International Journal of Molecular Veterinary Research, 2024, Vol.14, No.6, 261-268 http://animalscipublisher.com/index.php/ijmvr 264 contributes to rapid disease progression and high mortality (Wu et al., 2021). The virus's interaction with host metabolic pathways also promotes its replication, exacerbating the disease's impact on swine physiology (Ju et al., 2021). 5 Case Study 5.1 Background of the selected outbreak The African swine fever virus (ASFV) has been a significant threat to the global pig industry, with outbreaks causing severe economic losses. A notable outbreak occurred in China in 2018, marking the first report of ASFV in the region. This outbreak involved both high-virulence strains, which can cause up to 100% mortality, and low-virulence genotype I strains, complicating prevention and control efforts (Wang et al., 2022). The virus's ability to spread rapidly and its high mortality rate in domestic pigs have made it a critical concern for the swine industry worldwide (Afe et al., 2023). 5.2 Host cell responses during the outbreak During the outbreak, ASFV demonstrated its capacity to manipulate host cell responses to facilitate its replication and evade the immune system. The virus interacts with host proteins to suppress immune responses, such as inhibiting interferon expression and modulating cytokine production. ASFV proteins, like MGF110-7L, can induce stress responses in host cells, leading to translation suppression and stress granule formation, which are crucial for viral survival and replication (Figure 3) (Zhong et al., 2022). Additionally, ASFV exploits host cell machinery, such as the clathrin-mediated endocytosis pathway, to enter cells and establish infection (Chen et al., 2023). Figure 3 Schematic representation of the proposed role of ASFV MGF110-7L in subversion of the host protein translation (Adopted from Zhong et al., 2022) Image caption: ASFV-encoded MGF110-7L could trigger ER stress and activate the PERK and IRE1α-XBP1 branches of the UPR. The ER stress and UPR induction promotes the phosphorylation of eIF2α by activating the kinases PERK and PKR, resulting in host translation arrest and SG formation (Adopted from Zhong et al., 2022) 5.3 Outcomes and lessons learned The outbreak highlighted the need for improved understanding of ASFV-host interactions to develop effective control measures. The virus's ability to evade immune responses and manipulate host cell processes underscores the complexity of developing vaccines and antiviral strategies. Research into ASFV's interaction with host proteins has provided insights into potential targets for therapeutic intervention, such as the identification of host proteins involved in viral entry and replication (Chen et al., 2022). The outbreak also emphasized the importance of rapid response and containment measures to prevent the spread of ASFV in new regions. Overall, the lessons learned from this outbreak can guide future research and policy decisions to mitigate the impact of ASFV on the swine industry.
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