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At least 19 recordsLinked to original sources
PubMed1970

Pathogenesis of chronic disease associated with persistent lymphocytic choriomeningitis viral infection. II. Relationship of the anti-lymphocytic choriomeningitis immune response to tissue injury in chronic lymphocytic choriomeningitis disease.

Tissue injury (chronic disease) associated with persistent LCM infection is apparently caused by the host immune response to the virus. Employing parabiosis or cell transfer from hyperimmune donors to isologous virus carriers, the tissue injury of chronic disease could be initiated and/or intensified. Furthermore, the transfer of anti-LCM antibody to SWR/J carrier mice results in acute necrotizing inflammatory lesions in regions of viral persistence, followed by chronic mononuclear infiltrates quite similar to those seen after the transfer of immune cells. The pathogenesis of the nonglomerular tissue injury of chronic LCM disease is apparently at least in part related to the interaction of circulating anti-LCM antibody with viral antigen at the tissue site. Trapping of circulating virus-antibody complexes in the glomerular filter is apparently the major cause of the glomerulonephritis.

Animals↗
PubMed1984

Virus specificity of cytotoxic T lymphocytes generated during acute lymphocytic choriomeningitis virus infection: role of the H-2 region in determining cross-reactivity for different lymphocytic choriomeningitis virus strains.

We have compared the relatedness of five different strains of lymphocytic choriomeningitis virus (LCMV) as assessed by LCMV-specific cytotoxic T lymphocytes (CTL). Several different mouse strains were injected with each of the five LCMV strains, and the cross-reactivity of virus-specific CTL generated during the acute infection was tested by killing on a panel of target cells infected with the various LCMV strains. We found that the cross-reactivity pattern of LCMV-specific CTL generated in mice of H-2d haplotype (BALB/c WEHI and DBA/2) was strikingly different from that in mice of H-2b haplotype (C57BL/6 and C3H.Sw/Sn), suggesting that the fine specificity of LCMV-specific CTL is a function of the H-2 region. The characteristic cross-reactivity patterns were also observed in (C57BL/6 X DBA/2)F1 mice, demonstrating that the repertoire of the H-2b- and H-2d-restricted LCMV-specific CTL is not changed as a result of complementation by gene products of the other major histocompatibility haplotype. Studies with congenic BALB.B10 and (BALB.B10 X BALB/c)F1 mice firmly established that the characteristic cross-reactivity patterns of LCMV-specific CTL map to the H-2 region and are not influenced by background genes outside the major histocompatibility locus. These results suggest that LCMV determinants seen in the context of H-2d-restricting elements are different from those seen in the context of H-2b-restricting elements. Moreover, our studies show that CTL can be used as probes for dissecting differences among various LCMV strains, but the degree of relatedness between the different LCMV strains is not absolute when measured by CTL recognition. Since the H-2 region regulates the fine specificity of CTL generated during LCMV infection in its natural host, the degree of cross-protective immunity developed during a viral infection apparently depends on the major histocompatibility haplotype. The importance of these findings lies in understanding susceptibility or resistance of various host populations to viral infections and in designing vaccination programs to provide immunity.

Animals↗
PubMedDate not supplied

[Herpes simplex and lymphocytic choriomeningitis viruses in infections of the central nervous system--clinical and cerebrospinal fluid characteristics].

INTRODUCTION: A great number of various viruses are stated as the cause of acute infections and damages of the central nervous system. In most cases these are minor damages which exhibit as meningeal syndrome and a specific finding in the cerebrospinal fluid. According to the dominant location, central nervous system infections can take a form of meningitis, encephalitis or myelitis. Since the inflammatory process of the meninges can not be separated from the inflammatory process of the brain, we usually speak of meningoencephalitis. The etiological diagnosis of meningitis and encephalitis is established by isolating the virus from the cerebrospinal fluid and by finding the presence of the specific antibodies in the blood and in the cerebrospinal fluid. The most common causes of the viral meningitis are Enteroviruses, the Mumps virus, Arthropode borne viruses, the Herpes viruses, Adeno viruses and the Lymphocytic choriomeningitis virus. The aim of our study was to establish the correlation between the clinical features and immunological and cerebrospinal fluid changes and the degree of the damage to the blood-brain barrier during the infections of the central nervous system, caused by the Herpes Simplex virus and the Lymphocytic choriomeningitis virus. MATERIAL AND METHODS: From a group of 103 patients, who had been treated for viral meningitis and meningoencephalitis, a group of 27 patients with established specific viral etiology--Herpes Simplex virus and Lymphocytic choriomeningitis virus, had been taken into the account. Herpes Simplex infection had been proven by the complement binding reaction and the neutralisation test of the even samples of serum. The diagnosis of Lymphocytic choriomeningitis was confirmed by the immunofluorescence test of the pharynx swabs and cerebrospinal fluid. The clinical features, such as body temperature, encephalitic signs, and electroencephalographic findings had been followed and compared. RESULTS: Herpes Simplex infection had been found in 20 patients, Lymphocytic choriomeningitis had been proven in 7 patients. All the patients had increased body temperature. Only four of the patients exhibited encephalitic signs, all infected by the Herpes Simplex virus. Patients from the Herpes Simplex group showed various degrees of consciousness disturbances, ranging from somnolence to coma, while the Lymphocytic choriomeningitis patients exhibited none. Higher pleocytosis and protein level had been found in the Lymphocytic choriomeningitis group. DISCUSSION: Viral diseases of the central nervous system are the result of the direct damage of the brain and meninges by the virus and immunological processes. Herpes Simplex meningitis usually has a good prognosis. Lymphocytic choriomeningitis has longer course of the disease and exhibits more severe clinical features. CONCLUSION: In cases of the central nervous system infections, caused by Herpes Simplex virus or Lymphocytic choriomeningitis virus, the correlation between the severeness of clinical features and the degree of damage of the blood-brain barrier, the level of pleocytosis and the increase of the cerebrospinal fluid proteins had been established.

