Reacción a "Two mutations identified that make the avian flu virus more dangerous in the United States than in Europe"

The current situation with the highly pathogenic avian influenza (HPAI) H5N1 virus is generating great alarm worldwide, due to multiple outbreaks in wild birds, poultry, and mammals. This study analyzed the differences in pathogenicity between two H5N1 viruses belonging to clade 2.3.4.4b, but from different lineages: North American and Eurasian.

This work is highly relevant, since previous observations suggested that the more recent American lineage exhibits a greater capacity for systemic dissemination, as well as greater tropism and invasion of the nervous system (neurotropism and neuroinvasion), and adaptation to mammals. However, the molecular mechanisms underlying these changes are not fully understood.

Using both in vitro and in vivo models, the researchers provide solid evidence of some of the molecular mechanisms responsible for the increased pathogenicity of the virus and its possible adaptation to mammals. In particular, two key mutations in distinct viral genes (PB2-478I and NP-450N) were identified that significantly increase viral polymerase activity, resulting in enhanced replication capacity.

These mutations not only enhance viral replication but also promote immune cell infection and systemic dissemination, contributing to increased virulence. Furthermore, these changes could play a crucial role in virus adaptation to mammals.

In conclusion, this carefully designed study provides crucial scientific evidence on the genetic determinants associated with the virulence of the H5N1 avian influenza virus subtype. Given the continued global spread of this virus and its growing threat to public health, it is essential to strengthen epidemiological surveillance efforts, as well as to continue research focused on the molecular mechanisms of pathogenicity and virus adaptation to new mammalian species.