1887

Abstract

African swine fever is a devastating disease of domestic swine and wild boar caused by a large double-stranded DNA virus that encodes for more than 150 open reading frames. There is no licensed vaccine for the disease and the most promising current candidates are modified live viruses that have been attenuated by deletion of virulence factors. Like many viruses African swine fever virus significantly alters the host cell machinery to benefit its replication and viral genes that modify host pathways represent promising targets for development of gene deleted vaccines. Autophagy is an important cellular pathway that is involved in cellular homeostasis, innate and adaptive immunity and therefore is manipulated by a number of different viruses. Autophagy is regulated by a complex protein cascade and here we show that African swine fever virus can block formation of autophagosomes, a critical functional step of the autophagy pathway through at least two different mechanisms. Interestingly this does not require the gene that has been shown to interact with Beclin-1, an important autophagy regulator.

Funding
This study was supported by the:
  • biotechnology and biological sciences research council (Award BBS/E/I/00007039)
    • Principle Award Recipient: NotApplicable
  • biotechnology and biological sciences research council (Award BBS/E/I/00007037)
    • Principle Award Recipient: NotApplicable
  • biotechnology and biological sciences research council (Award BBS/E/I/00007034)
    • Principle Award Recipient: NotApplicable
  • biotechnology and biological sciences research council (Award BBS/E/I/00002120)
    • Principle Award Recipient: ChristopherL Netherton
  • biotechnology and biological sciences research council (Award BBS/E/I/00001709)
    • Principle Award Recipient: NotApplicable
  • This is an open-access article distributed under the terms of the Creative Commons Attribution License. This article was made open access via a Publish and Read agreement between the Microbiology Society and the corresponding author’s institution.
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2021-08-18
2024-04-26
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