Previous infection and immunity to one of the common cold coronaviruses may have put people at risk for more severe COVID illness and death, according to a new study.
At the start of the COVID pandemic, it was hoped that a pre-existing immunity to the common cold might protect you against COVID, but new evidence suggests that sometimes the opposite can happen.
The study in the Journal of Infectious Diseases examined immunity to various coronaviruses, including the SARS-CoV-2 virus that causes COVID, in blood samples taken from 155 COVID patients during the first months of the pandemic. Of these patients, 112 were hospitalized and provided sequential samples during their hospitalization.
These hospitalized patients experienced a large and rapid increase in antibodies targeting SARS-CoV-2 and several other coronaviruses. While big boosts in antibodies – protective proteins generated by the immune system – are usually a good thing, in this case it wasn’t.
The researchers found that these antibodies targeted parts of the spike protein (which sits on the surface of coronaviruses and helps them infect cells) that were similar to cold coronaviruses that the immune system remembered from previous infections.
Unfortunately, targeting these areas meant that antibodies could not neutralize the novel SARS-CoV-2 virus. When levels of these antibodies rose faster than levels of SARS-CoV-2 neutralizing antibodies, patients had more severe disease and a higher risk of death.
“In people who were sicker – those who were in intensive care or who died in hospital, the immune system responded robustly in a less protective way,” says lead author Martin Zand, senior associate dean of clinical research at the University of Rochester Medical Center. “It took longer for these patients for the immune system to make protective antibodies…unfortunately, too late for some.
This study adds to a growing body of evidence that a phenomenon called immune imprinting is at play in COVID immune responses. Zand, who is also co-director of the University of Rochester’s Institute for Clinical and Translational Sciences (UR CTSI), compares this phenomenon to an “immune distraction”: immunity to a threat (seasonal coronaviruses) hijacks the response immune to a similar new threat. (SARS-CoV-2). Immune fingerprinting has been linked to poor immune responses to other viruses, such as influenza, and may have implications for vaccine strategies.
According to some predictions, COVID is likely to be with us for a long time, with new, milder strains emerging and circulating on an annual or seasonal basis. If these predictions hold true, the study suggests that we will need to regularly develop new vaccines targeting new strains of SARS-CoV-2. Although none have hit the market yet, pharmaceutical companies like Pfizer and Moderna have been developing and testing new versions of their COVID vaccines as concerning new variants have emerged.
“We should expect the development of new vaccines to be a good thing,” Zand says. “That doesn’t mean the original science was wrong. It means that nature has changed. If we want an immune system that pays attention to the right things, we have to teach it new tricks with different vaccines. »
The study also analyzed 188 blood samples taken in the pre-COVID era (before December 2019) as controls. Some of the blood samples analyzed for the study were provided by the University of Rochester CTSI COVID-19 Biobank, a repository of blood samples from hundreds of patients with and without COVID infections that was developed by the University of Rochester CTSI and University of Rochester Medical Laboratories Shared Center Resources.
Funding for the study came, in part, from the National Institute of Allergy, Immunology, and Infectious Diseases; the National Center for the Advancement of Translational Sciences; and the Rochester Vaccine Fellowship.
Source: University of Rochester