AI Article Synopsis
- African swine fever virus (ASFV) causes a deadly disease in pigs and is linked to the ability of certain virulent strains to inhibit type I interferon (IFN) production, impacting the host immune response.
- ASFV encodes proteins that disrupt key immune signaling pathways, specifically targeting the cGAS-STING and JAK-STAT pathways, thereby reducing IFN production and antiviral responses.
- The review discusses the viral proteins involved in this immune suppression and explores their potential role in developing a live-attenuated vaccine for ASFV.
Article Abstract
African swine fever virus (ASFV) is the causative agent of a lethal disease in pigs. Highly virulent strains of ASFV are known to suppress the induction of type I interferons (IFNs), while naturally attenuated strains do not exhibit this capability. Thus, the ability to suppress IFN is assumed to be associated with viral virulence. ASFV genome encodes many proteins capable of disrupting crucial components of host immune response pathways. Notably, these viral proteins interfere with the induction of type I IFNs by targeting various steps of the cGAS-STING signaling pathway. Additionally, certain viral proteins impede the expression of interferon-stimulated genes by interfering with the JAK-STAT pathway. Consequently, ASFV proteins hamper both IFN production and the induction of antiviral responses by IFNs. This review article summarizes the viral proteins responsible for suppressing various steps of the cGAS-STING and JAK-STAT signaling pathways and discusses the potential application of this knowledge to the rational design of a live-attenuated ASFV vaccine.
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| http://dx.doi.org/10.1016/j.virol.2024.110317 | DOI Listing |
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