Flaviviruses such as Zika virus (ZIKV) and Kunjin virus (KUNV) are mosquito-borne human pathogens that acquire their envelope from host cell lipids. The functional role of lipid–protein interactions in viral glycoproteins, however, remains incompletely understood. This thesis investigates host-dependent lipid integration in flavivirus structural proteins and explores ultraviolet (UV) inactivation of enveloped RNA viruses.The first experimental branch developed a novel approach for generating infectious ZIKV particles in insect cells using a full-length infectious DNA clone, and employed structure-guided mutagenesis of the Kunjin prM glycoprotein to disrupt a conserved lipid pocket. Mutants exhibited reduced infectivity, smaller plaques, and host-dependent effects, while a bioinformatic survey identified conserved cholesterol-binding motifs (CRAC/CARC) across mosquito- and tick-borne flaviviruses.The second branch, in collaboration with the Civil Engineering Department, used a monochromatic UVC system to study viral inactivation at defined wavelengths. ZIKV was fully inactivated at 222 nm with 16 mJ/cm², while RSV showed wavelength-specific sensitivity at 250–270 nm.Together, these findings highlight the structural and functional relevance of lipid–protein interactions in flavivirus infectivity and identify UVC-based strategies for physical inactivation of enveloped RNA viruses. The results have implications for viral pathogenesis research and disinfection technologies