The Epidemiology of Lymphocytic Choriomeningitis in White Mice

Traub, E.

doi:10.1084/jem.64.2.183

Cited by 131 publications

(56 citation statements)

References 3 publications

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“…Of note, the absence of infiltrates in naive mice and in rLCMV/INDG-immune mice challenged with ARM (see Figure 4A) rendered analogous tests for these groups impossible. **P < 0.01. tally infected ARM carriers was clinically silent (data not shown), most likely due to antiviral CD8 + T cell tolerance (27,28). Moreover, rLCMV/INDG persisted in the CNS of carriers at comparable levels for at least 100 days (as determined by immunohistochemistry; data not shown) and remained restricted to neurons.…”

Section: Figurementioning

confidence: 92%

“…neonatal infection (<24 hours after birth) of mice with naturally occurring strains of lymphocytic choriomeningitis virus (LCMV; naturally occurring strain referred to as LCMVwt) is widely used to study viral persistence (27). Systemic infection involves the neonatal thymus (29) Measurements with MHC class I tetramers were carried out 7 and 50 days after infection and showed specific T cell frequencies around the detection limit (Figure 1A and data not shown).…”

Section: Introductionmentioning

confidence: 99%

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"Viral deja vu" elicits organ-specific immune disease independent of reactivity to self

Merkler

Horvath²,

Brück³

et al. 2006

Journal of Clinical Investigation

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Autoimmune diseases are often precipitated by viral infections. Yet our current understanding fails to explain how viruses trigger organ-specific autoimmunity despite thymic tolerance extending to many nonlymphohematopoietic self antigens. Additionally, a key epidemiological finding needs to be explained: In genetically susceptible individuals, early childhood infections seem to predispose them to multiple sclerosis (MS) or type 1 diabetes years or even decades before clinical onset. In the present work, we show that the innate immune system of neonatal mice was sufficient to eliminate an attenuated lymphocytic choriomeningitis virus (LCMV) from most tissues except for the CNS, where the virus persisted in neurons (predisposing virus). Virus-specific cytotoxic T cells (CTLs) were neither deleted nor sufficiently primed to cause disease, but they were efficiently triggered in adulthood upon WT LCMV infection (precipitating virus). This defined sequence of viral infections caused severe CNS inflammation that was histomorphologically reminiscent of rasmussen encephalitis, a fatal human autoimmune disease. Yet disease in mice was mediated by antiviral CTLs targeting an epitope shared by the precipitating virus and the predisposing virus persisting in neurons (déjà vu). Thus the concept of "viral déjà vu" demonstrates how 2 related but independently encountered viral infections can cause organspecific immune disease without molecular mimicry of self and without breaking self tolerance.

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Section: Figurementioning

confidence: 92%

Section: Introductionmentioning

confidence: 99%

"Viral deja vu" elicits organ-specific immune disease independent of reactivity to self

Merkler

Horvath²,

Brück³

et al. 2006

Journal of Clinical Investigation

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“…These infected hamsters have most recently been responsible for reported disease in humans (2,34). Additionally, reports of transplant-associated LCMV disease and fatality highlight the clinical relevance of arenaviral infection in immunocompromised individuals (15).…”

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confidence: 99%

Conserved Residues in Lassa Fever Virus Z Protein Modulate Viral Infectivity at the Level of the Ribonucleoprotein

