Treatment using phytochemicals for West Nile virus infection

Treatment for West Nile virus infection

抄録

West Nile virus (WNV) is a mosquito-borne neurotropic flavivirus that has become a major cause of arboviral neuroinvasive disease worldwide. The virus encodes three structural proteins (C, prM/M, and E) and seven non-structural proteins (NS1-NS5) that mediate viral entry, replication, assembly, and immune evasion. WNV is maintained in an enzootic cycle between Culex mosquitoes and avian reservoir hosts, whereas humans and horses are incidental dead-end hosts. Since its introduction into North America in 1999, WNV has spread widely and continues to cause recurrent outbreaks. Approximately 80% of infections are asymptomatic, while about 20% cause West Nile fever. Fewer than 1% progress to West Nile neuroinvasive disease, including meningitis, encephalitis, and acute flaccid paralysis, which are associated with considerable mortality and long-term neurological sequelae. Current treatment remains supportive because no approved antiviral therapy exists. Several licensed drugs, including favipiravir, remdesivir, interferon-α2b, statins, miconazole, cilnidipine, mycophenolate mofetil, nitazoxanide, teriflunomide, and minocycline, have demonstrated anti-WNV and/or neuroprotective effects in experimental studies. In addition, phytochemicals such as epigallocatechin gallate, apigenin, curcumin, hesperidin, hesperetin, quercetin, cianidanol, L-rhamnose, and palmatine inhibit viral entry or target key viral enzymes. Many of these compounds are present in Kampo medicines, including Senkyu-chacho-san, Keigai-rengyo-to, and Seijo-bofu-to. Although these formulations may provide complementary antiviral, anti-inflammatory, and immunomodulatory benefits, further in vitro, in vivo, and clinical studies are needed to establish their safety and efficacy against WNV.