Ukurasa 1 kutoka 2073 matokeo
There is an urgent need for therapeutic development to combat infections caused by Rift Valley fever virus (RVFV), which causes devastating disease in both humans and animals. In an effort to repurpose drugs for RVFV treatment, our previous studies screened a library of FDA-approved drugs. The most
Infection rates were compared in Culex pipiens and Aedes taeniorhynchus after they fed on Rift Valley fever (RVF) viremic hamsters or ingested similar doses of RVF virus from blood-soaked pledgets. Infection rates were significantly lower for mosquitoes that ingested virus from a pledget than for
In a study of the response in cattle to a live and an inactivated Rift Valley fever (RVF) vaccine prepared from cell cultures infected with RVF virus, the effects of varying doses and combinations of these vaccines were compared. The antibody response to a primary injection of either vaccines was
Rift Valley fever (RVF) is an emerging, vector-borne viral zoonosis that has significantly impacted public health, livestock health and production, and food security over the last three decades across large regions of the African continent and the Arabian Peninsula. The potential for expansion of
Rift Valley fever (RVF) is a zoonotic disease that primarily affects ruminant animals and can also cause fatal disease in humans. In the current report, we present the ultrastructural changes in the liver of a man aged 60 years who died from RVF in the Aseer Central Hospital, Abha, Saudi Arabia. The
Rhesus macaques, intravenously inoculated with virulent Rift Valley fever virus, develop viremia and biochemical evidence of liver damage and serve as a model for human disease. Some of these monkeys suffer more serious disease with hemorrhagic phenomena and approximately 20% die with frank
DNA vaccines have successfully induced effective antibody and cellular immune response to many viral pathogens. The antibody response of DNA immunization induction in mouse model with envelope glycoproteins of Rift Valley Fever Virus (RVFV), G (N + C), GN and GC was investigated. For this purpose,
Laboratory mice were inoculated with 3 different strains of Rift Valley fever virus (RVFV): namely, the prototype, the Nigerian, and the Lunyo variant strains of RVFV. Animals were inoculated with either infective mouse brain or serum by the i.c. or i.p. route and organs of inoculated animals
Rift Valley fever virus (RVFV) leads to varied clinical manifestations in animals and in humans that range from moderate fever to fatal illness, suggesting that host immune responses are important determinants of the disease severity. We investigated the immune basis for the extreme susceptibility
Rift Valley fever virus is an arbovirus found in Africa and the Middle East. Most infected individuals experience a mild self-limiting illness; however, some develop severe disease including hepatitis, hemorrhagic fever, or encephalitis. The biological reasons for these marked differences in disease
The large variation in individual response to infection with Rift Valley fever virus (RVFV) suggests that host genetic determinants play a role in determining virus-induced disease outcomes. These genetic factors are still unknown. The systemic inoculation of mice with RVFV reproduces major
Rift Valley Fever (RVF) is a zoonotic arbovirosis. Among animals, it mainly affects ruminants, causing abortions in gravid females and mortality among young animals. In humans, RVF virus infection is usually asymptomatic or characterized by a moderate fever. However, in 1 to 3% of cases, more severe
Rift Valley fever (RVF) is an emerging zoonosis of major public health concern in Africa and Arabia. Previous outbreaks attributed camelids a significant role in the epidemiology of Rift Valley fever virus (RVFV), making them an important target species for vaccination. Using three alpacas as
A congenic rat strain (WF.LEW) was derived from the susceptible Wistar-Furth (WF) (background strain) and the resistant LEW (donor strain) inbred strains and was used to evaluate the phenotypic expression of a dominant Mendelian gene that confers resistance to fatal hepatic disease caused by the
Infection of mice with Rift Valley fever virus (RVFV) reproduces major pathological features of severe human disease, notably the early-onset hepatitis and delayed-onset encephalitis. We previously reported that the Rvfs2 locus from the susceptible MBT/Pas strain reduces survival time after RVFV