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Biomedical subjects

J G Aaskov

Publications and source records attributed to J G Aaskov.

At least 37 records · Page 2Linked to original sources
PubMed1988

Interaction of Alphaviruses with the serum complement system is a function of method of purification.

The interaction of Sindbis and Ross River viruses with the serum complement system in vitro was influenced by the type of density gradient used to purify them. Sindbis virus purified on sucrose gradients activated the alternate serum complement pathway while Ross River virus prepared in an identical manner had no effect on C3 turnover in non-immune serum. Both viruses purified on tartrate gradients inhibited the spontaneous cleavage of C3 in normal serum. At least some of this inhibition appeared to be due to the presence of tartrate adsorbed to the surface of virions.

Alphavirus↗
PubMed1987

Ross River virus arthritis in Papua New Guinea.

In 1975 it was reported that antibodies to Ross River virus (RRV) were present in the sera of many population groups in Papua New Guinea. We describe here 3 cases of polyarthritis that occurred in Port Moresby, the capital of Papua New Guinea, during 1980-81 and in which the diagnosis of RRV infection was confirmed by serological tests, and 3 other cases in which serological tests suggested RRV infection but were not diagnostic. A possible case of fatal RRV encephalitis is also reported.

Adult↗
PubMed1987

Prolonged infection of human synovial cells with Ross River virus.

Primary cultures of human synovial cells shed infectious virus for 14 to 35 days following infection with isolates of Ross River virus which had been passaged in the C6/36 line of Aedes albopictus mosquito cells. No frank cytopathic effect was seen in infected synovial cells and they continued to replicate for the duration of the experiments.

Alphavirus↗
PubMed1987

A study of arthritis in Papua New Guinea.

A study was undertaken of 182 Melanesian patients with arthritis who were admitted to three major hospitals in Papua New Guinea between 1977 and 1982. There were 118 male and 64 female subjects, whose mean ages were 29 years and 25 years respectively. A diagnosis was made in 101 cases (55.5%) but in 81 cases, because assessment and management had been inadequate, a diagnosis could not be made. The commonest cause was infectious arthritis (44%), followed by rheumatoid arthritis (14%), gout (8%), and reactive arthritis (8%). In the 44 subjects with infectious arthritis, gonorrhea was the cause in 25 cases (57%) and in a further six cases (14%) it was attributed to Ross River virus infection. In five cases, arthritis was believed to be caused by Wuchereria bancrofti infection. In several cases, chronic arthritis was present in association with ankylosing spondylitis, psoriasis, systemic lupus erythematosus, dermatomyositis, or systemic sclerosis.

Adolescent↗
PubMed1987

Natural killer cells in viral arthritis.

Changes in natural killer (NK) cell activity were studied in patients with polyarthritis associated with rubella or Ross River virus infections. In 30 of 32 Ross River virus patients, peripheral NK cell activity was depressed at some stage of the disease but returned to normal levels as patients recovered from arthritic symptoms. Similar changes did not occur in rubella patients and no difference was found between changes in peripheral NK activity and serum interferon (IFN) levels in rubella patients with arthritis and those without. Neither the peak of NK cell activity in peripheral blood lymphocytes (PBL) recovered early in Ross River virus and rubella infections, nor the depression of NK cell activity late in Ross River virus infections could be correlated with changes in serum IFN levels. The decrease in PBL-NK cell activity in epidemic polyarthritis (EPA) patients could not be attributed solely to loss of NK cells from the peripheral circulation because limiting-cell-dilution (LCD) analyses indicated changes in peripheral NK cell activity were due to changes in both the number and lytic activity of NK cells. Despite the association between HLA-DR7 and EPA no differences were found in levels of peripheral NK cell activity in DR7+ and DR7- EPA patients. The demonstration that peripheral NK cells could kill autologous synovial cells suggested that NK cells in joints of EPA patients may contribute to the arthritis associated with Ross River virus infection.

Adult↗
PubMed1986

Hemadsorption immunosorbent technique for the detection of dengue immunoglobulin M antibody.

We developed a highly specific, sensitive, and economical hemadsorption immunosorbent technique for the detection of dengue-specific immunoglobulin M (IgM) antibody. The technique is based on the reaction of human sera with anti-human IgM immobilized onto a solid phase followed by the detection of dengue-specific IgM by the addition of a known quantity of dengue virus hemagglutinin and goose erythrocytes. Dengue-specific IgM-positive sera showed hemadsorption. IgM antibody specific for dengue virus was detected in 22 of 39 (56%) convalescent-phase sera from primary dengue infections and 8 of 10 (80%) convalescent-phase sera from secondary dengue infections. Additionally, 32 of 76 single sera from patients were positive for dengue IgM; these sera were previously uninterpretable by the hemagglutination inhibition test, as only a single serum specimen was available. No false-positive results were obtained with sera that were negative by the hemagglutination inhibition test for dengue virus. Crude dengue virus hemagglutinin preparations could be used without purification. Dengue-specific IgG did not interfere with the results, nor was there any cross-reactivity between dengue hemagglutinins and IgM specific for other viruses. Some cross-reactivity of the dengue-specific IgM was observed with Japanese encephalitis virus hemagglutinins, but this did not present any problems in the interpretation of results. This test is specific, inexpensive, highly reproducible, and simple to perform.

Antibodies, Viral↗
PubMed1985

Isolation of Ross River virus from epidemic polyarthritis patients in Australia.

