Key result
ASFV protein pF778R suppresses type I interferon response by weakening STAT1 nuclear accumulation.
Why the study?
ASFV causes high lethality in domestic swine with no effective vaccine, and the immune evasion roles of most ASFV-encoded proteins remain unknown.
Population
Preclinical model studying host immune response to African swine fever virus (ASFV)
Design
Preclinical
Authors
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May inform ASFV countermeasures in swine; leaves open whether this STAT1 mechanism extends to other hosts or viruses.
The ASFV protein pF778R evades host innate immunity by inhibiting the nuclear accumulation of activated STAT1, thereby attenuating the type I interferon response.
Chen et al. (2023) studied African swine fever virus infection. ASFV ribonuclease reductase large subunit pF778R was evaluated on Type I interferon (IFN) response and STAT1 nuclear translocation. ASFV protein pF778R negatively regulates the type I interferon response by weakening the nuclear accumulation of activated STAT1 without interfering with its phosphorylation or dimerization.
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