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At least 19 recordsLinked to original sources
PubMed1994

Development of a candidate vaccine against Ross River virus infection.

Ross River virus is a mosquito-borne alphavirus which causes several thousand cases of arthritis (epidemic polyarthritis) each year. In this study, binary ethylenimine (BEI) was used to destroy the infectivity of this virus without abolishing the antigenicity or immunogenicity of the virion. Mice immunized intramuscularly with BEI-inactivated virus, with or without Alhydrogel adjuvant, produced antibody which neutralized Ross River virus in vitro, and the mice also failed to develop viraemia when challenged intravenously with live virus. Serum neutralization and in vivo protection were greatest when BEI-inactivated virus was administered without adjuvant.

Adjuvants, Immunologic↗
PubMed1986

Epidemic polyarthritis and Ross River virus disease.

Ross River virus is a mosquito-transmitted alphavirus indigenous to Australia, Papua New Guinea and nearby islands, which recently appeared in other western and central South Pacific islands. Human infection can be manifest by varied constitutional disturbances, rash and rheumatic symptoms, known in Australia as epidemic polyarthritis and broadly similar to certain alphavirus diseases in other regions. Although usually short-lived, the rash can persist for 5 months. Rheumatic effects involve synovial joints, tendon and ligaments, and can continue or recur in peripheral joints and tissues as long as 6 years, though gradually improving without destructive changes. At different times, the disease can closely simulate rubella and other virus diseases, Henoch-Schönlein syndrome, rheumatoid and other chronic rheumatic diseases. Diagnosis rests upon geography, specific serology and judicious interpretation of clinical and supportive laboratory data. Skin and synovial lesions are characterized by infiltration of mononuclear cells. Their pathogenesis most likely depends on the reaction of these cells with persistent foci of virus disseminated during the early viraemic phase of infection.

Arthritis, Infectious↗
PubMed1987

Interferon treatment of experimental Ross River virus polymyositis.

Ross River virus (RRV), an alpha togavirus, causes an inflammatory myopathy in mice, which probably results from direct lytic effects of virus or viral products on myofibers. Administration of recombinant hybrid human leukocyte interferon-alpha A/D (rIFN-alpha A/D) ameliorates clinical illness and reduces mortality from 86 to 42%. Peak concentrations of virus are reduced by 1,000-fold in serum and by 30-fold in muscle, but anti-RRV antibody production is not altered. Treatment with rIFN-alpha A/D dramatically reduces inflammation and necrosis in muscle. Beneficial effects of rIFN-alpha A/D on experimental, RRV-induced polymyositis result in part from inhibition of viral replication and spread, though immunomodulation might also play an important role.

Animals↗
PubMed2000

Specific ablation of antiviral gene expression in macrophages by antibody-dependent enhancement of Ross River virus infection.

Ross River virus (RRV) is an indigenous Australian arthropod-borne alphavirus responsible for epidemic polyarthritis (EPA), myalgia, and lethargy in humans. Macrophages and monocytes have been associated with human RRV disease, and previous studies have shown that RRV is capable of infecting macrophages via both a natural virus receptor and by Fc receptor-mediated antibody-dependent enhancement (ADE). Similar to other viruses, such as human immunodeficiency virus and dengue virus, ADE infection results in dramatic RRV growth increases for in vitro macrophage cultures. This study demonstrates that RRV could resist lipopolysaccharide (LPS)-induced antiviral activity in macrophage cultures when infection was via the ADE pathway. Investigation of this infection pathway found that RRV was able to suppress the transcription and translation of key antiviral genes (tumor necrosis factor and inducible nitric oxide synthase) in LPS-stimulated macrophages by disrupting the transcription into mRNA of the genes coding for the associated transcription factors IRF-1 and NF-kappaB. The transcription of non-antiviral control genes was not perturbed by RRV-ADE infection, and de novo protein synthesis also was not significantly affected in RRV-ADE infected cells. The ADE pathway of infection allowed RRV to specifically target antiviral genes in macrophages, resulting in unrestricted virus replication. As ADE has been observed for several virus families and associated with disease and adverse vaccination outcomes, these findings may have broad relevance to viral disease formation and antiviral vaccination strategies.

