Immune imprinting is the tendency for someone’s initial exposure to a virus to bias their immune response when they meet the same virus again.
New studies
- Various new studies are now showing how imprinting is shaping people’s response to SARS-CoV-2. For example, those infected with the earliest strain or with the subsequent Alpha or Beta strains mount varying immune responses to a later Omicron infection, depending on the strain to which they were first exposed.
- Even exposure to Omicron itself doesn’t seem to help update the imprinted response of people previously infected with an older strain, which might explain why they can be reinfected.
About Immune Imprinting
- Imprinting was first observed by Jonas Salk and Thomas Francis in 1947 in people with influenza. They were the developers of the first flu vaccine, together with another scientist, Joseph Quilligan.
- They found that people who had previously had flu, and were then vaccinated against the current circulating strain, produced antibodies against the first strain they had encountered.
- Researchers gave the phenomenon the tongue-in-cheek name ‘original antigenic sin’, although today most researchers prefer to call it imprinting.
- The phenomenon can explain some observations from the past, such as the surprisingly high mortality among young adults during the 1918 influenza pandemic. Members of the older generation, exposed in their youth to a flu strain that closely matched the deadly H1N1 pandemic strain, had a more robust immune response than did younger adults, whose first exposure was to a mismatched strain.
- Imprinting equips the immune system with a memory of an invader that helps it prepare to do battle again.
- The key players are memory B cells, which are generated in lymph nodes during the body’s first exposure to a virus. These cells then keep watch in the bloodstream for the same foe, ready to develop into plasma cells that then churn out antibodies.
- The snag comes when the immune system encounters a similar, but not identical, strain of a virus. In this case, rather than generate new, B cells to produce tailored antibodies, the memory-B-cell response kicks in. This often leads to the production of antibodies that bind to features found in both the old and new strains, known as cross-reactive antibodies. They might offer some protection but are not a perfect fit to the new strain.
(Source: Nature)
