The cell-signaling protein, interferon type 1, has the potential to reduce H5N1 influenza virus' (bird flu virus) replication in mice, and can thus offer protection in the early stages of infection.
The research was conducted in Georgia.
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.
While not much is known about the pathogenic mechanisms of H5N1 influenza viruses, prior research has suggested that their ability to evade innate immune responses within the host, such as the type 1 interferon (IFN-a/B) response, contributes to virulence in mammals.
In the study, they used a mouse model to analyze the role of type 1 interferons in IFN a/ receptor-deficient and wild-type mice challenged with two avian influenza A viruses isolated from humans (HK/483 and HK/486).
The two viruses generally exhibit high and low lethality in mice.
The findings revealed that INF-a/B 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/B receptor-deficient mice.
However, pre-treatment with IFN-a/B significantly reduced replication of both viruses.
"These results suggest a role for the IFN-a/B 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," said the researchers.
The findings of the study have been reported in the Journal of Virology.