Genetic changes that accompanied shifts of low pathogenic avian influenza viruses toward higher pathogenicity in poultry

Abstract

Avian influenza viruses (AIV) of H5 and H7 subtypes exhibit two different pathotypes in poultry: infection with low pathogenic (LP) strains results in minimal, if any, health disturbances, whereas highly pathogenic (HP) strains cause severe morbidity and mortality. LPAIV of H5 and H7 subtypes can spontaneously mutate into HPAIV. Ten outbreaks caused by HPAIV are known to have been preceded by circulation of a predecessor LPAIV in poultry. Three of them were caused by H5N2 subtype and seven involved H7 subtype in combination with N1, N3, or N7. Here, we review those outbreaks and summarize the genetic changes which resulted in the transformation of LPAIV to HPAIV under natural conditions. Mutations that were found directly in those outbreaks are more likely to be linked to virulence, pathogenesis, and early adaptation of AIV.

Keywords: avian influenza virus; poultry; proteolytic cleavage site; virulence determinants.

Figure 1. Major genetic changes found in HPAIV that have directly evolved from LPAIV. Shown are the genetic changes found in the hemagglutinin (particularly proteolytic cleavage site; denoted as a red square) that accompanied shifts of low pathogenic avian influenza viruses from wild birds reservoir toward higher pathogenicity in land based poultry. The transition periods ranged from few days to several years. All outbreaks were eradicated while the exclamation mark refers to the on-going H7N3 outbreak in domesticated poultry in Mexico since June 2012.