Prolonged Infection of Human Synovial Cells with Ross River Virus

Journeaux, S. F.; Brown, W. G.; Aaskov, John

doi:10.1099/0022-1317-68-12-3165

Cited by 18 publications

(11 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The present study also provided evidence that CHIKV can persist and replicate in vivo in primates for extended periods, with vRNA and antigen detected in several organs and tissues for 3 months. Alphaviral persistence has been described in vitro, in human synovial fibroblasts and murine macrophages (57,58), and in vivo, in mouse muscle cells (59), up to 25 dpi with another arthrogenic alphavirus, RRV. The only study addressing in vivo persistence of alphavirus in humans found viral RNA 5 weeks after the onset of symptoms in 2 RRV disease patients (49).…”

Section: Discussionmentioning

confidence: 99%

Chikungunya disease in nonhuman primates involves long-term viral persistence in macrophages

Labadie¹,

Larcher²,

Joubert³

et al. 2010

J. Clin. Invest.

484

604

View full text Add to dashboard Cite

Chikungunya virus (CHIKV) is a mosquito-borne alphavirus that induces in humans a disease characterized by fever, rash, and pain in muscles and joints. The recent emergence or reemergence of CHIKV in the Indian Ocean Islands and India has stressed the need to better understand the pathogenesis of this disease. Previous CHIKV disease models have used young or immunodeficient mice, but these do not recapitulate human disease patterns and are unsuitable for testing immune-based therapies. Herein, we describe what we believe to be a new model for CHIKV infection in adult, immunocompetent cynomolgus macaques. CHIKV infection in these animals recapitulated the viral, clinical, and pathological features observed in human disease. In the macaques, long-term CHIKV infection was observed in joints, muscles, lymphoid organs, and liver, which could explain the long-lasting CHIKV disease symptoms observed in humans. In addition, the study identified macrophages as the main cellular reservoirs during the late stages of CHIKV infection in vivo. This model of CHIKV physiopathology should allow the development of new therapeutic and/or prophylactic strategies.

show abstract

Section: Discussionmentioning

confidence: 99%

Chikungunya disease in nonhuman primates involves long-term viral persistence in macrophages

Labadie¹,

Larcher²,

Joubert³

et al. 2010

J. Clin. Invest.

484

604

View full text Add to dashboard Cite

show abstract

“…In the absence of experimental evaluation of target cells, one could expect CHIKV to bind and infect a broad range of cell lines similarly to those infected by related Alphaviruses . To support this hypothesis, the related virus RRV was reported to persistently and productively infect a large variety of cells including human synovial cells (Cunningham and Fraser, 1985; Journeaux, Brown, and Aaskov, 1987), fibroblasts (Journeaux, Brown, and Aaskov, 1987), macrophages (Linn and Suhrbier, 1997; Linn et al, 1996) and CD4+ lymphocytes found in the mononuclear synovial effusion of patients with epidemic polyarthritis (Fraser and Becker, 1984). Similarly, VEEV can infect a broad array of human cell types (Kolokoltsov, Weaver, and Davey, 2005).…”

Section: Chikv Entry Into Human Cellsmentioning

confidence: 99%

Replication cycle of chikungunya: A re-emerging arbovirus

et al. 2009

View full text Add to dashboard Cite

Arboviruses (or arthropod-borne viruses), represent a threat for the new century. The 2005–2006 year unprecedented epidemics of chikungunya virus (CHIKV) in the French Reunion Island in the Indian Ocean, followed by several outbreaks in other parts of the world such as India, have attracted the attention of clinicians, scientists, and state authorities about the risks linked to this re-emerging mosquito-borne virus. CHIKV, which belongs to the Alphaviruses genus, was not previously regarded as a highly pathogenic arbovirus. However, this opinion was challenged by the death of several CHIKV-infected persons in Reunion Island. The epidemic episode began in December 2005 and four months later the seroprevalence survey report indicated that 236,000 persons, more than 30% of Reunion Island population, had been infected with CHIKV, among which 0.4–0.5% of cases were fatal. Since the epidemic peak, the infection case number has continued to increase to almost 40% of the population, with a total of more than 250 fatalities. Although information available on CHIKV is growing quite rapidly, we are still far from understanding the strategies required for the ecologic success of this virus, virus replication, its interactions with its vertebrate hosts and arthropod vectors, and its genetic evolution. In this paper, we summarize the current knowledge of CHIKV genomic organization, cell tropism, and the virus replication cycle, and evaluate the possibility to predict its future evolution. Such understanding may be applied in order to anticipate future epidemics and reduce the incidence by development and application of, for example, vaccination and antiviral therapy.

show abstract

“…Viral antigen had been demonstrated in leukocytes from joint effusions, and viral RNA has been demonstrated by PCR testing of synovial biopsy specimens (64,188). Human synovial cells can be productively infected with RRV in vitro (34,91). La Linn and coworkers (105,107) showed that macrophages could be persistently and productively infected with RRV and suggested this might play a role in persistence through the phagocytosis of dying cells by other macrophages.…”

Section: Immune Response Pathogenesis and Laboratory Diagnosis Immumentioning

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

Prolonged Infection of Human Synovial Cells with Ross River Virus

Cited by 18 publications

References 17 publications

Chikungunya disease in nonhuman primates involves long-term viral persistence in macrophages

Chikungunya disease in nonhuman primates involves long-term viral persistence in macrophages

Replication cycle of chikungunya: A re-emerging arbovirus

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

Contact Info

Product

Resources

About