ZIKV has been reported to affect the function of TJs through innate immunity, such as its ability to over activate the ERK/MAPK pathway, thereby disrupting the BTB to increase the permeability of TJs [47] and causes ZO-1 degradation via the production of inflammatory mediators, thus acting in the later stages of viral infection [48] (Figure 2). Here, TJP1 is linked to viral infectious disease.