Nancy Lapid

(Reuters.) – Here is a list of recent COVID-19 studies. There is some research that needs to be further investigated to verify the results and has yet to receive peer review certification.

Coronavirus victims are left with self attacking antibodies after being infected.

New findings show that survivors of SARS-CoV-2 infections have high levels antibodies, which can cause them to attack their organs and tissue, months after they are fully recovered.

There were 177 health care workers that had been treated for coronavirus-related infections before vaccines became available. All had chronic autoantibodies. Some of these could cause inflammation or nerve injury and can also inflict permanent damage to the skin, joints and nervous system. Susan Cheng, of Cedars-Sinai Smidt’s Heart Institute in Los Angeles said that it is unusual to find such a wide range of autoantibodies in patients or for them to remain elevated as long as six months. Researchers reported Thursday that patterns of elevated autoantibodies vary between men and women in the Journal of Translational Medicine.

Cheng stated that the antibody levels will remain elevated for at least six more months. It will be crucial to continue monitoring individuals. She is currently investigating whether elevated autoantibodies are associated with chronic symptoms in patients with COVID. Her group also plans to examine autoantibodies after infection with newer viruses.

Omicron reduces the effects of B cells but does not eliminate them

Researchers believe that the effects of antibodies from the immune system’s memory B cells against Omicron coronavirus could be substantial, even though they are weaker.

After the body has learned to recognize SARS/CoV-2 after an infection, or vaccination, the B cells produce new antibodies that neutralize the virus. A bioRxiv study that was submitted before peer review has been published. Researchers examined the strength and effectiveness of over 300 antibodies generated by memory cells from volunteers who were vaccinated.

In a joint email, Matthieu Mahevas from Universite de Paris and Pascal Chappert said “Omicron appeared to evade a very large portion of the memory B cell pool” and that it was “seems not to have been recognized by close to 30% of total antibody and 10% of all potent neutrizing antibodies.” They speculate that the strong proliferative ability of memory B cells to produce and multiply antibodies could compensate for their decreased effectiveness “in less than 2 days”.

They said that B cells work in conjunction with immune system components such as T cells to explain why many people who are vaccinated do not get sick enough to need hospitalization.

Cellular activity makes virus variants more powerful

Research has shown that, in addition to spike mutations which allow the coronavirus to break into cells and mutations that alter the virus’ behaviour inside cells are key factors for why certain variants were more transmissible.

Nevan Krogan of University of California San Francisco said that the results, published in Nature, suggest scientists need to “start looking at mutations other than the spike”, which had so far been the focus of most vaccines and anti-infective drugs. The Alpha variant was discovered by his research team. It causes the infected cells of an infection to increase their production rate for Orf9B. Orf9b causes cells to stop using TOM70 to signal to their immune systems. The researchers stated that the immune system responds less well to higher amounts of Orf9B, which disables TOM70 and allows the virus to evade detection.

Krogan stated that Orf9B has been increasing. “It is rare for mutations to ‘turn up’ proteins. This is a really sneaky virus. It was the same mutation that was detected on Delta. “And sure enough, nearly the exact same mutation is found on Omicron,” said he. This suggests similar effects to the immune system. These new findings could lead to drugs being developed that attack the interactions of Orf9b/TOM70.

Click for a Reuters graphic https://tmsnrt.rs/3c7R3Bl on vaccines in development.