Candid1, a live-attenuated Junin virus vaccine strain, was developed during the early 1980s to control Argentine hemorrhagic fever, a severe and frequently fatal human disease. Six amino acid substitutions were found to be unique to this vaccine strain, and their role in virulence attenuation in mice was analyzed using a series of recombinant viruses. Our results indicate that Candid1 is attenuated in mice through a single amino acid substitution in the transmembrane domain of the G2 glycoprotein. This work provides insight into the molecular mechanisms of attenuation of the only arenavirus vaccine currently available.

Lymphocytic choriomeningitis virus (LCMV) is the prototype of the family Arenaviridae. LCMV can be associated with severe disease in humans, and its global distribution reflects the broad dispersion of the primary rodent reservoir, the house mouse (Mus musculus). Recent interest in the natural history of the virus has been stimulated by increasing recognition of LCMV infections during pregnancy, and in clusters of LCMV-associated fatal illness among tissue transplant recipients. Despite its public health importance, little is known regarding the genetic diversity or distribution of virus variants. Genomic analysis of 29 LCMV strains collected from a variety of geographic and temporal sources showed these viruses to be highly diverse. Several distinct lineages exist, but there is little correlation with time or place of isolation. Bayesian analysis estimates the most recent common ancestor to be 1,000–5,000 years old, and this long history is consistent with complex phylogeographic relationships of the extant virus isolates.

Background: Rift Valley Fever Virus is a pathogen of humans and livestock that causes significant morbidity and mortality throughout Africa and the Middle East. A vaccine that would protect animals from disease would be very beneficial to the human population because prevention of the amplification cycle in livestock would greatly reduce the risk of human infection by preventing livestock epizootics. A mutant virus, constructed through the use of reverse genetics, is protective in laboratory animal models and thus shows promise as a potential vaccine. However, the ability to distinguish infected from vaccinated animals is important for vaccine acceptance by national and international authorities, given regulations restricting movement and export of infected animals.Results: In this study, we describe the development of a simple assay that can be used to distinguish naturally infected animals from ones that have been vaccinated with a mutant virus. We describe the cloning, expression and purification of two viral proteins, and the development of side by side ELISAs using the two viral proteins.Conclusion: A side by side ELISA can be used to differentiate infected from vaccinated animals. This assay can be done without the use of biocontainment facilities and has potential for use in both human and animal populations.

Marburg virus (MARV), the causative agent of Marburg virus disease, emerges sporadically in sub-Saharan Africa and is often fatal in humas. The natural reservoir for this zoonotic virus is the frugivorous Egyptian rousette bat (Rousettus aegyptiacus) that when infected, sheds virus in the highest amounts in oral secretions and urine. Being fruit bats, these animals forage nightly for ripened fruit throughout the year, including those types often preferred by humans. During feeding, they continually discard partially eaten fruit on the ground that could then be consumed by other Marburg virus susceptible animals or humans. In this study, using qRT-PCR and virus isolation, we tested fruit discarded by Egyptian rousette bats experimentally infected with a natural bat isolate of Marburg virus. We then separately tested viral persistence on fruit varieties commonly cultivated in sub-Saharan Africa using a recombinant Marburg virus expressing the fluorescent ZsGreen1. Marburg virus RNA was repeatedly detected on fruit in the food bowls of the infected bats and viable MARV was recovered from inoculated fruit for up to 6 h.

Lassa virus (LASV), is a significant cause of severe, often fatal, hemorrhagic fever in humans throughout western Africa, with an estimated 100,000 infections each year. No vaccines are commercially available. We report the development of an efficient reverse genetics system to rescue recombinant LASV and to investigate the contributions of the long 5′ and 3′ noncoding regions (NCRs) of the S genomic segment toinvitrogrowth andinvivovirulence. This work demonstrates that deletions of large portions of these NCRs confer an attenuated phenotype and are a first step toward further insights into the high virulence of LASV.