PB1-F2, present in most influenza A viruses, induces secondary bacterial pneumonia in mice, according to study in Cell Host & Microbe.
A protein in influenza A virus (IAV) increases the deadliness of resulting bacterial infections, according to researchers at the department of infectious diseases at St. Jude Children’s Research Hospital.
Investigators examined the interaction between influenza and bacterial infection by studying a newly discovered IAV protein, PB1-F2. The gene encoding PB1-F2 is present in nearly all IAVs including highly pathogenic avian IAVs that have infected humans and the IAV associated with the 1918 pandemic, report the scientists.
The researchers found that expression of PB1-F2 increased the incidence of and exacerbated secondary bacterial pneumonia in a mouse model. Intranasal delivery of a synthetic peptide derived from a portion of PB1-F2 had the same effects.
The team also found that an influenza virus engineered to express a version of PB1-F2 identical to that in the 1918 pandemic strain was more virulent in mice and led to more severe bacterial pneumonia.
The study appears in the October issue of Cell Host & Microbe.
