Genetic stability of ross river virus during epidemic spread in nonimmune humans

Burness, A. T. H.; Pardoe, Ingrid U.; Faragher, S.G.; Vrati, Sudhanshu; Dalgarno, L.

doi:10.1016/0042-6822(88)90129-8

Cited by 21 publications

(17 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Evolution of the virus is slow (21), and it remains genetically homogeneous over large geographic areas (119,176). This stability suggests that temporal or spatial changes in virulence are unlikely to occur.…”

Section: Clinical Manifestationsmentioning

confidence: 99%

Ross River Virus Transmission, Infection, and Disease: a Cross-Disciplinary Review

2001

View full text Add to dashboard Cite

SUMMARY Ross River virus (RRV) is a fascinating, important arbovirus that is endemic and enzootic in Australia and Papua New Guinea and was epidemic in the South Pacific in 1979 and 1980. Infection with RRV may cause disease in humans, typically presenting as peripheral polyarthralgia or arthritis, sometimes with fever and rash. RRV disease notifications in Australia average 5,000 per year. The first well-described outbreak occurred in 1928. During World War II there were more outbreaks, and the name epidemic polyarthritis was applied. During a 1956 outbreak, epidemic polyarthritis was linked serologically to a group A arbovirus (Alphavirus). The virus was subsequently isolated from Aedes vigilax mosquitoes in 1963 and then from epidemic polyarthritis patients. We review the literature on the evolutionary biology of RRV, immune response to infection, pathogenesis, serologic diagnosis, disease manifestations, the extraordinary variety of vertebrate hosts, mosquito vectors, and transmission cycles, antibody prevalence, epidemiology of asymptomatic and symptomatic human infection, infection risks, and public health impact. RRV arthritis is due to joint infection, and treatment is currently based on empirical anti-inflammatory regimens. Further research on pathogenesis may improve understanding of the natural history of this disease and lead to new treatment strategies. The burden of morbidity is considerable, and the virus could spread to other countries. To justify and design preventive programs, we need accurate data on economic costs and better understanding of transmission and behavioral and environmental risks.

show abstract

Section: Clinical Manifestationsmentioning

confidence: 99%

Ross River Virus Transmission, Infection, and Disease: a Cross-Disciplinary Review

2001

View full text Add to dashboard Cite

show abstract

“…Anti-idiotypic antibody and virus mutant studies have established the importance of the region to cell binding (23,35,39,41,42). Studies have also demonstrated that amino acid changes within this domain affect the ability of an alphavirus to infect different vertebrate cell types (3,36,38) and productively infect the arthropod vector (45).The prototype SIN virus strain, AR339, and viruses derived from this strain have limited infection and transmission potential in Aedes aegypti, the vector of yellow fever and dengue viruses. Approximately 40% of mosquitoes orally infected with AR339 virus develop disseminated infections in head tissues by 14 days postinfection (p.i.)…”

mentioning

confidence: 99%

mentioning

confidence: 99%

Deletions in the Putative Cell Receptor-Binding Domain of Sindbis Virus Strain MRE16 E2 Glycoprotein Reduce Midgut Infectivity in Aedes aegypti

Myles

Pierro

Olson

2003

J Virol

View full text Add to dashboard Cite

The Sindbis virus (Alphavirus; Togaviridae) strain MRE16 efficiently infects Aedes aegypti mosquitoes that ingest a blood meal containing 8 to 9 log 10 PFU of virus/ml. However, a small-plaque variant of this virus, MRE16sp, poorly infects mosquitoes after oral infection with an equivalent titer. To determine the genetic differences between MRE16 and MRE16sp viruses, we have sequenced the MRE16sp structural genes and found a 90-nucleotide deletion in the E2 glycoprotein that spans the 3 end of the coding region for the putative cell-receptor binding domain (CRBD). We examined the role of this deletion in oral infection of mosquitoes by constructing infectious clones pMRE16ic⌬E200-Y229 and pMRE16ic, representing MRE16 virus genomes with and without the deletion, respectively. A third infectious clone, pMRE16ic⌬E200-C220, was also constructed that contained a smaller deletion extending only to the 3 terminus of the CRBD coding region. Virus derived from pMRE16ic replicated with the same efficiency as parental virus in vertebrate (BHK-21) and mosquito (C6/36) cells and orally infected A. aegypti. Viruses derived from pMRE16ic⌬E200-Y229 and pMRE16ic⌬E200-C220 replicated 10-to 100-fold less efficiently in C6/36 and BHK-21 cells than did MRE16ic virus. Each deletion mutant poorly infected A. aegypti and dramatically reduced midgut infectivity and dissemination. However, all viruses generated nearly equal titers (ϳ6.0 log 10 PFU/ml) in mosquitoes 4 days after infection by intrathoracic inoculation. These results suggest that the deleted portion of the E2 CRBD represents an important determinant of MRE16 virus midgut infectivity in A. aegypti.Sindbis (SIN) viruses are cycled principally between Culex species of mosquitoes and avian vertebrate hosts (6,7,37). SIN viruses also have been isolated from Aedes species of mosquitoes (7). The general features of arthropod-borne virus infection of mosquitoes have been described previously (13). The virus enters the lumen of the midgut with ingestion of a blood meal and replicates in the midgut epithelial cells. Virus then escapes the midgut, enters the hemolymph, and disseminates to other tissues, including head and salivary glands. Following multiplication in the salivary glands, virus is transmitted through saliva to a susceptible vertebrate host. However, our understanding of the molecular determinants of vector-pathogen interaction is minimal.SIN viruses have a positive-sense, single-stranded RNA genome (11.7 kb) with a 5Ј cap and a poly(A) tail (36). The 5Ј two-thirds of the genome translates two, N-coterminal nonstructural polyproteins that are posttranslationally cleaved to form the viral replication machinery. Translation of the 3Ј third of the genome requires the transcription of subgenomic 26S RNA from the full-length negative-sense RNA intermediate and generates the structural proteins. The 26S RNA is translated into a polyprotein that is co-and posttranslationally cleaved to form the viral capsid (C) protein and envelope glycoproteins (E1 and E2). The glycoproteins o...

show abstract

“…However, it loses its power relatively rapidly as strains diversify. Partial R N A sequencing has been adopted more recently to link larger groups of virus strains within a serotype in distinct lineages or genotypes (Rico-Hesse, 1990;Rico-Hesse et al, 1987;Burness et al, 1988). Nucleic acid hybridization using synthetic oligonucleotide probes is yet another approach for revealing epidemiological linkages (Kerschner et al, 1986).…”

Section: Discussionmentioning

confidence: 99%

Type 3 poliovirus/Finland/1984 is genetically related to common Mediterranean strains

Pöyry

Kinnunen

Kapsenberg

et al. 1990

Journal of General Virology

View full text Add to dashboard Cite

Genetic stability of ross river virus during epidemic spread in nonimmune humans

Cited by 21 publications

References 21 publications

Ross River Virus Transmission, Infection, and Disease: a Cross-Disciplinary Review

Ross River Virus Transmission, Infection, and Disease: a Cross-Disciplinary Review

Deletions in the Putative Cell Receptor-Binding Domain of Sindbis Virus Strain MRE16 E2 Glycoprotein Reduce Midgut Infectivity in Aedes aegypti

Type 3 poliovirus/Finland/1984 is genetically related to common Mediterranean strains

Contact Info

Product

Resources

About