Paramyxoviridae constitutes an RNA-genome virus family that includes the emergent and deadly Nipah (NiV) and Hendra (HeV) viruses. These viruses possess substantial pandemic potential and exhibit an expansive host range, a characteristic underpinned by their conserved ephrin receptors. Being a highly virulent zoonotic pathogen, NiV has caused recurrent outbreaks in Southeast Asia with mortality rates ranging from 40% to 100% among infected individuals. While fruit bats serve as natural reservoirs, other mammals such as pigs, donkeys, dogs, cats, and hamsters can also be permissive to NiV infection, typically through close contact or exposure to bodily fluids. This pronounced ability to spill over combined with a lack of approved vaccines or treatments for NiV infection underscore the urgent nature of studying NiV pathogenesis. This thesis investigates the unexplored functions of NiV glycoproteins and delineates their immunomodulatory and cellular modulatory functions. First, we shed light on the immunomodulatory role of NiV G, a receptor-binding protein, in counteracting the interferon-stimulated gene tetherin. This study applied various molecular techniques with the aim of deciphering the interactions between pathogen and host and thereby unraveling how NiV strategically evades certain antiviral functions. Second, proteomic analyses revealed mitochondrial number to increase during live NiV infection. While the precise molecular mechanisms underlying these modulations remain unclear, this study of NiV glycoproteins and their multifaceted roles serves as a step towards refining our understanding. Our findings contribute to the ongoing effort to understand NiV pathogenesis and enhance our knowledge of virus-host interactions involving both immune and cellular pathways.