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Rift Valley Fever Virus (RVFV) antigens primarily consist of the surface glycoproteins Gn and Gc, and the internal nucleocapsid (N) protein. The Gn and Gc glycoproteins are critical for viral attachment to host cells and subsequent membrane fusion, making them the primary targets for neutralizing antibodies and vaccine development. The N protein is highly conserved and abundant during infection, serving as a major target for diagnostic assays and T-cell mediated immunity. RVFV is a zoonotic Phlebovirus that causes significant outbreaks of Rift Valley Fever, characterized by symptoms ranging from mild flu-like illness to severe complications such as viral hemorrhagic fever, encephalitis, and ocular disease. Therapeutic strategies targeting these antigens include the development of monoclonal antibodies to block viral entry and live-attenuated or viral-vectored vaccines designed to elicit long-lasting protective immunity. Additionally, small molecule antivirals like Favipiravir target the replication machinery associated with the viral complex to reduce viral load during acute infection.
Vaccines utilize these antigens to induce neutralizing antibodies and T-cell responses; antiviral drugs like Favipiravir inhibit the viral RNA-dependent RNA polymerase to prevent replication of the viral genome associated with these antigens.
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