Alphavirus Infections↗
PubMed2006

Role of Verrallina funerea (Diptera: Culicidae) in transmission of Barmah Forest virus and Ross River virus in coastal areas of eastern Australia.

Verrallina funerea (Theobald) (Diptera: Culicidae) is a brackish water mosquito species found most commonly in Indonesia, Papua New Guinea, and the northeastern coastal regions of Australia. Aspects of the vector competence of this species for Barmah Forest virus (family Togaviridae, genus Alphavirus, BFV) and Ross River virus (family Togaviridae, genus Alphavirus, RRV), two medically important arboviruses in Australia, were investigated. Laboratory-reared Ve. funerea were moderately susceptible to experimental infection with BFV (median cell culture infectious dose of 10(3.6) per mosquito) and were capable of transmission to suckling mice (52% after a 9-12-d extrinsic incubation period). Maximum salivary gland infections for BFV (65%) and RRV (50%) were observed 8 and 10 d postinfection, respectively. To examine any regional differences in vector competence, field populations (separated by up to 200 km) of Ve. funerea and Aedes vigilax (Skuse) from southeastern Queensland and northern New South Wales were fed BFV and RRV, and subsequent infection rates were compared. For both viruses, no statistically significant variations in body, disseminated, or salivary gland infection rates were found in either Ve. funerea or Ae. vigilax. The results from this study indicate that Ve. funerea may have an important role as an amplification vector during outbreaks of both viruses and that local government authorities should rapidly treat brackish water habitats to control this species during periods of increased disease activity.

Alphavirus↗
PubMed1998

Molecular genetic study of the interaction of Sindbis virus E2 with Ross River virus E1 for virus budding.

Glycoprotein PE2 of Sindbis virus will form a heterodimer with glycoprotein E1 of Ross River virus that is cleaved to an E2/E1 heterodimer and transported to the cell plasma membrane, but this chimeric heterodimer fails to interact with Sindbis virus nucleocapsids, and very little budding to produce mature virus occurs upon infection with chimeric viruses. We have isolated in both Sindbis virus E2 and in Ross River virus E1 a series of suppressing mutations that adapt these two proteins to one another and allow increased levels of chimeric virus production. Two adaptive E1 changes in an ectodomain immediately adjacent to the membrane anchor and five adaptive E2 changes in a 12-residue ectodomain centered on Asp-242 have been identified. One change in Ross River virus E1 (Gln-411-->Leu) and one change in Sindbis virus E2 (Asp-248-->Tyr) were investigated in detail. Each change individually leads to about a 10-fold increase in virus production, and combined the two changes lead to a 100-fold increase in virus. During passage of a chimeric virus containing Ross River virus E1 and Sindbis virus E2, the E2 change was first selected, followed by the E1 change. Heterodimers containing these two adaptive mutations have a demonstrably increased degree of interaction with Sindbis virus nucleocapsids. In the parental chimera, no interaction between heterodimers and capsids was visible at the plasma membrane in electron microscopic studies, whereas alignment of nucleocapsids along the plasma membrane, indicating interaction of heterodimers with nucleocapsids, was readily seen in the adapted chimera. The significance of these findings in light of our current understanding of alphavirus budding is discussed.

Amino Acid Sequence↗
PubMed2004

Human immunodeficiency virus type 1-derived lentivirus vectors pseudotyped with envelope glycoproteins derived from Ross River virus and Semliki Forest virus.

