CoV-2 reach this maximum viral load much faster.

A virus that "masks" its presence with the immune system

However, despite the large viral load induced by SARS-CoV-2 in the body, the latter seems to react with a long delay on ignition. " The virus acts like a ninja, its replication resulting in a lower inflammation and production ofinterfering Says Jasper Chan Fok-woo, another study co-author. These are precisely the interfering, molecules of the family of cytokines, which participate in the effectiveness of the immune response. " While SARS-CoV activates 11 markers of Genoa pro-inflammatory of the 13 possible types, SARS-CoV-2 activates only 5 Says the study. This weak immune response explains why the virus manages to develop so quickly and also the lightness or even the absence of symptoms in many patients, who unknowingly have a very high viral load and are therefore likely to spread the disease insidiously.

But how does the virus so pass incognito in the body? Researchers are on this point only hypotheses. " If the 2019 SARS-CoV-2 and the 2003 SARS-CoV-2 bind and enter the cells hostsvia ACE2 (the receiver to which the protein viral), the mechanism by which the former overcomes the immune response and suppresses the production of interferons as well as pro-inflammatory cytokines to achieve a higher degree of replication viral is still elusive "Admit the authors. SARS-CoV-2 may contain protein antagonists different or more strongly expressed interferon.

Less than 48 hours to prevent virus replication

All of this partly explains why most patients with the new coronavirus are much more contagious and much earlier than with SARS 2003, which makes the disease more difficult to detect. It also complicates treatment, since you have less than 48 hours to administer antivirals able to limit replication of the virus, against a period of 7 to 10 days with SARS.

In addition, the drugs anti-inflammatory which limit the overly strong immune response, which is rather effective in the case of SARS, are completely useless at the start of infection with SARS-CoV-2 since the latter has its own inflammatory self-limiting mechanism. On the other hand, beta-interferon-type products (cytokines mediating antiviral activity) could be useful, says Yuen Kwok-yung at South China Morning Post. This study, limited to a small number of samples, does not in itself represent the variety of immune responses induced by SARS-CoV-2. But it highlights all the difficulty that we are currently facing for fight the virus and his diffusion.

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