Host pathogenesis factors involved in African Swine Fever Virus infection (ASFV host factors)

Host pathogenesis factors involved in African Swine Fever Virus (ASFV) infection comprise a wide array of porcine cellular proteins and pathways that the virus exploits to facilitate its life cycle and evade host defenses. ASFV primarily targets macrophages and monocytes, utilizing host endocytic pathways such as macropinocytosis and clathrin-mediated endocytosis for entry (Galindo & Alonso, 2017). Once inside, the virus relies on host transport machinery, including dynein and microtubules, to move to the perinuclear region where it establishes viral factories (Dixon et al., 2013). Key host factors identified include the scavenger receptor CD163, which has been investigated as a potential entry mediator, and various heat shock proteins like Hsp70 that assist in viral protein folding (Popescu et al., 2017; Wang et al., 2021). Furthermore, ASFV modulates host signaling pathways, such as the cGAS-STING and NF-kappaB pathways, to suppress the production of interferons and other pro-inflammatory cytokines (Zhuo et al., 2020). Because ASFV is a complex virus with no current vaccine, these host factors are being investigated as potential targets for host-directed antiviral therapies. Experimental compounds like statins (which disrupt cholesterol-dependent entry) and various kinase inhibitors have shown efficacy in reducing viral titers in vitro, although their clinical application in livestock is limited by potential toxicity and the need for high specificity (Gaudreault et al., 2020).

Other names

African Swine Fever Virus host factorsASFV host-virus interactionsHost determinants of ASFV infectionPorcine host factors for ASFV

Inhibition of host-mediated viral entry, uncoating, genome replication, or assembly through the modulation of cellular pathways.