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Updated: Mar 30, 2026
Using Reverse Genetics to Manipulate the NSs Gene of the Rift Valley Fever Virus MP-12 Strain to Improve Vaccine Safety and Efficacy
Published on: November 1, 2011
Mapping a Major Gene for Resistance to Rift Valley Fever Virus in Laboratory Rats
Catherine M Busch1, Ralph J Callicott1, Clarence J Peters1
1From the Department of Veterinary Pathobiology, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, 4467 TAMU, College Station, TX 77843-4467 (Busch and Womack); the Animal Resource Center, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9037 (Callicott); the Department of Pathology, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555-0609 (Peters); and the Department of Microbiology and Immunology, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555-0609 (Morrill).
Abstract:
The Rift Valley Fever virus (RVFV) presents an epidemic and epizootic threat in sub-Saharan Africa, Egypt, and the Arabian Peninsula, and has furthermore recently gained attention as a potential weapon of bioterrorism due to its ability to infect both livestock and humans. Inbred rat strains show similar characteristic responses to the disease as humans and livestock, making them a suitable model species. Previous studies had indicated differences in susceptibility to RVFV hepatic disease among various rat strains, including a higher susceptibility of Wistar-Furth (WF) compared to a more resistant Lewis (LEW) strain. Further study revealed that this resistance trait exhibits the pattern of a major dominant gene inherited in Mendelian fashion. A genome scan of a congenic WF.LEW strain, created from the susceptible WF and resistant LEW strains and itself resistant to infection with RVFV, revealed 2 potential regions for the location of the gene, 1 on chromosome 3 and the other on chromosome 9. Through backcrossing of WF.LEW rats to WF rats, genotyping offspring using SNPs and microsatellites, and viral challenges of 3 N1 litters, we have mapped the gene to the distal end of chromosome 3.
