Measurement of Antibodies to Machupo Virus by the Indirect Fluorescent Technique

Cj, Peters; Pa, Webb; Km, Johnson

doi:10.3181/00379727-142-37060

Cited by 54 publications

(15 citation statements)

References 2 publications

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“…Others [de Bracco et al, 1978;Lewis et al, 1975;Peters et al, 1973;Wulff and Lange, 19751 infections, but they have not emphasized the possible gains in diagnostic time relative to infection. Although truncated, our results confirm the ability of the IFAT, compared to the SN, to rapidly detect Machupo virus infection in rhesus monkeys, and of the DFAT, compared to plaque titration, to detect infection in cell culture.…”

Section: Discussionmentioning

confidence: 99%

“…Indirect fluorescent antibody testing (IFAT) has become a common serological tool for the evaluation of natural and laboratory arenavirus infection, commonly requiring only 2-4 hrs to perform. It often provides an alternate spectrum of virus-specific antibody assessment to virus neutralization [Lewis et al, 1975;Peters et al, 1973;Peters, 1984;Wulff and Lange, 1975;Wulff et al, 19781. This report presents IFAT results from eight Machupo-infected monkeys and results of a safety test conducted on antigen slides that conflicts with a previous report [Peters et al, 19731.…”

mentioning

confidence: 99%

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Indirect immunofluorescence, serum neutralization, and viremia responses of rhesus monkeys (Macaca mulatta) to Machupo virus

Gonder

Eddy²

1986

Journal of Medical Virology

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Although indirect immunofluorescent antibody tests (IFAT) have been developed for several arenaviruses, none has been applied to the rhesus monkey model for Bolivian hemorrhagic fever (caused by the arenavirus Machupo). We infected eight rhesus monkeys with Machupo virus and bled them weekly for determination of viremia and for serum antibody detection by IFAT and serum neutralization (SN) testing. Viremia peaked day 14 post-inoculation (PI), when two of eight animals had low IFAT titers. At day 21 PI, the six surviving monkeys had elevated IFAT titers and diminished viremias. SN titers were not observed until 28 days PI, when three of four survivors had low titers. Results of the IFAT were available more rapidly than the SN, and detected increased serum antibody titers earlier than the SN. Acetone fixation did not completely inactivate BHF antigen spot slides.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Indirect immunofluorescence, serum neutralization, and viremia responses of rhesus monkeys (Macaca mulatta) to Machupo virus

Gonder

Eddy²

1986

Journal of Medical Virology

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“…Indirect fluoresecent antibody (IFA) titers against Junin virus were determined according to the method of Peters et al [15]. Plaque reduction neutralization (PRN) titers were performed on Vero cells by the method of Webb et al [12].…”

Section: Serological Assaysmentioning

confidence: 99%

Viral Strain Dependent Differences in Experimental Argentine Hemorrhagic Fever (Junin Virus) Infection of Guinea Pigs

Kenyon¹,

Green²,

Maiztegui³

et al. 1988

Intervirology

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Guinea pigs infected with low-passage Junin virus of human origin showed viral strain dependent differences in mortality, LD₅₀, time to death, and in viral spread and distribution. Different Junin strains appeared to cause at least two broad patterns of Argentine hemorrhagic fever in guinea pigs. A number of strains of Junin virus caused a viscerotropic type of illness in which virus replicated predominantly in lymph nodes, spleen, and bone marrow. With the most severe visceral forms of Argentine hemorrhagic fever, the guinea pigs became viremic, developed necrosis of spleen, lymph nodes, and bone marrow, showed gastric hemorrhages, and all animals died within 13–15 days. Other Junin strains induced a neurological type of illness with transient viral replication in and lymphocyte depletion of spleen and lymph nodes, with no detectable viremia or viral replication in bone marrow. Subsequently, virus was found in the brain with varying severities of polioencephalitis, and the guinea pigs frequently showed rear leg paralysis before death occurred 28–34 days after inoculation. Not all animals infected with a neurotropic strain developed all these signs. One viral strain induced some signs characteristic of both patterns of illness. Although the disease forms in the guinea pig model did not strictly correlate with those observed in the humans from which these strains were obtained, the different strains of Junin virus consistently caused very different patterns of illness in infected guinea pigs.

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“…Sera were heated at 56 °C for 30 rain and tested, as previously described [10], for LCMV-antibody titers by an indirect immunot]ourescent antibody test (IFAT) and an in vitro assay for neutralizing-antibody used for arenaviruses [16,32]. Briefly, in the IFAT assay, dilutions of test sera were incubated with slides of accto;~e fixed, LCMVinfected, Vero-cells and with slides of fixed uninfected control, Vero-cells.…”

Section: Lc M V-antibody Assaysmentioning

confidence: 99%

Immunosuppression-induced susceptibility of inbred hamsters (Mesocricetus auratus) to lethal-disease by lymphocytic choriomeningitis virus infection

Genovesi

Peters

1987

Archives of Virology

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The role of the immune response in the pathogenesis of lethal and non-lethal lymphocytic choriomeningitis virus (LCMV)-infections of young adult Syrian golden hamsters (Mesocricetus auratus) of different strains was examined using immunosuppressive treatment with cyclophosphamide or with whole-body gamma-irradiation. In all hamsters, the LCMV strains, WE and Armstrong (ARM), caused systemic infections and induced comparable serum LCMV-antibody titers. However, lethal wasting-disease occurred which was hamster-strain and virus-strain dependent. With WE-inocula, MHA and PD4 inbred hamsters were all susceptible to lethal-disease and failed to completely eliminate infection. All LSH and CB inbred hamsters resisted lethal-disease and totally cleared WE-infection. Random colony-bred LVG hamsters and inbred LHC hamsters were intermediate in WE-susceptibility; some died with wasting, while others survived with minimal to no illness. ARM was avirulent for all hamsters and infections were totally cleared. By immunosuppressive treatment, all hamsters were rendered completely susceptible to lethal-disease by WE, and had unresolved infections and diminished serum LCMV-antibody titers. Immunosuppression also rendered all hamster strains partially susceptible to lethal infection by ARM. The hamster immune response was thus shown to suppress LCMV-infection and protect against lethal illness.

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Measurement of Antibodies to Machupo Virus by the Indirect Fluorescent Technique

Cited by 54 publications

References 2 publications

Indirect immunofluorescence, serum neutralization, and viremia responses of rhesus monkeys (Macaca mulatta) to Machupo virus

Indirect immunofluorescence, serum neutralization, and viremia responses of rhesus monkeys (Macaca mulatta) to Machupo virus

Viral Strain Dependent Differences in Experimental Argentine Hemorrhagic Fever (Junin Virus) Infection of Guinea Pigs

Immunosuppression-induced susceptibility of inbred hamsters (Mesocricetus auratus) to lethal-disease by lymphocytic choriomeningitis virus infection

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