Influenza is famous for its ability to mutate and evolve but are mutations always the virus’ friend? Jesse Bloom discusses his work on influenza escape from serum through mutation and how mutations affect influenza virus function and transmission.

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Julie’s Biggest Takeaways

Influenza is famous for its ability to mutate and evolve through two major mechanisms:

• Antigenic drift occurs when a few mutations accumulate in the influenza genome and lead to seasonal changes.
• Antigenic shift occurs when two influenza strains recombine their genomes to form one previously unknown in human populations.

Avian influenza has caused thousands of zoonotic cases, in which the virus is transmitted from birds to people. This causes serious disease but the virus doesn’t easily pass from person-to-person, limiting how many people are affected. When a zoonotic case becomes easily transmissible between people, as is suspected occurred in the 1918 influenza pandemic, the outcome can be very serious for many, many people.

During antigenic drift, the virus accumulates mutations randomly throughout its genome. Mutations in the hemagglutinin (HA) glycoprotein gene are the mutations most likely to affect the ability of antibodies to attach and block HA during viral infection of a new host cell. The circulating human H3N2 influenza A virus accumulates approximately 3-4 mutations annually within its HA gene, representing a 0.5-1% change. On average, it takes 5-7 years of these mutations accumulating until a viral strain can reinfect a previously infected person.

The changes in the influenza sequence are responsible for waning immunity against the annually circulating strain. This was demonstrated when a flu strain from the 1950s was inadvertently reintroduced in the 1970s; older people who had previously been infected were protected against this exact same strain.

Influenza viruses can escape from sera, which contains many different antibodies, similar to how they can escape from a single monoclonal antibody: through mutations in major antibody binding sites. However, the mutations that allow escape from one person’s serum are different from the mutations that allow escape from another person’s serum. This means the strains that escape one person’s immune system may only be able to infect those with similar immunity.

 

Links for This Episode

• MTM Listener Survey, only takes 3 minutes. Thanks!
• Jesse Bloom’s lab website
• Guns Germs and Steel by Jared Diamond
• Lee J.M. et al. Mapping Person-to-Person Variation in Viral Mutations that Escape Polyclonal Serum Targeting Influenza Hemagglutinin.eLife. August 2019.
• Xue K.S. et al. Cooperating H3N2 Influenza Virus Variants are not Detectable in Primary Clinical Samples.mSphere. January 2018.
• Francis Arnold at ASM Microbe:Innovation by Evolution: Bringing New Chemistry to Life

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