Abstract
Autophagy is a relevant cellular defense mechanism that directly eliminates intracellular pathogens and has a crucial role for innate and adaptive immune responses. Some viruses have developed tools to counteract this cellular response. A179L, the viral Bcl2 homolog of African swine fever virus, interacts with proapoptotic Bcl2 family proteins to inhibit apoptosis. Here we report that this gene manipulates autophagy by interacting with Beclin 1 through its BH3 homology domain. At subcellular level, A179L colocalized with Beclin 1 at mitochondria and the endoplasmic reticulum. Virus infection inhibited autophagosome formation in cells; however, when autophagy was induced prior to or at the time of infection the number of infected cells was severely decreased.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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African Swine Fever Virus / genetics*
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African Swine Fever Virus / metabolism
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Animals
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Apoptosis
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Apoptosis Regulatory Proteins / genetics*
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Apoptosis Regulatory Proteins / metabolism
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Autophagy / genetics
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Beclin-1
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Chlorocebus aethiops
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Endoplasmic Reticulum / metabolism*
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Endoplasmic Reticulum / virology
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Gene Expression Regulation
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Host-Pathogen Interactions / genetics
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Membrane Proteins / genetics*
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Membrane Proteins / metabolism
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Mitochondria / metabolism*
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Mitochondria / virology
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Molecular Mimicry
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Phagosomes / metabolism*
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Phagosomes / virology
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Protein Binding
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Protein Structure, Tertiary
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Proto-Oncogene Proteins c-bcl-2 / chemistry
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Proto-Oncogene Proteins c-bcl-2 / genetics
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Proto-Oncogene Proteins c-bcl-2 / metabolism
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Time Factors
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Vero Cells
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Viral Envelope Proteins / chemistry
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Viral Envelope Proteins / genetics*
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Viral Envelope Proteins / metabolism
Substances
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Apoptosis Regulatory Proteins
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BECN1 protein, human
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Beclin-1
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Membrane Proteins
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Proto-Oncogene Proteins c-bcl-2
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Viral Envelope Proteins