A new study led by University professor Sarah Cobey in the Ecology and Evolution Department in collaboration with institutions including Harvard University and the University of Pennsylvania shows flu vaccine efficacy can be influenced by immune responses, which differ from person to person based on their past interactions with the flu.
In the past, aside from incorrect predictions about the flu season’s strongest strain, mutations occurring inside chicken eggs where the vaccines are grown have been cited to explain low vaccine effectiveness. Data from Cobey’s study suggest this is not the only source of variables causing vaccines to fail.
“Overall, vaccination works, but to improve flu vaccines, we need to understand the basic dynamics of the immune response better,” Cobey wrote in an e-mail to The Maroon. “There’s a shortage of good longitudinal studies that track how the immune response in people evolves over time from infection and vaccination, and one of the goals of my lab is to fit mathematical models to these data to try to infer what’s going on.”
Each year, researchers use predictive models to identify which flu strain will be the most prevalent that season. Identifying the proper flu strains to use in vaccines already presents its challenges, but even if researchers identify the exact strain that becomes most widespread in a given year, vaccine efficacy ultimately depends on the immune system’s ability to create antibodies that accurately target the disease. Flu vaccines function by introducing the immune system to a flu strain in order to initiate antibody production. After the body has produced antibodies in response to the vaccine, the body may now use those antibodies to ward off an actual infection. However, not all antibodies have the same ability to recognize or attack infections; the study found that certain antibodies take precedence over others depending on when and how many times a person has contracted the flu or has been vaccinated.
As flu strains change minimally from year to year, it is very likely that antibodies may recognize the disease, but the parts of the virus that the antibodies recognize may no longer be the critical part of the virus that must be neutralized to prevent illness. As a result, people who have contracted the flu or been previously vaccinated may produce an immune response targeted at parts of the new strain that will not ward off infection. According to the study, antibodies created from interactions with the flu early in life often respond over recently developed antibodies, meaning that even if a person has been vaccinated for the proper strain, the antibodies created by the vaccine may not be prompted to react against the disease in a person with prior contact to different flu strains.
While the study makes the breakthrough assertion that immune responses play a larger role in vaccine effectiveness than previously known, egg mutations are not irrelevant as a source of error. Egg mutations have been shown to cause erroneous immune responses, which has led vaccine developers to use alternative growth mediums such as insect cells or dog kidney cells to minimize mutation.
The study’s findings have led Cobey to two larger research questions: “Why does the vaccine not induce a strong response in some people, and how does the vaccine interact with pre-existing responses to determine the specificities (or viral targets) of the antibodies that are induced?” As the pursuit for more effective flu vaccines continues, Cobey believes that these questions will guide the direction of future research.