Molecular Pathogens 2024, Vol.15, No.4, 209-218 http://microbescipublisher.com/index.php/mp 214 inhibit interferon (IFN) signaling and other immune responses, making it difficult to pinpoint specific targets for vaccine development (Figure 2)(Gallardo et al., 2018; Dixon et al., 2019; Zhu et al., 2023). Another challenge is the lack of comprehensive understanding of the virus-host interactions at the molecular level. The virus primarily infects macrophages and monocytes, cells that play crucial roles in the immune response. However, the exact mechanisms by which ASFV modulates these cells to evade the immune system are not fully understood (Dixon et al., 2019). Advanced techniques such as quantitative proteomics and transcriptome analysis have been employed to identify differentially expressed proteins and genes during ASFV infection, but these methods require sophisticated equipment and expertise, which may not be readily available in all research settings (Zhu et al., 2019; Lv et al., 2022; Song et al., 2024). Figure 2 Mechanisms of apoptosis inhibition by ASFV. Pathways by which ASFV inhibits induction of apoptosis in infected cells are shown as red icosahedra with the name of the protein inside. The ASFV pA179 L Bcl-2 family protein binds to and inhibits several BH3 only domain pro-apoptotic proteins. The pA224 L IAP-family protein binds to and inhibits caspase 3 and activates NF-kB signalling thus increasing expression of anti-apoptotic genes including cFLIP, cIAP2 and c-rel. The pDP71 L protein recruits protein phosphatase 1 to dephosphorylate eIF-2α restoring global protein synthesis and inhibiting transcriptional activation of pro-apoptotic CHOP. The pEP153R protein inhibits activation of the p53 protein (Adopted from Dixon et al., 2019) The study by Dixon et al. (2019) demonstrated the mechanisms by which various genes within the ASFV genome help the virus evade the host immune system by inhibiting interferon (IFN) signaling and other immune responses. ASFV-encoded proteins, such as the MGF360 and MGF505 families, are capable of suppressing IFN production and signaling within host cells, making it difficult to precisely target specific proteins in vaccine development. The presence of these mechanisms not only enhances the virus's pathogenicity but also complicates vaccine design, making a deep understanding of these processes crucial for effective antiviral strategies.
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