Ross River virus (RRV) and Semliki Forest virus (SFV) are two alphaviruses that have a high degree of amino acid homology, as well as a very broad host range. We show here that envelope glycoproteins derived from both viruses can pseudotype human immunodeficiency virus type 1 (HIV-1)-derived lentivirus vectors. Both RRV and SFV glycoproteins considerably expand the host range of the lentivirus vector, and vectors can be efficiently concentrated by ultracentrifugation. A systematic analysis comparing the alphaviral glycoproteins to the vesicular stomatitis virus glycoprotein (VSV-G) revealed that lentivirus vectors incorporate RRV glycoproteins with an efficiency comparable to that of VSV-G. Both pseudotypes have comparable physical titers, but infectious titers with the RRV pseudotype are lower than with VSV-G. Incorporation of SFV glycoproteins into lentivirus vector is less efficient, leading to decreased physical and infectious titers. The transduction rates with VSV-G-, RRV-, and SFV-pseudotyped lentivirus vectors into adherent cell lines can be significantly increased by using a combination of Polybrene and plates coated with CH-296 recombinant fibronectin fragments. Together, our data suggest that RRV and SFV glycoproteins might be suitable as alternatives to VSV-G for pseudotyping lentivirus vectors.

Animals↗
PubMed2000

Adaptive mutations in Sindbis virus E2 and Ross River virus E1 that allow efficient budding of chimeric viruses.

Alphavirus glycoproteins E2 and E1 form a heterodimer that is required for virus assembly. We have studied adaptive mutations in E2 of Sindbis virus (SIN) and E1 of Ross River virus (RR) that allow these two glycoproteins to interact more efficiently in a chimeric virus that has SIN E2 but RR E1. These mutations include K129E, K131E, and V237F in SIN E2 and S310F and C433R in RR E1. Although RR E1 and SIN E2 will form a chimeric heterodimer, the chimeric virus is almost nonviable, producing about 10(-7) as much virus as SIN at 24 h and 10(-5) as much after 48 h. Chimeras containing one adaptive change produced 3 to 20 times more virus than did the parental chimera, whereas chimeras with two changes produced 10 to 100 times more virus and chimeras containing three mutations produced yields that were 180 to 250 times better. None of the mutations had significant effects upon the parental wild-type viruses, however. Passage of the triple variants eight or nine times resulted in variants that produced virus rapidly and were capable of producing >10(8) PFU/ml of culture fluid within 24 h. These further-adapted variants possessed one or two additional mutations, including E2-V116K, E2-S110N, or E1-T65S. The RR E1-C433R mutation was studied in more detail. This Cys is located in the putative transmembrane domain of E1 and was shown to be palmitoylated. Mutation to Arg-433 resulted in loss of palmitoylation of E1. The positively charged arginine residue within the putative transmembrane domain of E1 would be expected to alter the conformation of this domain. These results suggest that interactions within the transmembrane region are important for the assembly of the E1/E2 heterodimer, as are regions of the ectodomains possibly identified by the locations of adaptive mutations in these regions. Further, the finding that four or five changes in the chimera allow virus production that approaches the levels seen with the parental SIN and exceeds that of the parental RR illustrates that the structure and function of SIN and RR E1s have been conserved during the 50% divergence in sequence that has occurred.

Adaptation, Physiological↗
PubMed1996

Chimeric Sindbis-Ross River viruses to study interactions between alphavirus nonstructural and structural regions.

Sindbis virus and Ross River virus are alphaviruses whose nonstructural proteins share 64% identity and whose structural proteins share 48% identity. Starting from full-length cDNA clones of both viruses, we have generated two reciprocal Sindbis-Ross River chimeric viruses in which the structural and nonstructural regions have been exchanged. These chimeric viruses replicate readily in several cell lines. Both chimeras grow more poorly than do the parental viruses, with the chimera containing Sindbis virus nonstructural proteins and Ross River virus structural proteins growing considerably better in both mosquito and Vero cell lines than the reciprocal chimera does. The reduction in replicative capacity in comparison with the parental viruses appears to result at least in part from a reduction in RNA synthesis, which suggests that the structural proteins or sequence elements within the structural region interact with the nonstructural proteins or sequence elements within the nonstructural region, that these interactions are required for efficient RNA replication, and that these interactions are suboptimal in the chimeras. The chimeras are able to infect mice, but their growth is attenuated. Western equine encephalitis virus, a virus widely distributed throughout the Americas, has been previously shown to have arisen by natural recombination between two distinct alphaviruses, but other naturally occurring recombinant alphaviruses have not been found. The present results suggest that most nonstructural/structural chimeras that might arise by natural recombination will be viable but that interactions between different regions of the genome, some of which were previously known but some of which remain unknown, limit the ability of such recombinants to become established.

