ETIDIOH - NEW

Abstract High pathogenicity (HP) avian influenza viruses (AIV) generally evolve from low pathogenicity (LP) precursors after transmission from wild birds to chickens (Gallus gallus domesticus) and turkeys (Meleagris gallopavo), causing severe economic losses worldwide. Turkeys are more susceptible to AIV infection than chickens and are considered potential bridging hosts that facilitate the emergence of HPAIV . Beyond the polybasic cleavage site (pCS) in hemagglutinin (HA), little is known about other virulence determinants of HPAIV in these species. In 2015, HPAIV H7N7 and its LP ancestor were isolated from the same chicken farm, which differed by 16 nonsynonymous mutations across all eight gene segments, in addition to the pCS. Here we identify the genetic determinants, including the pCS, that contributed to the HPAIV H7N7 virulence, transmission, replication, and tissue distribution in chickens and turkeys. Notably, the non-structural (NS1) or matrix (M) proteins ’ encoding segments...

Abstract Evaluating the trade-off hypothesis for the evolution of virulence using empirical data poses significant challenges. The hypothesis suggests that pathogens evolve to maximize transmissibility, but fatality imposes limits as there are diminishing gains in transmissibility . In this study, we analyzed a secondary dataset of influenza virus infections in ferrets (Mustela putorius furo), categorized by Hemagglutinin (HA) and Neuraminidase (NA) subtypes . Subgroups defined by the H7/N9 and H7/N7 combinations exhibited fatality rates of approximately 30% and reached cumulative viral titers close to 7.5 (log10 titer/mL). These levels represent intermediate fatality rates , as the H5/N6 and H5/N1 subgroups had higher fatality rates but reached lower cumulative viral titers. Using cumulative viral titer as a proxy for potential secondary transmissions, the analysis suggests that intermediate fatality rates are associated with higher numbers of secondary transmissions . However, there ...