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One of the ongoing mysteries surrounding the spread of the H5N1 bird flu virus has been that among clusters, genetically related blood relatives are far more likely to be co-infected than other household members.
This has led to speculation that their might be some genetic predisposition to catching the virus, that some people have, and others do not.
An intriguing, but unproven theory.
While the study below is on genetically inbred mice - and may not apply to humans – it gives tantalizing evidence that certain genetic factors may determine host susceptibility to the virus.
At least in mice.
First, an overview from Science Daily.
Genes May Determine Susceptibility To H5N1 Avian Influenza A Virus Infection
ScienceDaily (Oct. 26, 2009) — A new study found genetic variations in mice affect their susceptibility to and severity of H5N1 avian influenza A virus infection suggesting that humans who contract the virus may be genetically predisposed.
Below is the abstract from the Journal of Virology, and as you can see, the pedigree of this project is impressive. (Reparagraphed for readability)
(A.C.M. Boon, J. deBeauchamp, A. Hollmann, J. Luke, M. Kotb, S. Rowe, D. Finkelstein, G. Neale, L. Lu, R.W. Williams, R.J. Webby. 2009. Host genetic variation affects resistance to infection with a highly pathogenic H5N1 influenza A virus in mice. Journal of Virology, 83. 20: 10417-10426.)
Received 12 March 2009/ Accepted 21 July 2009Despite the prevalence of H5N1 influenza viruses in global avian populations, comparatively few cases have been diagnosed in humans. Although viral factors almost certainly play a role in limiting human infection and disease, host genetics most likely contribute substantially.
To model host factors in the context of influenza virus infection, we determined the lethal dose of a highly pathogenic H5N1 virus (A/Hong Kong/213/03) in C57BL/6J and DBA/2J mice and identified genetic elements associated with survival after infection. The lethal dose in these hosts varied by 4 logs and was associated with differences in replication kinetics and increased production of proinflammatory cytokines CCL2 and tumor necrosis factor alpha in susceptible DBA/2J mice.
Gene mapping with recombinant inbred BXD strains revealed five loci or Qivr (quantitative trait loci for influenza virus resistance) located on chromosomes 2, 7, 11, 15, and 17 associated with resistance to H5N1 virus. In conjunction with gene expression profiling, we identified a number of candidate susceptibility genes. One of the validated genes, the hemolytic complement gene, affected virus titer 7 days after infection.
We conclude that H5N1 influenza virus-induced pathology is affected by a complex and multigenic host component.
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