Recombinant Rift Valley Fever Virus Glycoprotein (aa 691-1139)[His]

Rift Valley Fever (RVF) is a zoonosis caused by Rift Valley Fever Virus (RVFV) transmitted by mosquito bites, which can lead to large-scale abortions and deaths of newborn young animals such as sheep, goats, and cattle during pregnancy, causing serious losses to the livestock industry. Most people show self-limiting fever after infection, and a few infected people develop severe symptoms such as hemorrhagic fever, meningoencephalitis, fulminant hepatitis and even blindness.

RVFV belongs to the genus Phlebovirus and has a lipid envelope with a surface composed of glycoproteins Gn and Gc forming a heterodimer. The viral genome is a three-segmented, single-stranded negative-stranded RNA, named L, M, and S segments based on segment size, encoding the RVFV RNA-dependent RNA polymerase (RdRp), envelope glycoprotein precursor (GPC), and nucleocapsid protein (NP), respectively. The M and S segments encode the nonstructural proteins NSm and NSs, respectively, where NSs is an important virulence factor of RVFV that antagonizes the host's type I interferon pathway, and NSm is thought to inhibit apoptosis induced by viral infection. The GPC encoded by the M segment is lysis by host proteases into two glycoproteins, Gn and Gc, which contain the major viral neutralization epitopes and are important antigens for the development of novel vaccines for RVFV. The L segment encodes the largest protein of the virus, the L protein, whose main function is to act as an RNA polymerase and play an important role in viral replication and transcription.

Figure 1. Schematic of the RVFV genome
(Source: Wright D, et al. 2019)

After invading the body, RVFV is transported to peripheral lymph nodes through lymphatic conduits, where it replicates and then enters the circulatory system, after which it further infects important target organs such as the liver, spleen, and kidneys. The virus continues to replicate in the target organ, further causing high levels of viremia, with characteristic hemorrhage and altered serum biochemical markers in severe cases. During infection, the virus suppresses the host's natural antiviral immune response through the anti-interferon action of the NS protein. In the acquired immune response, the body produces neutralizing antibodies against Gn/Gc within 4-8 days of infection. There is no specific treatment for RVFV infection, and vaccination is the most economical and effective means of controlling the spread of the virus.

RVFV Glycoprotein