03.05.2013

Maurer-Stroh et al (2013) Virology Journal

The H7N3 avian influenza strain infected chickens in Mexico last summer and led to the culling of millions of birds. In a study published in Virology Journal, Maurer-Stroh and co-authors investigated the cleavage site of the new virus. According to this study, the H7N3 avian influenza strain which caused outbreaks in chicken farms in June/July 2012 in Mexico has a new extended cleavage site which is the likely reason for its high pathogenicity in these birds. This cleavage site appears to have been naturally acquired and was not present in the closest low pathogenic precursors. Different from recent cleavage site insertions, the origin of the insert here is not from the viral genome but from host 28S ribosomal RNA (rRNA) instead. This is a novelty for a natural acquisition as a similar insertion has so far only been observed in a laboratory strain before. Given the abundance of viral and host RNA in infected cells, the acquisition of a pathogenicity-enhancing extended cleavage site through a similar route by other low-pathogenic avian strains in future does not seem unlikely.