Key result
African swine fever virus I10L protein inhibits autolysosome formation by disrupting RAB7-HOPS-dependent SNARE assembly.
May guide ASF countermeasures in swine; leaves open whether SNARE modulators restore flux in infected macrophages.
ASFV: African swine fever virus; GEF: guanine nucleotide exchange factor; GFP: green fluorescent protein; HOPS: homotypic fusion and vacuole protein sorting; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; PAMs: primary alveolar macrophages; RAB7: RAB7, member RAS oncogene family; siRNA: small interfering RNA; SNAP29: synaptosome associated protein 29; SNARE: soluble N-ethylmaleimide-sensitive factor attachment protein receptor; SQSTM1/p62: sequestosome 1; STX17: syntaxin 17; TM: transmembrane domain; VAMP8: vesicle associated membrane protein 8; VPS39: VPS39 subunit of HOPS complex; VPS41: VPS41 subunit of HOPS complex; YKT6: YKT6 vesicular SNARE protein.
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Chen et al. (2026) studied African swine fever virus infection. African swine fever virus I10L protein was evaluated on autolysosome formation. African swine fever virus I10L protein inhibits autolysosome formation by disrupting RAB7-HOPS complex-dependent SNARE complex assembly.
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