Key result
Human influenza C virus and swine influenza D virus (sharing 50% sequence identity) replicated differentially in guinea pigs, resulting in disparate viral shedding and tissue tropism.
Why the study?
Antivirals against influenza A and B viruses are ineffective against influenza C virus, mandating the need to study its pathobiological aspects.
Guinea pigs are a suitable animal model to study the pathobiology of influenza C virus, which exhibits differential tissue tropism compared to influenza D virus.
Guinea pig model enables ICV receptor and pathogenesis studies; leaves open human translation.
Similar to influenza A and B, ICV infections are seen associated with bacterial and viral co-infections which complicates the assessment of its real clinical significance. Further, the antivirals against influenza A and B viruses are ineffective against ICV which mandates the need to study the pathobiological aspects of this virus. Here we demonstrated that the respiratory tract of guinea pigs possesses specific viral receptors for ICV. We also compared the replication kinetics and pathogenesis of huICV and swIDV, as these viruses share 50% sequence identity. The tissue tropism and pathology associated with huICV in guinea pigs are analogous to the mild respiratory disease caused by ICV in humans, thereby demonstrating the suitability of guinea pigs to study ICV. Our comparative analysis revealed that huICV and swIDV replicated differentially in the guinea pigs suggesting that the type-specific genetic differences can result in the disparity of the viral shedding and tissue tropism.
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Sreenivasan et al. (2023) studied Influenza C and D virus infection. Human influenza C virus (huICV) vs. Swine influenza D virus (swIDV) was evaluated on Replication kinetics, pathogenesis, and tissue tropism. Human influenza C virus and swine influenza D virus (sharing 50% sequence identity) replicated differentially in guinea pigs, resulting in disparate viral shedding and tissue tropism.
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