Animals↗
PubMedDate not supplied

A candidate Ross River virus vaccine: preclinical evaluation.

A killed Ross River virus vaccine is being developed in an effort to prevent the, ca 5000 cases of epidemic polyarthritis which occur in Australia each year. The symptoms of epidemic polyarthritis commonly last 30-40 weeks and 25% of patients have symptoms for a year or more. There is no cure. Although there was some strain to strain variation, particularly after a single injection, outbred and inbred strains of mice all produced significant levels of anti-Ross River virus antibody after intramuscular (i.m.) injection with 24 h BEI inactivated, sucrose gradient purified, Ross River virus vaccine. Mice immunized i.m. with two 20 micrograms doses of vaccine or live virus produced similar levels of neutralizing antibody but the reaction of IgG 2a and IgG 2b antibody from these two groups of mice to Ross River virus proteins in western blots differed. Antibody from BALB/c mice immunized with this vaccine neutralized all strains of Ross River virus tested, in vitro, albeit to different degrees.

Animals↗
PubMed2002

Ross River virus: ecology and distribution.

Ross River virus is the most common mosquito-borne pathogen in Australia, and approximately 5000 human cases are reported annually. The infection is not fatal, but there is considerable morbidity associated with a debilitating polyarthritis that is the major symptom. The virus is annually active in most regions of Australia, but exists as strains that vary in virulence. Native macropods are thought to be the natural vertebrate hosts, although horses and humans may be involved during epidemic activity, and vertical transmission of the virus occurs in mosquitoes. Different mosquito species are involved as vectors in various regions and in different seasonal and environmental conditions. In coastal areas the saltmarsh mosquitoes Aedes camptorhynchus and Ae. vigilax are the most important vectors in southern and northern regions, respectively, whereas in inland areas Culex annulirostris is the most important vector, although various Aedes species can be involved depending on region and conditions, and the epidemiology of the disease and vector control imperatives vary with circumstance concomitantly.

Alphavirus Infections↗
PubMed1981

Experimental viral polymyositis: age dependency and immune responses to Ross River virus infection in mice.

Ross River virus (RRV) causes an age-dependent myositis in mice. Infected 4-week-old mice develop no clinical signs, but 1-week-old mice develop weakness and myositis. Humoral and cell-mediated immune responses to RRV in the two age groups are comparable, and immunosuppression does not alter age-dependent resistance to clinical disease. Immunosuppression of 1-week-old mice protracts clinical signs and reduces muscle inflammation but does not alter muscle necrosis or regeneration. These studies suggest that immune responses do not determine age dependency of RRV myositis and that muscle necrosis results from direct viral lysis of muscle fibers.

Age Factors↗
PubMed2000

Characterization of epitopes for virus-neutralizing monoclonal antibodies to Ross River virus E2 using phage-displayed random peptide libraries.

Ross River virus (RRV) is the predominant cause of epidemic polyarthritis in Australia, yet the antigenic determinants are not well defined. We aimed to characterize epitope(s) on RRV-E2 for a panel of monoclonal antibodies (MAbs) that recognize overlapping conformational epitopes on the E2 envelope protein of RRV and that neutralize virus infection of cells in vitro. Phage-displayed random peptide libraries were probed with the MAbs T1E7, NB3C4, and T10C9 using solution-phase and solid-phase biopanning methods. The peptides VSIFPPA and KTAISPT were selected 15 and 6 times, respectively, by all three of the MAbs using solution-phase biopanning. The peptide LRLPPAP was selected 8 times by NB3C4 using solid-phase biopanning; this peptide shares a trio of amino acids with the peptide VSIFPPA. Phage that expressed the peptides VSIFPPA and LRLPPAP were reactive with T1E7 and/or NB3C4, and phage that expressed the peptides VSIFPPA, LRLPPAP, and KTAISPT partially inhibited the reactivity of T1E7 with RRV. The selected peptides resemble regions of RRV-E2 adjacent to sites mutated in neutralization escape variants of RRV derived by culture in the presence of these MAbs (E2 210-219 and 238-245) and an additional region of E2 172-182. Together these sites represent a conformational epitope of E2 that is informative of cellular contact sites on RRV.

