Homologous recombination does not play a major role in the evolution of the human influenza A virus according to a recent Fogarty-supported study published in the Journal of Virology.
Homologous recombination, or "crossing over," is a process that occurs naturally during the formation of organisms. Recombination allows chromosomes to shuffle their genetic material, increasing the potential for genetic diversity. The influenza A virus has the ability to quickly generate both antigenic variants that can escape host immunity, as well as genotypes that provide resistance to antiviral drugs typically used to combat flu.
Human Influenza A Virus.
Influenza A viruses are a major source of respiratory disease in humans, causing 36,000 deaths each year in the U.S. and occasionally starting widespread pandemics, according to the CDC. As much as 20 percent of the U.S. population gets the flu every year and more than 200,000 people are hospitalized.
The dynamic nature of the virus and its ability to evolve are of major concern to the global health community. New influenza viruses emerge as a result of a process called antigenic shift, which prompts a sudden and major change in influenza A viruses. If these changes result in a new influenza A virus subtype that can infect humans and spread easily from person to person--an influenza pandemic can occur.
In order to determine the extent of homologous recombination in human influenza A virus, the authors assembled a data set of 13,852 sequences representing all eight segments and of both major circulating subtypes of the virus, H3N2 and H1N1.
The study concludes that no sequence of human influenza A virus contains a clear signature of the action of homologous RNA recombination. As over 10,000 different sequences were analyzed, the authors contend that if it occurs at all, homologous recombination plays only a very minor role in the evolution of human influenza A virus.
Homologous Recombination is Very Rare or Absent in Human Influenza A Virus. Maciej F. Boni, Yang Zhou, Jeffrey K. Taubenberger, Edward C. Holmes. J. Virol. doi:10.1128/JVI.02683-07
To read the study, visit: http://jvi.asm.org/cgi/reprint/JVI.02683-07v1