The Genetics of the Flu
The Flu is a virus which is contracted and cannot be inherited or passed down through generations genetically. However, the genetic make-up of the virus, as well as how it operates is of great interest to researchers world-wide.
Influenza A, the primary strand of the Flu, is a textbook example of a re-emerging virus. Its genetic properties and ecological diversity account for this. Infact, history has shown us how re-emegent the virus is.
Antigenic drift produces highly pathogenic strains of Influenza
Antigenic drift, on the other hand, is a mode of change involving the random accumulation of mutant genes of the virus. This drift can cause a loss of effectiveness for a certain vaccine, or effective evasion of the immune system. Like other RNA viruses, the flu's mutations occur rapidly because its polymerase has no proofreading mechanism easily allowing for changes to rise.
Viral gene segments of Influenza A are generally from 890 to 2341 nucleotides long. The 3' end has anywhere from 20 to 45 noncoding nucleotides, and the 5' has 23 to 61 noncoding nucleotides depending, varying from segment to segment. Transcription and replication of the viral RNA always occurs in the nucleus of an infected cell. Here, the switch from transcription to replication happens in the later stages of infection as it requires the synthesis of viral proteins.
Influenza A virions responsible for the
Hong Kong Flu (H3N2) of 1968 which killed 1 million people.
Today, researchers are working as hard as possible to keep ahead of antigenic shift and drift. This task is overwhelming because each new copy of the virus is a mutant from the previous version. Because of a lack of a proofreading mechanism, approximately 1 nucleotide is incorrectly copied during a cell's infection with influenza which results in a mutation. These mutation grow into strain-wide resistances, like H3N2's 91% resistance rate against M2 Inhibitors, once a common treatment, in 2005.