US Pharm. 2018;43(4):4.

The mass media makes a lot of the supposed ineffectiveness of this season’s flu vaccine program, yet reports often fail to tell the whole story. For example, news stories sounded the alarm about vaccine effectiveness (VE) of 36% for the 2017–2018 season (through February 3, 2018), but this is not unprecedented: The VE of the H3N2 component of the flu vaccine in the 2012–2013 season was just 3% more efficacious—protecting 39% of immunized individuals.

That season, public-health experts blamed adaptations in egg-grown vaccines. A recent study in Clinical Infectious Diseases, however, indicates that poor immune responses, as opposed to egg adaptations, may have contributed to low VE that year, according to researchers from the University of Chicago, Harvard University, and others.

“Egg adaptations have variable effects,” said Sarah Cobey, PhD, assistant professor of ecology and evolution at the University of Chicago and lead author of the study. “Sometimes they matter and sometimes they don’t, but what seems to make the most difference is immune history.”

Variability in immunization efficacy by age group would seem to support this theory. For the 2017–2018 flu campaign, reported VE varied among individual age groups: 25% VE against A(H3N2); 51% VE in children aged 6 months to 8 years; 67% VE against A(H1N1)pdm09; and 42% VE against B (mostly B/Yamagata, not in IIV3).

Researchers believe that a phenomenon known as “original antigenic sin” influences reduced VE. Influenza vaccines cause the immune system to generate antibodies that recognize the virus strains that individuals are most likely to encounter. These antibodies target unique sites on the virus, latching on and disabling it. The next time the immune system comes in contact with the virus, it reactivates the same immune cells. The problem with this process, however, is that the virus alters slightly each year and the recognized virus sites may not be the crucial ones responsible for virus neutralization season to season.

Complicating this, explain researchers, the antibodies produced from our earlier encounters with the flu—from either vaccines or infections—take precedence over those created by subsequent inoculations.

Enhanced insight into the mechanisms responsible for the body’s immune response to influenza and other viruses won’t necessarily lead directly to more effective vaccines, however. “There hasn’t been enough consumer and medical demand to shift to more effective vaccines,” Cobey said. “Until recently, there also hadn’t been as much research on the complexity and variation in the immune response to influenza.”

For the 2018–2019 Northern Hemisphere influenza season, vaccines are recommended to protect against the following strains: A/Michigan/45/2015 (H1N1)pdm09-like virus; A/Singapore/INFIMH-16-0019/2016 (H3N2)-like virus; a B/Colorado/06/2017-like virus (B/Victoria/2/87 lineage); and a B/Phuket/3073/2013-like virus (B/Yamagata/16/88 lineage).

Should these flu vaccines not “measure up” in the coming fall and winter, maybe we should consider the impact of individual immune responses and other, to-be-discovered factors before condemning them as poorly designed or manufactured.

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