Molecular Pathogens 2024, Vol.15, No.4, 209-218 http://microbescipublisher.com/index.php/mp 212 Figure 1 ASFV pH240R inhibits inflammasome activation by interacting with NLRP3 (Adopted from Huang et al., 2023) Image caption: (A) iGLuc activity in HEK293T cells using the iGLuc-based NLRP3 inflammasome system. HEK293T cells were transfected with different doses of a plasmid expressing pH240R in the presence of the components of the iGLuc-based NLRP3 inflammasome system as indicated. (B) Co-IP analysis of interaction between overexpressed pH240R and NLRP3, ASC, or caspase-1 in HEK293T cells. HEK293T cells were transfected with a plasmid encoding pH240R, along with a plasmid encoding HA-tagged NLRP3, ASC, or caspase-1. (C) Co-IP analysis of the interaction between overexpressed pH240R and NLRP3. HEK293T cells were mock-transfected or transfected with a plasmid expressing HA-NLRP3 or Flag-pH240R alone or both. (D) Co-IP analysis of the interaction between pH240R and NLRP3 in PAMs infected with ASFV. PAMs were infected with ASFV (MOI, 1) for 24 h, and then the cells were collected to perform co-IP with anti-pH240R antibody. (E) The subcellular localization of overexpressed pH240R and NLRP3 in HEK293T cells. HEK293T cells were transfected with a plasmid expressing HA-NLRP3 or Flag-pH240R alone or both. (G) Schematic representation of the full-length NLRP3 and its truncated mutants. (H) Co-IP analysis of the interaction between HA-NLRP3 and Flag-pH240R or its deletion mutants in HEK293T cells. HEK293T cells were transfected with a plasmid expressing Flag-pH240R alone or together with HA-NLRP3 or its deletion mutants (Adopted from Huang et al., 2023) 4.2 Alteration of chemokine production ASFV also modulates the host's chemokine production to facilitate immune evasion. The virus has been observed to decrease the expression of chemokines that recruit neutrophils and CD8+ T effector cells, thereby avoiding these critical components of the immune response. This reduction in chemokine production helps the virus evade neutrophil extracellular traps and CD8+ T cell-mediated cytotoxicity, which are essential for controlling viral infections (Zhu et al., 2019). Moreover, transcriptome analyses have revealed that ASFV infection enhances chemokine-mediated signaling pathways and neutrophil chemotaxis in porcine alveolar macrophages (PAMs). This dysregulation of the chemokine axis not only aids in immune evasion but also promotes virus replication by altering host metabolic pathways (Ju et al., 2021). The virus's ability to modulate chemokine production is further evidenced by the
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