International Journal of Molecular Veterinary Research, 2024, Vol.14, No.6, 261-268 http://animalscipublisher.com/index.php/ijmvr 263 Furthermore, ASFV encodes several apoptosis inhibitors, which help in evading host defenses and prolonging the survival of infected cells (Dixon et al., 2019). The virus's ability to modulate immune responses is crucial for its persistence in natural hosts and domestic pigs (Netherton et al., 2019). Figure 2 ASFV proteins modulating the cGAS/STING and NF-κB signaling pathway (Adopted from Afe et al., 2023) 3.3 Resource reallocation for viral assembly ASFV reprograms host cellular machinery to allocate resources for viral assembly. The virus infects macrophages, utilizing clathrin-and cholesterol-dependent endocytosis for entry, which is essential for a productive infection (Galindo et al., 2015). ASFV also influences the host's cellular machinery of protein synthesis, ensuring that viral proteins are synthesized efficiently. This reallocation of resources is critical for the assembly and maturation of new viral particles, facilitating the spread of the virus within the host (Dolata et al., 2023). 4 Outcomes of ASFV Infection 4.1 Cytopathic effects on host cells African swine fever virus (ASFV) primarily targets porcine macrophages, leading to significant cytopathic effects. The virus enters these cells through clathrin- and cholesterol-dependent endocytosis, which is crucial for successful viral replication (Galindo et al., 2015). ASFV infection results in the modulation of host cell gene expression, including the upregulation of pro-inflammatory cytokines and the downregulation of anti-inflammatory cytokines, contributing to excessive tissue inflammation and apoptosis (Yang et al., 2021a). The virus also affects cellular homeostasis by interacting with host proteins, which can lead to cell death and tissue damage (Guo et al., 2021). 4.2 Immune system evasion and suppression ASFV has developed sophisticated mechanisms to evade and suppress the host immune system. It inhibits MHC Class II antigen processing and presentation, thereby avoiding detection by CD8+T effector cells (Zhu et al., 2019). The virus also suppresses macrophage activation and induces immune-suppressive cytokines, which help it evade both innate and adaptive immune responses (Afe et al., 2023). ASFV encodes several apoptosis inhibitors, which prevent the host from effectively clearing the infection (Dixon et al., 2019). Additionally, ASFV can modulate host immune signaling pathways, such as cGAS-STING and NF-κB, to further suppress antiviral responses. 4.3 Impacts on swine physiology and disease progression ASFV infection in domestic pigs leads to acute hemorrhagic fever with a high mortality rate, often reaching 100% in naive herds (Netherton et al., 2019). The virus causes severe physiological disruptions, including elevated body temperature, bleeding, and ataxia. ASFV's ability to modulate host immune responses and induce apoptosis
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