Highly pathogenic avian influenza H5N1 viruses increasingly pose a serious public health risk as cases of interspecies transmission from birds to humans continue to rise. Over 400 laboratory-confirmed human cases and 250 deaths from H5N1 virus infection have been reported since 2003. Much is still unknown about the pathogenic mechanisms of H5N1 influenza viruses, but prior research suggests that their ability to evade innate immune responses within the host, such as the type 1 interferon (IFN-a/B) response, contributes to the virulence of these viruses in mammals.
In the study researchers used a mouse model to analyze the role of type 1 interferons in IFN a/β receptor-deficient and wild-type mice challenged with two avian influenza A viruses isolated from humans (HK/483 and HK/486). These two viruses generally exhibit high and low lethality in mice. Results showed that INF-a/β receptor-deficient mice lost significantly more weight and were faster to succumb to death than wild-type mice. Both the HK/483 and H/K 486 virus caused a similar systemic infection in INF-a/β receptor-deficient mice, however, pretreatment with IFN-a/β significantly reduced replication of both viruses.
"These results suggest a role for the IFN-a/β response in the control of H5N1 virus replication both in vivo and in vitro, and as such it may provide some degree of protection to the host in the early stages of infection," say the researchers.