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. 2022 Oct 18;11(10):1200. doi: 10.3390/pathogens11101200

Figure 2.

Figure 2

Multiple viruses regulate TJs expression through the innate immune pathway. HIV infection can activate MAPK, thereby upregulating NF-κB, and disrupting TJs, and the NF-κB and MAPK pathways involved by IL-17 participate in the repair process of the barrier. ZIKV infection can over activate the ERK/MAPK pathway and destroy BTB. Inflammatory cytokines/chemokines caused by JEV infection, such as IP-10 can regulate the expression of TJs, which is considered as the main cause of BBB destruction. Early JEV infection leads to significant upregulation of IP-10, which induces TNF-α via the JNK-c-Jun signaling pathway, and TNF-α directly contributes to BBB decomposition by inhibiting the expression of ZO-1, OCLN, and CLDN-5. DENV infection downregulates the ex-pression of TNF-α, cause a significant decrease in ZO-1 expression and peripheral localization in epithelial and endothelial cells. In the process of RABV infection, IFN-λ maintains the integrity of ZO-1 in the BBB to reduce neuroinflammation. Meanwhile, the downregulation of ZO-1 and OCLN is resulted from the activating JNK/MAPK pathway by PCV2 infection.