Rift Valley Fever Vaccine

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Rift Valley Fever

Rift Valley Fever (RVF) is a contagious acute animal disease that occurs mainly in Africa. The disease is caused by Rift Valley Fever virus (RVFV), which primarily infects domesticated animals such as sheep, goats, cattle, etc., and the high mortality rate often leads to huge economic losses in the epidemic area. People infected with the virus usually do not show symptoms or only show mild discomforts such as fever, headache, and myalgia. In about 2% of cases, the disease would progress into hemorrhagic fever. In general, the patient will recover within 2-7 days after the disease occurs. 1% of people will die after suffering from this disease, and the mortality rate of livestock infected with the virus is comparable high.

The causative agent of the disease, the Rift Valley Fever Virus, belongs to the Bunyaviridae family. The genome of the virus is a three-part negative single-stranded RNA encoding a total of six proteins, including two glycoproteins G(C) and G(N), nucleocapsid protein N, viral polymerase L, and 2 non-structural proteins NSs and NSm. The outer structure of the virus is a lipid membrane that surrounds the virus and is composed of two glycoproteins RVFV spreads through mosquito vectors and can also be transmitted through contact with tissues of infected animals.

Fig.1 Countries in which Rift Valley fever (RVF) is endemic. (Dungu B and Lubisi BA, 2018)

Fig.2 Countries where RVF vaccines have been implemented. (Dungu B and Lubisi BA, 2018)

Pathogenesis of the Virus

The glycoproteins of the RVFV are required for the virus to enter the host cell, and it releases the viral genome to the cytoplasm by fusion with the endosomal membrane of the target cell. In addition, studies found that the non-structural protein NSs encoded by the viral genome can directly affect the host's immune system and play a role in pathogenicity. NSs work by interfering with the host's interferon antiviral response, an important component of the immune system against viral infections. NSs could interact with and bind to the subunit necessary for RNA polymerase I and II, competitively inhibit their binding to another transcription factor, thus blocking the assembly of transcription factor complex, and ultimately cause inhibition of host antiviral responses. In addition, NSs are capable of binding to the SAP30 protein of the host cell and forming a complex, which can result in the deacetylation of histones, rendering the IFN promoter unable to be transcriptionally activated, thereby blocking the expression of interferon. Moreover, NSs can interfere with the activity of double-stranded RNA-dependent protein kinase R, hence affecting the host's cellular immune response. The filamentous structure formed by NSs in the nucleus of the host cell enables the virus to interact with specific regions of the host DNA, enhancing viral infectivity and down-regulating the host's antiviral response.

The Development of Rift Valley Fever Vaccine

Basic strategies for preventing RVF infection in humans are vaccinating RVFV-vulnerable animals. At present, some RVF vaccines that are being used in livestock are listed below.

Live Attenuated Virus Vaccine

Vaccination is an effective method to control RVF in epidemic area. Smithburn vaccine is the first RVF vaccine prepared in 1949 through serially passaging in the mouse brain using the RVFV virus Entebbe strain. Subsequently, the neurotropic strain of the virus was attenuated in the same manner, and the obtained vaccine containing the mouse brain extract was sold in South Africa from 1951 to 1968. In addition, the modified live virus vaccine using BHK-21 cell for expansion production has also been extended to other South African countries. These vaccines are able to elicit long-lasting protection in vaccinated animals, however, they may cause miscarriage or fetal malformation or even cause reassortment of the virus with pathogenic RVFV. Therefore such vaccines are only used for non-pregnant animals. Clone 13, a novel live attenuated vaccine for RVF, is made from a plaque clone of the RVFV 74HB59 strain. The attenuation of the virus is achieved by truncation of the NSs gene of the virus genome. A single dose inoculation of the vaccine could provide protection in animals and the vaccine has been widely used in South Africa. MP-12 is also a live attenuated vaccine which is licensed in the US for prevention RVF infection in animals. The vaccine is based on Egyptian AH548 strain and safety as well as efficacy both in animals and humans have been shown via a single injection, but further clinical trials need to be carried out for human use.

Inactivated Virus Vaccine

RVF ZH501 and Menya/Sheep/258 are two inactivated RVF vaccines prepared by the Veterinary Serum and Vaccine Research Institute in Egypt using RVFV Menya strains. The two vaccines are inactivated by binary ethylenimine and formalin respectively. South Africa also used the RVFV field strain to prepare a formalin-inactivated vaccine that is safe for pregnant animals, but the vaccine requires booster immunization for protection within 3-4 weeks after the initial immunization. TSI-GSD-200, also a formalin-inactivated vaccine based on Entebbe strain, is now an Investigational New Drug in the US. Prime-boost immunization with this vaccine could maintain protection against RVF.

Creative Biolabs has advanced and extensive experience in viral vaccines, especially in the field of Rift Valley Fever virus. Through our proven vaccine development platform, led by a leading research and development team, we are able to design and prepare a variety of safe and effective Rift Valley Fever vaccines to meet different needs. At the same time, we can help customers complete the specific operations of vaccine development and evaluation in the most cost-effective way, greatly simplifying your process of vaccine development.

Reference

1. Dungu B, Lubisi BA. (2018). “Rift Valley fever vaccines: current and future needs”. Curr Opin Virol. 29, 8-15.

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