Influenza A epidemics

Flu is generally considered to be a mild disease, but influenza can be a major killer of the aged and the immune compromised. Even though the body mounts a strong and effective immune reaction to influenza infections, and the individual is immune from reinfection upon recovery, the virus is able to mount periodic epidemics in which prior immunity to related strains is no protection. The solution to this apparent enigma is found in the broad host range of influenza A and the unique ability of influenza A (but not B or C) genomic segments to be independently packaged into individual virion particles during infection. Such a situation leads to a very inefficient packaging process, but allows for rapid dissemination of a favorable mutation. If there is a mixed infection of two different influenza A virus strains in the same cell, significant genetic changes can arise and will provide a significant evolutionary advantage to the progeny.

Since most immune protection against a viral infection is directed against surface components of any virus (the membrane glycoproteins in the case of influenza virus), one can predict that the antigenic properties of these surface proteins will change or "drift" over time. This drift is due to the random accumulation of amino acid changes (mutations), along with the slight selective advantage of a virus that has a surface protein not as efficiently recognized by the immune system as those of the virus that induced immunity in the first place. Such drift is found in many viruses and other pathogens.

Cytoplasm

Receptor-mediated endocytosis

Influenza A virion

Receptors

MMVN^

WWW 8 separate

RNP's released

Nucleus

10 viral mRNA's

Translation

Viral protein

Rough endoplasmic reticulum, Golgi apparatus

Trans-splicing

Eight RNPs sense strand

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