Amino Acid Sequence↗
PubMed2004

Spatial-temporal analysis of Ross River virus disease patterns in Queensland, Australia.

Ross River virus is the most common vector-borne disease in Australia, with the majority of notifications being in Queensland. This study describes a retrospective spatial analysis of Queensland Ross River virus disease notifications spanning a 10-year period. Notifications were mapped to the local government area (LGA) of the residence of the patient. Ross River virus disease outbreaks within each LGA were detected by applying a Poisson model. Estimates of the seasonal incidence rates indicated wide variation between seasons and LGAs. Positive spatial autocorrelation between LGAs experiencing outbreaks indicated that LGAs within the same region often experience outbreaks at the same time. A hierarchical cluster analysis of the outbreak data was used to group LGAs with similar temporal outbreak patterns. This analysis highlights the variability in Ross River virus disease notification rates across Queensland, and provides a robust method for identifying disease outbreaks.

Adolescent↗
PubMed1996

Ross River virus and Barmah Forest virus infection. Commonly asked questions.

Ross River virus infection and Barmah Forest virus infection are two commonly reported arboviral diseases in Australia. Ross River virus has long been recognised as a cause of epidemic polyarthritis and polyarticular disease. Clinical disease as a result of Barmah Forest virus infection has only been identified since 1988 and Australia is the only country in which this virus has been detected. Severe and prolonged symptoms can occur as a result of infection with either virus and may result in significant distress to the patient. This article reviews some of the issues that patients raise in relation to both Ross River virus and Barmah Forest virus disease including the source of infection, the duration of symptoms and measures to prevent infection.

Adult↗
PubMed1981

Evidence for transplacental transmission of Ross River virus in humans.

Immunoglobulin M antibody to Ross River virus was found in the cord blood of 11 368 children born to mothers who were pregnant during the epidemic of Ross River virus infection in Fiji, in 1979. Since IgM antibody does not normally cross the human placenta, these findings are suggestive of in-utero infection. Antibody to Ross River virus was also present in eight of the 11 mothers of children with IgM-positive cord blood. One of the mothers with IgM-negative blood had no detectable haemagglutination-inhibiting antibody to Ross River virus. All children appeared normal at birth.

Antibodies, Viral↗
PubMed2002

The Quasi-Biennial Oscillation and Ross River virus incidence in Queensland, Australia.

Ross River virus (RRV) is the most important vector-borne disease in Australia. The National Notifiable Diseases Surveillance System has confirmed that its incidence is often greatest in the state of Queensland, where there is a clear seasonal pattern as well as interannual variability. Previous studies have examined relationships between large-scale climate fluctuations (such as El Niño Southern Oscillation) and vector-borne disease. No previous study has examined such relationships with the Quasi-Biennial Oscillation (QBO), another large-scale climate fluctuation. We employ time-series analysis techniques to investigate cycles inherent in monthly RRV incidence in Queensland, Australia, from January 1991 to December 1997 inclusive. The presence of a quasi-biennial cycle in the RRV time series that is out of phase with the climatic QBO is described. Quantitative analyses using correlograms and periodograms demonstrate that the quasi-biennial cycle in the RRV time series is statistically significant, at the 95% level, above the noise. Together with the seasonal cycle, the quasi-biennial cycle accounts for 77% of the variance in Queensland RRV cases. Regression analysis of QBO and summer rainfall in three climatic zones of Queensland indicates a significant association between QBO and rainfall in the subtropical southeastern part of the state. These results suggest an indirect influence of the QBO on RRV incidence in Queensland, via its influence on climate in this region. Our findings indicate that the QBO may be a useful predictor of RRV at several months lead, and might be used by public health authorities in the management and prevention of this disease.

Alphavirus Infections↗