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Continued adaptation of A/H2N2 viruses during pandemic circulation in humans. | LitMetric

AI Article Synopsis

  • The H2N2 influenza virus caused a pandemic in 1957 and remained in circulation until 1968, with low human immunity and ongoing wild bird presence raising concerns about its transmissibility.
  • Research using ferrets showed that six avian A/H2N2 viruses did not transmit between them, indicating a potentially low pandemic risk for these strains.
  • The study revealed that human A/H2N2 viruses adapted over time, particularly the 1958 strain, which had a more stable hemagglutinin that improved its ability to infect humans, but changes in receptor binding and stability did not significantly impact airborne transmissibility.

Article Abstract

Influenza A viruses of the H2N2 subtype sparked a pandemic in 1957 and circulated in humans until 1968. Because A/H2N2 viruses still circulate in wild birds worldwide and human population immunity is low, the transmissibility of six avian A/H2N2 viruses was investigated in the ferret model. None of the avian A/H2N2 viruses was transmitted between ferrets, suggesting that their pandemic risk may be low. The transmissibility, receptor binding preference and haemagglutinin (HA) stability of human A/H2N2 viruses were also investigated. Human A/H2N2 viruses from 1957 and 1958 bound to human-type α2,6-linked sialic acid receptors, but the 1958 virus had a more stable HA, indicating adaptation to replication and spread in the new host. This increased stability was caused by a previously unknown stability substitution G205S in the 1958 H2N2 HA, which became fixed in A/H2N2 viruses after 1958. Although individual substitutions were identified that affected the HA receptor binding and stability properties, they were not found to have a substantial effect on transmissibility of A/H2N2 viruses via the air in the ferret model. Our data demonstrate that A/H2N2 viruses continued to adapt during the first year of pandemic circulation in humans, similar to what was previously shown for the A/H1N1pdm09 virus.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10721047PMC
http://dx.doi.org/10.1099/jgv.0.001881DOI Listing

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