Exploring therapeutic potential of claudin in Flavivirus infection: A review on current advances and future perspectives.

Flavivirus such as Dengue, Zika, West Nile, Japanese encephalitis, and yellow fever virus, composed of single-stranded positive-sense RNA, predominantly contaminated through arthropods. Flavivirus infection characterises from asymptomatic signs to severe hemorrhagic fever and encephalitis. The host's immune system detects these viruses and provides a defence mechanism to sustain their life and growth. However, flaviviruses through different mechanisms compromise the host's immune defence. The current pharmacotherapeutic strategies against Flavivirus infection target different stages of the Flavivirus life cycle and its proteins. On the contrary, the host's immune defence mechanism is equally important to restrict their growth. It has been suggested that flaviviruses compromise claudins to sustain their life and growth inside the mammalian cells. This review primarily focuses on the effect of Flavivirus on claudins (CLDNs), transmembrane proteins that form tight junctions in mammalian cells. CLDNs are crucial in viral entry and pathogenesis by regulating paracellular permeability, particularly in tissues and the blood-brain barrier. Recent studies indicate that the Dengue and Zika viruses can potentially be treated by targeting specific CLDNs-specifically CLDN 1, CLDN 5, and CLDN 7 to inhibit viral entry and fusion. Additionally, it highlights the current challenges and future prospects in developing claudin-based antiviral agents against Flavivirus infections.