Intrahost HA #polymorphisms and culture #adaptation shape antigenic profiles of #H3N2 #influenza viruses

Loss of a morph is associated with asymmetric character release in a radiation of woodland salamanders - preLights

A biological phenomenon triggers faster evolution rates in woodland salamanders

Ecology and sexual conflict drive the macroevolutionary dynamics of female-limited colour polymorphisms

Sexual conflict over mating has been documented in many species, both in the field and in experimental studies. In pond damselflies (family Coenagrionidae), sexual conflict maintains heritable female colour polymorphisms, with one female morph typically being a male mimic. However, it is not known whether sexual conflict can also explain the evolutionary origin of female-limited colour morphs, and if so, what ecological factors play a role in this macroevolutionary transition, by modulating the strength of the conflict. Furthermore, the effects of sexual conflict on phylogenetic diversification remain controversial, in particular, whether sexual conflict elevates speciation rates, extinction rates, or both. Here, we use phylogenetic comparative methods to show that female colour polymorphisms are more likely to evolve when population densities at breeding sites are high, and that these demographic conditions are more common at high latitudes and in open landscapes. We show that female-limited polymorphisms typically evolve from sexually dimorphic ancestors through the addition of a male-like female morph, consistent with the hypothesis of selection for male mimicry. Female colour polymorphisms increase both speciation and extinction rates, leading to higher evolutionary turnover of polymorphic lineages. We conclude that female colour polymorphisms evolve in a predictable fashion, and are likely driven by ecological conditions that increase the rate of pre-mating interactions and thus the intensity of sexual conflict. The effects of female colour polymorphisms on extinction differ from previous intraspecific studies and indicate contrasting long-term effects of sexual conflict at micro- and macroevolutionary scales. ### Competing Interest Statement The authors have declared no competing interest.

Top 10 discoveries about ancient people from DNA in 2023

This year's highlights include ways of finding ancient relatives, how some phenotypes evolved in ancient people, and trace evidence from artifacts.

Autism Linked With DNA Our Ancestors Inherited From Neanderthals

Some time deep in our evolutionary past, most likely more than once, a significant amount of Neanderthal DNA became mixed in with our own, influencing everything from how we now fight illness to even our appearance.

The impact of PA/I38 substitutions and PA polymorphisms on the susceptibility of zoonotic influenza A viruses to baloxavir - Archives of Virology

Genetic reassortment of avian, swine, and human influenza A viruses (IAVs) poses potential pandemic risks. Surveillance is important for influenza pandemic preparedness, but the susceptibility of zoonotic IAVs to the cap-dependent endonuclease inhibitor baloxavir acid (BXA) has not been thoroughly researched. Although an amino acid substitution at position 38 in the polymerase acidic protein (PA/I38) in seasonal IAVs reduces BXA susceptibility, PA polymorphisms at position 38 are rarely seen in zoonotic IAVs. Here, we examined the impact of PA/I38 substitutions on the BXA susceptibility of recombinant A(H5N1) viruses. PA mutants that harbored I38T, F, and M were 48.2-, 24.0-, and 15.5-fold less susceptible, respectively, to BXA than wild-type A(H5N1) but were susceptible to the neuraminidase inhibitor oseltamivir acid and the RNA polymerase inhibitor favipiravir. PA mutants exhibited significantly impaired replicative fitness in Madin-Darby canine kidney cells at 24 h postinfection. In addition, in order to investigate new genetic markers for BXA susceptibility, we screened geographically and temporally distinct IAVs isolated worldwide from birds and pigs. The results showed that BXA exhibited antiviral activity against avian and swine viruses with similar levels to seasonal isolates. All viruses tested in the study lacked the PA/I38 substitution and were susceptible to BXA. Isolates harboring amino acid polymorphisms at positions 20, 24, and 37, which have been implicated in the binding of BXA to the PA endonuclease domain, were also susceptible to BXA. These results suggest that monitoring of the PA/I38 substitution in animal-derived influenza viruses is important for preparedness against zoonotic influenza virus outbreaks.