Risk Factors for Cluster Outbreaks of Avian Influenza A H5N1 Infection, Indonesia

Abstract

The type of exposure and the genealogical relationship between index cases and their contacts impacts the risk of clustering. The study adds evidence that AI H5N1 infection is influenced by, and may even depend on, host genetic susceptibility.

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“…Our findings of temporal peaks in influenza virus activity in Greece are consistent with data reported from Vietnam and other South East Asian countries (Finkelman et al, 2007), while avian influenza virus seasonal peak was, also consistent with studies conducted in Germany, Thailand, Indonesia and other regions (Liu et al, 2015) (Probst et al, 2012 (Loth et al, 2011) (Aditama et al, 2011). No correlation observed between influenza types recorded in humans and animals in Greece.…”

Host genetic determinants of influenza pathogenicity

“…Although the vast majority of cases of avian influenza arising in humans involve bird-tohuman transmission [3][4][5][6], clusters of such infections occur within families, suggesting that human-to-human transmission occurs [40][41][42][43][44] and that host genetic determinants may therefore play a contributory role. Alternatively, such familial clustering of infection may simply occur because of increased exposure in the absence of genetic susceptibility [45].…”

Engineering H5N1 avian influenza viruses to study human adaptation

“…56). When such information is considered in light of statistically significant clustering of non-humantransmitted (that is, presumably avian-acquired) household cases in genetically related versus unrelated persons 57,58 , a reasonable explanation seems to us to be that H5N1 is so poorly adapted to humans that exposure does not normally lead to infection or even the development of a detectable immune response 57,59 , except in persons with specific but undefined genetic susceptibilities, many of whom become cases [60][61][62] . There are few data on what the basis of such genetic susceptibilities may be, although recent evidence has linked severe human influenza to a minor IFITM3 allele 63 , supporting the suspicion that genetic determinants of influenza infection and replication in humans do exist.…”