(Reuters) – Antibodies to common-cold viruses, collectively known as hCoV, may hamper the body’s response to SARS-CoV-2, according to new data. Earlier studies have disagreed on whether previously acquired hCoV antibodies protect against SARS-CoV-2 infection.

“A major contributing factor to the discrepancies … is that they were not able to examine the level of hCoV antibodies in the same individual before and after infection,” said Maureen McGargill of St. Jude Children’s Research Hospital in Memphis.

Comparing before-and-after blood samples from people infected with the virus that causes COVID-19, her team found that SARS-CoV-2 infection caused hCoV antibody levels to rise, indicating that to some extent, the viruses appeared similar to the immune system.

But when they compared 121 people who became infected with SARS-CoV-2 and 1,081 who did not, they found that higher baseline levels of hCoV antibodies did not protect against SARS-CoV-2. Instead, they reported in Cell Host Microbe, higher baseline levels of hCoV antibodies were associated with higher levels of SARS-CoV-2 antibodies, which are a sign of more severe COVID-19.

Furthermore, mice whose immune systems had been primed to generate antibodies to attack common-cold viruses appeared less able to generate antibodies that neutralize SARS-CoV-2, the researchers also found.

The findings suggest that hCoV antibodies impair the antibody response to SARS-CoV-2, likely due to the boosting of antibodies that cross-react to SARS-CoV-2 but do not neutralize it, McGargill said.

SOURCE: https://bit.ly/3ILRLlJ Cell Host Microbe, online December 7, 2021.

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