Swine ANP32A Supports Avian Influenza Virus Polymerase

Author:

Peacock Thomas P.1ORCID,Swann Olivia C.1ORCID,Salvesen Hamish A.2ORCID,Staller Ecco1ORCID,Leung P. Brian1ORCID,Goldhill Daniel H.1ORCID,Zhou Hongbo3,Lillico Simon G.2ORCID,Whitelaw C. Bruce A.2ORCID,Long Jason S.1ORCID,Barclay Wendy S.1ORCID

Affiliation:

1. Department of Infectious Diseases, Imperial College London, London, United Kingdom

2. The Roslin Institute and Royal (Dick) School of Veterinary Studies, University of Edinburgh, Edinburgh, United Kingdom

3. State Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, Hubei, People’s Republic of China

Abstract

Avian influenza viruses can jump from wild birds and poultry into mammalian species such as humans or swine, but they only continue to transmit if they accumulate mammalian adapting mutations. Pigs appear uniquely susceptible to both avian and human strains of influenza and are often described as virus “mixing vessels.” In this study, we describe how a host factor responsible for regulating virus replication, ANP32A, is different between swine and humans. Swine ANP32A allows a greater range of influenza viruses, specifically those from birds, to replicate. It does this by binding the virus polymerase more tightly than the human version of the protein. This work helps to explain the unique properties of swine as mixing vessels.

Funder

National Natural Science Foundation of China

Wellcome Trust

UKRI | Biotechnology and Biological Sciences Research Council

Publisher

American Society for Microbiology

Subject

Virology,Insect Science,Immunology,Microbiology

Reference40 articles.

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