International Journal of Molecular Veterinary Research, 2024, Vol.14, No.5, 185-193 http://animalscipublisher.com/index.php/ijmvr 187 the host's immune response and enhancing viral replication (Wang et al., 2023). The pMGF505-7R protein inhibits IL-1β and type I IFN production by interacting with components of the NF-κB signaling pathway and the NLRP3 inflammasome, which are essential for initiating antiviral responses (Li et al., 2021). These structural proteins are crucial for ASFV's ability to cause disease and evade host defenses. In summary, ASFV's virulence is mediated by a combination of specific genes and structural proteins that enable the virus to evade the host's immune system and enhance its pathogenicity. Understanding these factors is essential for developing effective vaccines and therapeutic strategies against ASFV. Figure 2 Expression analysis and functional classification of ASFV genes (Adopted from Lv et al., 2022) Image caption: (A) Heatmap shows the expression levels for the 184 viral genes in the ASFV SY18 and HuB20 strains. (B) Nucleotide mutations, deletions and insertions in ORFs and the noncoding regions between ASFV SY18 and HuB20 genomes. (C) The functional classification of the detected 184 ASFV genes in SY18 and HuB20 strains, annotated with the most enriched function and divided into 6 clusters. (D) Validation of randomly selected ASFV gene expression by real-time PCR. At 6, 12, 24, and 48 hours after PAMs were infected with ASFV SY18 and HuB20 strain (MOI= 3), the transcriptional level of CP530R, I226R, E146L (highly expressed in the SY18 strain infected group) and MGF_505-2-R, D205R, CP204L (highly expressed in the HuB20 strain infected group) were detected by RT-qPCR. The fold-difference was measured by the 2-DDCt method. The RNA levels were normalized to the corresponding b-actin (Adopted from Lv et al., 2022)
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