Researchers have described a new mechanism by which influenza A viruses (IAV) alter the host immune system and make them more or less susceptible to often deadly co-occurring bacterial infections. The role of the PDZ-binding motif of IAV in susceptibility to bacterial superinfections (BSI) is presented in an article published in Viral Immunology, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers.
The Centers for Disease Control and Prevention (CDC) estimates that influenza kills 12,000 to 56,000 Americans each year. A major complication of influenza is the development of secondary bacterial infections, which exacerbate the severity of the disease.
A team of researchers led by Kelly Shepardson and Agnieszka Rynda-Apple, Montana State University, Bozeman, and Victor C. Huber, Sanford School of Medicine, University of South Dakota, Vermillion, demonstrated that the PDZ-bm determines the hosts susceptibility to BSI by controlling production of the cytokines IFN-α/ß. This newly identified mechanism of action for manipulating host immunity and controlling BSI severity specifically involves the regulation of IFN-ß. It is described in detail in the article titled "A Novel Role for PDZ-Binding Motif of Influenza A Virus Nonstructural Protein 1 in Regulation of Host Susceptibility to Postinfluenza Bacterial Superinfections."
"In the current issue of Viral Immunology, Shepardson and colleagues show that the non-structural-1 protein (NS1) of the virus can regulate innate immunity and susceptibility to secondary bacterial infections. Deletion of a key section of the NS1 from the virus resulted in 100% survival and decreased bacterial burden in superinfected mice," says David L. Woodland, PhD, editor in chief of Viral Immunology and adjunct member of the Trudeau Institute in Saranac Lake, N.Y. "These finding suggest that NS1 regulates the time dependent type I interferon response during influenza virus infection, which in turn determines susceptibility to secondary bacterial infections."
Source: Mary Ann Liebert, Inc.