Capul

Torre

Buchmeier

2011

J Virol

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Arenaviruses are negative-strand RNA viruses that cause human diseases such as lymphocytic choriomeningitis, Bolivian hemorrhagic fever, and Lassa hemorrhagic fever. No licensed vaccines exist, and current treatment is limited to ribavirin. The prototypic arenavirus, lymphocytic choriomeningitis virus (LCMV), is a model for dissecting virus-host interactions in persistent and acute disease. The RING finger protein Z has been identified as the driving force of arenaviral budding and acts as the viral matrix protein. While residues in Z required for viral budding have been described, residues that govern the Z matrix function(s) have yet to be fully elucidated. Because this matrix function is integral to viral assembly, we reasoned that this would be reflected in sequence conservation. Using sequence alignment, we identified several conserved residues in Z outside the RING and late domains. Nine residues were each mutated to alanine in Lassa fever virus Z. All of the mutations affected the expression of an LCMV minigenome and the infectivity of virus-like particles, but to greatly varying degrees. Interestingly, no mutations appeared to affect Z-mediated budding or association with viral GP. Our findings provide direct experimental evidence supporting a role for Z in the modulation of the activity of the viral ribonucleoprotein (RNP) complex and its packaging into mature infectious viral particles.Arenaviruses are the causative agents of a number of human diseases, including lymphocytic choriomeningitis, Lassa fever, and Bolivian hemorrhagic fever. These viruses are carried asymptomatically in wild rodents and are transmitted through contact with contaminated excretions. Endemic infection in these rodents maintains a reservoir of virus that can reemerge in human populations as outbreaks (1,18,30) or as novel pathogenic species (6). No FDA-licensed vaccines exist for these viruses, and current antiarenaviral therapy is limited to the off-label use of the nucleoside analogue ribavirin, which has had mixed success in treating cases of arenaviral hemorrhagic fever (HF) disease, while being associated with significant side effects (5).The prototypic arenavirus, lymphocytic choriomeningitis virus (LCMV), is ubiquitous in wild rodents and can infect domesticated mice and hamsters. These infected hamsters have most recently been responsible for reported disease in humans (2, 34). Additionally, reports of transplant-associated LCMV disease and fatality highlight the clinical relevance of arenaviral infection in immunocompromised individuals (15). In addition, congenital transmission of LCMV has been implicated in a variety of clinical conditions that affect mainly the retina and brain (3, 4).Arenaviruses are enveloped viruses bearing a bi-segmented, negative-sense RNA genome. Each segment contains two open reading frames (ORFs) in the ambisense orientation that are separated by a noncoding intergenic region (IGR) and bounded at their 5Ј and 3Ј ends by untranslated regions (UTRs) that are critical for the control of viral R...

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“…Traub's findings (6)(7)(8) that mice infected in utero with lymphocytic choriomeningitis fail to produce complement-fixing antibodies have already been mentioned. Kerr and Robertson reported that the antibody response to Trichomom~s Joaus is reduced considerably in calves injected intramuscularly with this organism shortly after birth (29).…”

mentioning

confidence: 95%

Inhibition of Tuberculin Skin Hypersensitivity in Guinea Pigs by Injection of Tuberculin and Intact Tubercle Bacilli During Fetal Life

Weiss

1958

The Journal of Experimental Medicine

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Female guinea pigs were subjected to laparotomy at different stages of pregnancy, and their fetuses injected through the uterine walls with one of the following preparations: Old Tuberculin, tubercle bacilli of the BCG strain killed by heat or exposure to phenol, and living BCG. A large number of the animals injected in utero with Old Tuberculin failed to develop skin hypersensitivity to P.P.D. following vaccination with 200 or 800 γ phenol-killed tubercle bacilli (BCG) in early adulthood. Normal control animals were sensitized by vaccination with such quantities of phenolized BCG. The failure of animals which had been injected with Old Tuberculin in fetal life to respond hypersensitively to P.P.D. after adult vaccination with tubercle bacilli is ascribed to their acquisition of a state of immunological tolerance to tuberculoprotein (tuberculin tolerance). Fetal injection with killed BCG conferred a state of tolerance on a few of the animals, and rendered others tuberculin-sensitive. Fetal injection with living BCG sensitized most of the animals to tuberculin, even when fetal exposure was as early as 46 days before birth, and induced tolerance in none. Fetuses of the same litter, injected simultaneously with identical inocula, often responded differently, some becoming tolerant to tuberculin, others developing hypersensitivity, and still others remaining immunologically unaffected, becoming neither sensitive nor tolerant. The state of tuberculin tolerance induced in these experiments was limited. When tolerant animals were revaccinated with living BCG several weeks after vaccination with phenol-killed bacilli, they developed as high a degree of tuberculin skin sensitivity as the originally non-tolerant animals.

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The Epidemiology of Lymphocytic Choriomeningitis in White Mice

Cited by 131 publications

References 3 publications

"Viral deja vu" elicits organ-specific immune disease independent of reactivity to self

"Viral deja vu" elicits organ-specific immune disease independent of reactivity to self

Conserved Residues in Lassa Fever Virus Z Protein Modulate Viral Infectivity at the Level of the Ribonucleoprotein

Inhibition of Tuberculin Skin Hypersensitivity in Guinea Pigs by Injection of Tuberculin and Intact Tubercle Bacilli During Fetal Life

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