Computational studies have predicted RVFV Gc to be a class II viral fusion protein, and previous experiments with other viruses of the Bunyaviridae family support Gc being the main determinant of cell fusion. Fusion assays Ibrutinib utilizing Gn and Gc of Bunyamwera virus found that deletions in Gc prevented syncytia formation. Additional experiments with La Crosse and Tahyna viruses identified Gc as a fusion protein using chimeras, site-directed mutagenesis, and cell-cell-fusion assays. Although it has been widely acknowledged that the RdRp is fundamental to replication and transcription of the RNA virus genome, other roles for the RVFV RdRp have not been previously explored. We found that RdRp was not required for the efficient cellular release of virus or packaging of N and genome. However, RVF-VLPs that lack RdRp, or express a catalytically inactive RdRp, cannot be complemented in trans. Complementing in trans with viral components required for transcription/replication is not unprecedented. Studies with the Ebola virus, which is a nonsegmented negative-sense RNA virus, investigated the viral components necessary for the generation of infectious particles. The Ebola virus VP30 protein, which is required for replication/ transcription by the RdRp, could be complemented in trans for restoration of activity in Ebola-VLP-infected target cells. Recently it was discovered that trans expressed influenza virus RdRp can replicate viral ribonucleoproteins and become incorporated into progeny vRNPs, however only cis RdRp could transcribe vRNPs. This Trichostatin A result suggests that the cis RdRp is somehow different from the trans RdRp. Our complementation studies suggest that a similar phenomenon may be occurring with RVFV RdRp, such that a catalytically active RdRp must be packaged in order for trans expressed RdRp to transcribe a reporter gene. We have illuminated roles for each of the viral components in the assembly, cellular release, and infectivity of RVFV. The interaction of genome and N with Gn triggers release of virus. Our results illustrate a novel mechanism for the efficient generation of infectious virus particles. The design and screening of therapeutics targeting the Gn cytoplasmic tail may offer a novel target for inhibition of both virus release and packaging of the RdRp and encapsidated genome. NAFLD represents a spectrum of changes in the liver that are closely associated with obesity, type II diabetes and other manifestations of the metabolic syndrome. The accumulation of triglycerides in the liver, known as steatosis, is the initial and requisite event in the pathogenesis of NAFLD. Over time, steatosis may progress to steatohepatitis, which is becoming a major contributor to chronic liver disease including cirrhosis and primary liver cancers in the United States. Weight reduction and exercise are the only widely accepted treatments for patients with NAFLD.