TITLE:
Mechanisms of African Swine Fever Virus Host Cell Invasion: Viral and Host Determinants
AUTHORS:
Kabengwe Bahati Marcelino, Guijie Fang
KEYWORDS:
African Swine Fever Virus, ASFV, Viral Entry, Host Cell Invasion, CD163, Siglec-1, Macropinocytosis, Endosomal Escape, Immune Evasion, Signaling Pathways
JOURNAL NAME:
Open Journal of Veterinary Medicine,
Vol.15 No.12,
December
11,
2025
ABSTRACT: African Swine Fever Virus (ASFV) is a highly contagious and lethal pathogen affecting domestic and wild swine, causing significant economic losses to the global pork industry. Understanding the mechanisms of ASFV invasion and host-pathogen interactions is critical for developing effective control strategies. This review synthesizes findings to elucidate the molecular and cellular processes underlying ASFV entry, replication, immune evasion, and pathogenesis. Literature findings show that ASFV employs multiple entry pathways, including clathrin-mediated endocytosis, macropinocytosis, and phagocytosis, facilitated by interactions between viral proteins (e.g., p72, p54, p30) and host receptors (e.g., CD163, Siglec-1). Following internalization, scientists further illustrate that the virus undergoes endosomal trafficking, with acidification triggering capsid disassembly and genome release. ASFV then exploits host transcription and translation machinery, utilizing viral enzymes (e.g., DNA polymerase, helicase) to replicate within permissive macrophages and dendritic cells. Multiple studies have confirmed that the virus evades innate immune responses by inhibiting interferon signaling (via proteins like A238L and I329L), blocking apoptosis (through A224L and EP153R), and modulating inflammatory cytokines. Additionally, ASFV disrupts antigen presentation by downregulating MHC class I and II, impairing T-cell responses. Recent studies highlight the role of viral non-structural proteins (e.g., pMGF505-7R, pDP71L) in immune suppression and autophagy manipulation. Furthermore, other studies have identified that host genetic factors, including polymorphisms in immune-related genes (e.g., RELA, TNF-α), influence susceptibility to ASFV. Environmental factors, such as tick vectors (Ornithodoros spp.), further complicated transmission dynamics. While progress has been made in vaccine development (e.g., live-attenuated strains, subunit vaccines), challenges remain due to viral genetic diversity and immune evasion strategies. This comprehensive analysis underscores the complexity of ASFV-host interactions and highlights gaps in current knowledge, emphasizing the need for multidisciplinary approaches to combat this devastating pathogen.