African swine fever virus virion proteins (ASFV) (ASFV)

African swine fever virus (ASFV) is a large, enveloped, double-stranded DNA virus that causes a lethal hemorrhagic disease in domestic and wild pigs, characterized by mortality rates approaching 100% in acute cases [Gaudreault et al., 2020]. The virion is structurally complex, comprising several layers: an internal nucleoid, a core shell, an inner lipid membrane, an icosahedral capsid, and an outer envelope [Wang et al., 2019]. The virion surface proteins, including p72 (B646L), p54 (E183L), p30 (CP204L), and p12, are essential for the virus's life cycle, mediating attachment to host macrophages and facilitating entry and assembly [Alejo et al., 2018]. These proteins are the primary targets for vaccine development and diagnostic tools, as they are highly immunogenic and critical for viral infectivity [Rock, 2017]. Despite extensive research, the complexity of the ASFV genome and its sophisticated immune evasion strategies have hindered the development of a safe and effective vaccine [Sánchez-Vizcaíno et al., 2015]. Current therapeutic strategies explore the use of small-molecule inhibitors targeting viral enzymes or structural proteins, as well as live-attenuated and subunit vaccine candidates [Dixon et al., 2019]. ASFV primarily infects monocytes and macrophages, employing mechanisms to evade the host's innate and adaptive immune systems [Galindo and Alonso, 2017]. The high environmental stability of the virus and the lack of cross-protection between different genotypes further exacerbate the challenge of controlling outbreaks globally [Dixon et al., 2020].

Other names

African swine fever virus structural proteinsAfrican swine fever virus particlesASFV surface proteinsp72p54p30p12CD2v

Inhibition of viral attachment and entry into host macrophages; disruption of viral DNA replication; induction of protective immune responses through neutralizing antibodies and T-cell activation [Dixon et al., 2019; Rock, 2017].