Changes in ability of equine flu virus to reproduce and survive charted in study

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Equine flu virus samples isolated 40 years apart tested in a study in Scotland.
File image by Hanne Hasu

Key changes to the H3N8 equine influenza virus since it jumped from birds to horses about 60 years ago include a reduced ability to cause tissue damage, scientists have found.

However, this reduction in virulence is tempered by the fact it has improved its ability to replicate and move from cell-to-cell in horses.

H3N8 equine influenza virus is the only subtype currently circulating in equine populations, as other avian-origin subtypes such as H7N7 became extinct.

H3N8 was first reported in the United States in 1963 and has been circulating uninterruptedly in equine populations since. Equine flu is characterised by lesions, mostly in the upper and middle respiratory tract.

Julien Amat and his fellow researchers said understanding the consequences of long-term virus adaptations after viral emergence is important for pandemic preparedness.

Researchers in the University of Glasgow study noted that the mechanisms and consequences of genome evolution on viral fitness following host shifts are poorly understood. Viral fitness – its ability to reproduce and survive – is multifactorial and thus difficult to quantify, they said.

Influenza A viruses circulate broadly among wild birds and have jumped into and become endemic in a range of mammals, including humans, pigs, dogs, seals, and horses.

In their study, reported in PLOS Pathogens, the researchers used equine flu virus samples collected 40 years apart to look at changes related to viral fitness due to genome-wide changes acquired during long-term adaptation.

They undertook laboratory-based experimental infections using equine tracheal tissue samples using the earliest H3N8 equine flu virus sample, isolated in 1963, and another from 2003, after continuous circulation in horses for 40 years.

The later virus showed increased resistance to interferon, an improved ability to replicate, and a more efficient cell-to-cell spread in cells and tissues.

However, despite replicating at higher levels and spreading over larger areas of the respiratory epithelium, the 2003 virus induced milder lesions in the laboratory tissue experiments compared to the 1963 virus.

The findings suggest that adaptations in the virus led to reduced tissue pathogenicity, they said.

“Our results reveal previously unknown links between virus genotype and the host response to infection, providing new insights on the relationship between virus evolution and fitness,” they said.

Overall, the study showed that the H3N8 virus evolved towards enhanced replication and cell-to-cell spread but reduced tissue damage, confirming that viral fitness is adaptive and does not necessarily result in higher virulence.

“Our work provides new insights on a central aspect of virus adaptation following emergence and highlights the need for context dependency in evolutionary theory,” they said.

The study team comprised Amat, Veronica Patton, Caroline Chauché, Daniel Goldfarb, Joanna Crispell, Quan Gu, Alice Coburn, Gaelle Gonzalez, Daniel Mair, Lily Tong, John Marshall Francesco Marchesi and Pablo Murcia, all with the University of Glasgow; and Luis Martinez-Sobrido, with the Texas Biomedical Research Institute in San Antonio, Texas.

Amat JAR, Patton V, Chauché C, Goldfarb D, Crispell J, Gu Q, et al. (2021) Long-term adaptation following influenza A virus host shifts results in increased within-host viral fitness due to higher replication rates, broader dissemination within the respiratory epithelium and reduced tissue damage. PLoS Pathog 17(12): e1010174.

The study, published under a Creative Commons License, can be read here

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