RESUMEN
The ability of low pathogenic (LP) avian influenza viruses (AIV) of the subtypes H5 and H7 to mutate spontaneously to highly pathogenic (HP) variants is the main reason for their stringent control. On-the-spot evidence from the field of mutations in LPAIV to render the virus into nascent HP variants is scarce. Epidemiological investigations and molecular characterization of two spatiotemporally linked outbreaks caused by LP, and subsequently, HPAIV H7N7 in two-layer farms in Germany yielded such evidence. The outbreaks occurred within 45 days on farms 400 m apart. The LP progenitor virus was identified on both farms, with its putative HP inheritor cocirculating and then dominating on the second farm. As postulated before, mutations in the hemagglutinin cleavage site (HACS) proved to be the most decisive change in the genome of HPAIV, in this case, it was mutated from monobasic (LP) PEIPKGR*GLF into polybasic (HP) PEIPKRKRR*GLF. The full-length genome sequences of both viruses were nearly identical with only ten coding mutations outside the HACS scattered along six genome segments in the HPAIV. Five of these were already present as minor variants in the LPAIV quasispecies of the LPAI-only affected farm. H7-specific seroconversion of part of the chicken population together with the codetection of LPAIV HACS sequences in swab samples of the HPAI outbreak farm suggested an initial introduction of the LP progenitor and a subsequent switch to HPAIV H7N7 after the incursion. The findings provide rare field evidence for a shift in pathogenicity of a notifiable AIV infection and re-inforce the validity of current approaches of control measures to curtail low pathogenic H5 and H7 virus circulation in poultry.
