Tolerance to Junin virus in thymectomized mice

Schmuñis, Gabriel A.; Weissenbacher, Mercedes; Parodi, A. S.

doi:10.1007/bf01241444

Cited by 14 publications

(5 citation statements)

References 12 publications

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“…In addition to the similarity of appearance, the Tacaribe complex viruses share a number of biological properties with LCM virus, such as production of persistent tolerant infections in rodents (11) and dependence of the mechanism of pathogenesis on the integrity of the thymusdependent lymphoid system (7,9,(18)(19)(20)(21).…”

mentioning

confidence: 99%

Serological Relationship of the Tacaribe Complex of Viruses to Lymphocytic Choriomeningitis Virus

Rowe

Pugh

Webb

et al. 1970

J Virol

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By means of the indirect fluorescent-antibody test, cross serological reactivity was demonstrated between lymphocytic choriomeningitis (LCM) virus and the viruses of the Tacaribe complex. Antisera to all members of the Tacaribe complex reacted with LCM virus; LCM antisera gave significant staining of Amapari virus, but minimal or inconsistent reactions with Tacaribe virus, and no reaction with two other viruses of the Tacaribe complex. A low level cross-reaction was observed in complement fixation tests of Machupo and Pichinde antisera against LCM antigen. Immunization with Tacaribe and Amapari viruses did not protect mice against challenge with LCM virus. Because of the identical appearance of the virions, the sharing of antigens, and the many biological similarities between LCM and the Tacaribe complex viruses, it is proposed that they be considered as constituting a new taxonomic group of viruses.

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mentioning

confidence: 99%

Serological Relationship of the Tacaribe Complex of Viruses to Lymphocytic Choriomeningitis Virus

Rowe

Pugh

Webb

et al. 1970

J Virol

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“…The role of the cellular immune response in the pathogenesis of encephalitis induced by Junin virus infection of mice has been exten sively studied employing thymectomized new born mice [2][3][4][5] or animals treated with anti metabolites [6] or antithymocyte serum [7]. Several workers have suggested that the brain lesions were due to destruction of infected cells acting as targets for specifically sensitized T lymphocytes.…”

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confidence: 99%

Junin Virus Infection in Genetically Athymic Mice

et al. 1983

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The progression of Junin virus infection was studied in congenitally athymic mice. Immunocompetent littermates were used as infected controls. As expected, the latter developed lethal encephalitis, with viremia and considerable viral replication in the brain. The mortality rate was almost 100%; the few surviving controls exhibited high serum neutralizing antibody levels and a total absence of virus in blood and brain. In contrast, nude mice did not contract the disease; all survived with persistent viremia and virus in brain, but no serum neutralizing antibodies were detected. These results confirm previous research on thymectomized mice and those treated with anti-lymphocyte serum and tend to support the important role of cellular immunity in the pathogenesis of this viral disease.

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“…Previous work on newborn immuno competent mice has demonstrated that both neurologic disease and virus clearance are mediated by thymus-dependent lympho cytes; the absence of cell response precludes disease and leads to virus persistence without Abs, as shown in nude [2], thymectomized [6], and antithymocyte serum-treated mice [10].…”

Section: Discussionmentioning

confidence: 99%

“…When immunocompetent newborn mice are infected with Junin virus, virus titers in the brain climb during the first 10 days and the animals succumb to encephalitis due to a thymus-dependent cellular response [5,6]. However, in nu/nu newborn mice, Junin vi rus replicates but induces persistent central nervous system (CNS) infection with high viremia, and animals survive without neuro logic illness [2].…”

Section: Discussionmentioning

confidence: 99%

Induction of Junin Virus Persistence in Adult Athymic Mice

et al. 1986

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To determine the role of T lymphocytes in adult mice infected with Junin virus, 60-day-old athymic (nu/nu) mice and their immunocompetent (nu/+) littermates were inoculated intracerebrally with 10³ TCD50 of the XJ strain. None of them exhibited neurologic illness during a 6-month observation period, and mortality was 3% for nu/nu and 7% for nu/+ animals. The main features in infected nu/nu mice were: (i) high viral titers in brain, reaching a late peak (6.5 log/ml) 32 days postinoculation and persisting at least 6 months; (ii) low, late viremia appearing simultaneously with the viral peak in the central nervous system (CNS) and persisting up to 3 months after infection; (iii) absence of signs of neurologic disease or histologic lesions in brain and almost no mortality; and (iv) lack of detectable circulating antibodies either in IgM or in other immunoglobulins (Igs). Circulating anti-Junin antibodies were demonstrated in IgM and other Igs in immunocompetent mice, although no infectious virus or histologic lesions could be detected. These results show an important role for T lymphocytes in the clearence of Junin virus in the CNS, as demonstrated by viral persistence induced in adult athymic mice.

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Tolerance to Junin virus in thymectomized mice

Cited by 14 publications

References 12 publications

Serological Relationship of the Tacaribe Complex of Viruses to Lymphocytic Choriomeningitis Virus

Serological Relationship of the Tacaribe Complex of Viruses to Lymphocytic Choriomeningitis Virus

Junin Virus Infection in Genetically Athymic Mice

Induction of Junin Virus Persistence in Adult Athymic Mice

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