Research led by the Università della Svizzera Italiana in Switzerland suggests autoantibodies against specific chemokines are linked with better outcomes after infection with SARS-CoV-2.
Writing in Nature Immunology, the researchers suggest that these autoantibodies could help to reduce excessive inflammation and immune dysregulation that, if left unchecked, could result in symptoms such as those experienced by long COVID patients.
It has become clear over the last few years that infection with SARS-CoV-2 has a broad range of outcomes in different patients ranging from asymptomatic/mild to severe. Similarly, a significant percentage of people who have COVID-19 experience long-lasting effects, or long COVID.
“Some evidence points to a role for immune dysregulation and autoimmunity as contributors to long COVID, although virus persistence has also been proposed,” write the authors.
“Overall, however, there is little understanding of the biology underlying long COVID and the reasons behind the differences in COVID-19 manifestation.”
High levels of inflammation caused by chemokines and other inflammatory cytokines are behind much of the damage caused around the body in severe COVID-19 cases. Chemokines attract neutrophils and monocytes to infection sites around the body, by doing this they sustain high inflammation levels and cause tissue damage and fibrosis.
It has previously been suggested that “auto” antibodies developed by the body against type I interferon (IFN) and similar immune molecules are linked with poor COVID-19 outcomes, but a comprehensive study of chemokine autoantibodies or their effects over time has not been completed before.
The research team assessed samples from three cohorts, comprising 219 people in total who experienced different severities and duration of COVID-19. They found that the presence of autoantibodies against specific chemokines after infection seemed to be protective against developing long COVID at one year after infection.
“Previously it had been observed that autoantibodies are common in severe COVID patients, those who end up in intensive care,” said Jonathan Muri, postdoctoral fellow at the Institute for Research in Biomedicine (IRB, affiliated with the Università della Svizzera italiana) and co-author of the study, in a press statement. “Instead, in this case we discovered the opposite.”
“The immune system in some cases is a double-edged sword,” says Mariagrazia Uguccioni, co-director of the study. “It is important to activate it promptly to neutralize the coronavirus, but it must also be turned off at the right time, otherwise it can do damage.”
