It was previously thought that after initial infection your body creates antibodies tohelp your immune system in the future. But did you know that a common cold you had at a young age can affect how your react to covid today? Depending on the specific spike protein, your body may have a positive or negative response to future variants. An article by Rachel Brazil describes this as “original antigenic sin”(OAS) and has been linked to the differing immune responses to COVID-19.
THE HISTORY BEHIND OAS.
In 1960, Thomas Francis Jr, a US epidemiologist, noted that the immune system seemed to be ‘permanently programmed’ to produce specific antibodies against the first strain of flu it encountered. These antibodies would then reactivate when a flu virus shared similar epitopes to that of the first strain. Relating to SARS-CoV-2, the varying coronaviruses cause different immune responses from person to person. Similar to this, we learned about memory cells in AP Bio. Once the adaptive immune response takes place memory B, helper T, and cytotoxic cell are created to support future immunity to that specific virus.
Microbiologist at the University of Pennsylvania in Philadelphia, Scott Hensley, spoke with the author of the original article about his team’s work with OAS. “Much like flu, most of us are infected with these common coronaviruses by the age of five or six,” says Hensley. It’s surprising to learn that a coronaviruses have been around for many years before the pandemic. What’s even more surprising is that a simple cold we had as a kid can affectus even today. Hensley and his group analysed blood serum samples taken before the pandemic. Their findings were that the samples had antibodies that defended against a ‘common cold’ coronavirus called OC43. These antibodies could also bind to the SARS-Cov-2 spike protein. Hesley’s group then took samples from before and after SARS-Cov-2 infection for testing. Results showed that infection boosted the production of the antibodies that bind to OC43. They also found that these OC43-binding antibodies bound to the S2 subunit of the SARS-CoV-2 spike protein(due to its similar structure to that in OC43). On the other hand, the antibodies did not bind to the S1 region of the SARS-CoV-2 spike and were unable to stop the virus entering cells.
IS THIS A GOOD OR BAD THING?
Hensly’s group once again were studying OAS, but focused on its effects during the 2009 H1N1 pandemic. Their study showed that past infection to other historical flu strains provided protection against the H1N1 virus. While this may seem good, OAS also has drawbacks. The body may produce antibodies that could be used for other virus strains, but they may not be the best fit for the specific virus. As a result of this the ill equipped antibodies bind to the antigens preventing the body from creating more protective response.
In her article Brazil mentions Aldolfo García-Sastre, director of the Global Health and Emerging Pathogens Institute at the Icahn School of Medicine at Mount Sinai in New York City. García-Sastre observed the levels of the OC43 binding antibodies in patients hospitalized with COVID-19 in Spain. He found an increase in levels of OC43 binding antibodies along with antibodies for HKU1(another betacoronavirus). García-Sastre claimed that, “We looked for a correlation between people mounting higher [levels of] antibodies against these conserved epitopes versus having less protective immunity against SARS-COV-2, and there was a slight correlation”.
THE VERDICT: THERE ISN’T ONE…YET
Because of the varying reactions that follow OAS, the debate on whether or not it is to be seen as beneficial is polarizing. Though th, scientists are still working to find ways to use it in potential vaccines. Comment below to let us know your opinion on the matter!