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However, it is not known whether deletion or variation in the PL motif of NS1 proteins influence the virulence of H9N2 viruses in the poultry host.
It is likely that Bangladeshi H9N2 viruses are evolving to adapt and replicate efficiently in the poultry host because genes mostly comprising the nucleoprotein complex (NP, PA and PB1) are the most heterogeneous.
Poultry host density is often considerably higher than the virus would encounter in the wild, and in intensive systems the high density is maintained throughout the life of the flock.
In contrast, the capacity to colonize and infect ruminant host species is most likely the result of a small number of host jumps by S. aureus strains of human origin which were followed by genetic adaptation to ruminants, in a similar fashion to the recently reported poultry host switch by a subtype of the successful human CC5 lineage (Lowder et al. 2009).
Avian influenza surveillance shows that G1-like viruses may have been introduced into Pakistan and the Middle East after 1997 and could have continued to circulate in the poultry host for a few years, eventually leading to a well-defined genetic subgroup (H9N2_Mideast A/B/C/D lineages), as reported previously.
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In some instances, AIV strains from poultry hosts have increased pathogenicity for poultry species [9], [10], and have acquired an ability to infect mammalian hosts [11], [12], [13], and/or have caused fatal infections in humans [14], [15].
However, a vast number of poultry hosts serve as a reservoir, providing a sufficient population basis for accumulating such mutations [ 52].
The variation found in resistance patterns might have resulted from exposure to different antimicrobial drugs, resulting in different selection pressure on E. faecalis in the human and poultry hosts.
Conservation of the SRRPs and SecA2-SecY2 cluster in all six L. reuteri strains from pig MLSA lineages IV and V (this work) and in most strains from rodents (MLSA lineages I and III) but not in isolates from human and poultry hosts (MLSA lineages II and VI) may explain host-specific differences in L. reuteri biofilm formation [ 12].
Furthermore, the impact of agriculture upon bacterial evolution has been demonstrated in Staphylococcus aureus where the majority of isolates from chickens are the descendants of a single human-to-poultry host jump that occurred approximately 38 years ago (range, 30 to 63 years ago) in Poland [56].
They are repeatedly associated with poultry outbreaks but are also found in non-poultry hosts.
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