Ross River virus was isolated from two out of four seronegative serum samples obtained from epidemic polyarthritis patients in Australia. Virus isolated from each patient was found to be phenotypically diverse. These isolations suggest that previous failure to isolate virus from epidemic polyarthritis patients in this country may have been due to failure to obtain material (serum) from patients early enough in the course of the disease and to the use of relatively insensitive isolation techniques.

Alphavirus↗
PubMed1985

Interaction of Ross River virus with the complement system.

In the absence of virus-specific antibody, Ross River virus failed to activate either the classical or alternative complement pathways. Instead, it inhibited the cleavage of C3 via both pathways. The virus did not appear to act by disrupting C3bBb complexes or by preventing cleavage of factor B by factor D. Instead Ross River virus was found to interfere with the actual cleavage of C3 by activated factor B (C3bBb) of the alternative pathway and C4b2a of the classical pathway.

Alphavirus↗
PubMed1985

The inflammatory response in the synovium of a patient with Ross River arbovirus infection.

Ross River virus has been incriminated in the etiology of many sporadic and epidemic cases of polyarthritis in Australia and the Pacific. Both synovium and synovial exudate fluid recovered from the knee of an epidemic polyarthritis patient showed a predominantly mononuclear leucocyte infiltrate. Infectious virus could not be recovered from the synovial exudate. Functional natural killer cells were detected in the synovial fluid. Their level of cytotoxic activity was similar to that detected in the peripheral circulation.

Arthritis, Infectious↗
PubMed1984

Characterization of Ross River viruses isolated from patients with polyarthritis in New Caledonia and Wallis and Futuna Islands.

Viruses isolated during 1979 and 1980 from patients with polyarthritis in New Caledonia and Wallis and Futuna Islands have been found to be more closely related to Ross River virus than any other regional Alphavirus. On the basis of virulence in suckling mice the majority of these isolates were found to be more closely related to the NB5092 strain of Ross River virus than to the prototype T48 strain.

Alphavirus↗
PubMed1983

Epidemic polyarthritis in Australia, 1980-1981.

Information concerning their clinical illness was obtained by self-administered questionnaire from 528 patients who suffered from epidemic polyarthritis in Australia during 1980 and 1981. The clear and uniform clinical picture which has emerged from this study should facilitate the diagnosis of this disease. The illness begins suddenly with the onset of acute aching in the muscles and joints, followed by a maculopapular rash in between 40% and 78% of patients, and extensive polyarthritis. This affects chiefly the ankles, fingers, knees and wrists, usually serially, but no joint is spared. Estimates of incubation time suggest that it ranges from three to 21 days (mean, nine days). Women, especially housewives, are the group most frequently affected. Exposure to mosquitoes is an important predisposing factor; the implications of this for prevention and future research are considered. The mechanism of the survival of the virus in nature remains poorly understood.

Adult↗
PubMed1983

Cell-mediated immune response to Ross River virus in mice: evidence for a defective effector cell response.

Spleen cells recovered from mice during a primary infection with Ross River virus showed a virus-specific proliferative response when challenged in vitro. The majority of the proliferating cells were T-lymphocytes. In contrast, there was little detectable migration inhibition factor production by these spleen cells and little or no virus-specific cytotoxic activity. Sub-cutaneous challenge with virus elicited a weak delayed type hypersensitivity reaction.

Animals↗
PubMed1983

Detection by ELISA of IgM antibodies to Ross River virus in serum from patients with suspected epidemic polyarthritis.

An ELISA method for the detection of IgM antibody to Ross River virus in the serum of patients with suspected epidemic polyarthritis has been developed. None of the reagents is infectious or toxic and the use of purified virus minimizes the risk of non-specific reactions to non-viral products. In a positive reaction the ELISA substrate changes colour from yellow to purple, enabling serum antibody titres to be read by eye.

Antibodies, Viral↗
PubMed1981

Epidemic polyarthritis in northeastern Australia, 1978-1979.

In a study of epidemic polyarthritis in central and northern Queensland, clinical disease was observed most frequently in urban-dwelling adult females. Clinical and subclinical infections were detected year round, although the majority of clinical infections occurred between the months of January and June. In the communities studied, there were approximately 50 subclinical infections for each clinical infection. There was no detectable association between any HLA-A or HLA-B phenotypes and epidemic polyarthritis.

Adolescent↗
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↗
PubMed1981

Regulation in vitro of human natural killer (NK) cell activity.

The natural killer cell activity of PBL from epidemic polyarthritis patients was depressed early after onset of symptoms but returned to normal as the patient recovered. This study found that the in vitro culture of Ross River virus, the agent responsible for epidemic polyarthritis, with PBL resulted in enhanced rather than depressed NK cell activity. Evidence was also obtained that NK cell activity could be suppressed by suppressor-T lymphocytes generated by culture of PBL with high concentrations of Concanavalin A. This suppressive activity was not due to release of a soluble mediator(s) by the suppressor T cells.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1981

Specific and non-specific immunological changes in epidemic polyarthritis patients.

T-lymphocytes from epidemic polyarthritis patients exhibited a virus specific proliferative response when exposed to Ross River virus in vitro. The magnitude of this response was greater than that of lymphocytes from asymptomatic seropositive donors. The natural killer cell activity of peripheral blood mononuclear leucocytes from these patients was depressed early in disease but returned to normal levels as the severity of the symptoms decreased. Although no in vivo role can yet be assigned to natural killer cells in epidemic polyarthritis, changes in their activity appeared to be more closely associated with the presence or absence of disease symptoms than were levels of anti-viral antibody or the ability or T-lymphocytes from peripheral blood to proliferate on re-exposure to Ross River virus.

Antibodies, Viral↗