Adult↗
PubMed2000

Lymphocytic choriomeningitis virus: an underdiagnosed cause of congenital chorioretinitis.

PURPOSE: To elucidate the role and clinical spectrum of congenital lymphocytic choriomeningitis virus infection as a cause of chorioretinopathy, congenital hydrocephalus, and macrocephaly or microcephaly in the United States. METHODS: We performed complete ophthalmologic surveys of all residents at Misericordia, a home for the severely mentally retarded in Chicago, and prospectively evaluated all patients with chorioretinitis or chorioretinal scars during a 36-month period at Children's Memorial Hospital, also located in Chicago. Sera for patients demonstrating chorioretinal scars (a sign of intrauterine infection) were tested for Toxoplasma gondii, rubella virus, cytomegalovirus, and herpes simplex virus and lymphocytic choriomeningitis virus antibodies. RESULTS: Four of 95 patients examined at the home had chorioretinal scars, and two of these patients had normal T. gondii, rubella virus, cytomegalovirus, and herpes simplex virus titers and dramatically elevated titers for lymphocytic choriomeningitis virus. Three of 14 cases of chorioretinitis at the hospital had normal T. gondii, rubella virus, cytomegalovirus, and herpes sim-plex virus titers and elevated lymphocytic choriomeningitis virus antibody titers. (A fourth case, diagnosed in 1996, was reported 2 years ago.) CONCLUSIONS: Lymphocytic choriomeningitis virus was responsible for visual loss in two of four children secondary to chorioretinitis in a population of severely retarded children. The six new cases of lymphocytic choriomeningitis virus chorioretinitis identified in these two populations over the last 3 years, compared with the total number ever reported in the United States (10 cases), suggests that lymphocytic choriomeningitis virus may be a more common cause of congenital chorioretinitis than previously believed. Because its consequences for visual and psychomotor development are devastating, we conclude that the workup for congenital chorioretinitis should include lymphocytic choriomeningitis virus serology, especially if T. gondii, rubella virus, cytomegalovirus, and herpes simplex virus titers are negative.

Antibodies, Viral↗
PubMed2000

Lymphocytic choriomeningitis virus chorioretinitis mimicking ocular toxoplasmosis in two otherwise normal children.

PURPOSE: To report unilateral macular lesions, mimicking toxoplasmic scars, in two children with serological evidence for lymphocytic choriomeningitis virus infection. METHODS: Case reports. RESULTS: Patients were 4 and 5 years old, with negative toxoplasma serologies and no sign of rubella, cytomegalovirus, or herpes simplex infection (TORCH evaluation). Lymphocytic choriomeningitis virus infection was detected in both cases by enzyme-linked immunosorbent assay and confirmed by Western immunoblotting. The modes of infection were unknown; no history of symptomatic systemic lymphocytic choriomeningitis virus infection was reported, and lymphocytic choriomeningitis virus serologies were negative in the mothers of the patients. Neurological examinations and brain magnetic resonance imaging were normal. CONCLUSION: Our observations suggest that chorioretinal scars can be an isolated manifestation of lymphocytic choriomeningitis virus infection.

Animals↗
PubMed1984

Two epizootics of lymphocytic choriomeningitis virus occurring in laboratory mice despite intensive monitoring programs.

Two epizootics of lymphocytic choriomeningitis virus in mice occurred within two months in one research facility consisting of several widely separated rooms. These outbreaks developed despite intensive institutional monitoring policies designed to prevent introduction and spread of lymphocytic choriomeningitis virus. Evidence derived from serological and virological assays and interviews with the concerned investigators suggested that a single transplantable tumor carried in mice may have been responsible for spread of the virus. However, the tumor was not contaminated with lymphocytic choriomeningitis virus at the time of its introduction into the mouse facility. The origin of the virus responsible for the outbreaks was not definitively established although data supported an hypothesis that the virus was introduced into the research facility by a wild or feral mouse. Virus spread from infected mice to humans did not occur, as measured by serological tests. However, a large and valuable animal facility was depopulated for safety reasons. Absorption of sera with lymphocytic choriomeningitis virus antigen proved a necessary and reliable method for confirming specificity of lymphocytic choriomeningitis virus fluorescence-positive reactions.

Animals↗
PubMed1965

Lymphocytic-choriomeningitis virus in hamster tumor: spread to hamsters and humans.

A passage line of a spontaneous hamster fibrosarcoma is contaminated by the virus. of lymphocytic choriomeningitis. Tumors from animals receiving implants when newborn contain high titers of infectious lymphocytic-choriomeningitis virus and complement-fixing antigen, and hamsters receiving implants when weanlings develop high titers of complement-fixing antibody against lymphocytic-choriomeningitis virus. In contrast with the specific reactions of tumorous hamsters to the initiating virus in virus-induced tumors, the development of complement-fixing antibody to lymphocytic-choriomeningitis virus does not depend on the development of tumors. Infant hamsters bearing the tumor have a generalized subclinical infection and seem able to spread virus to other hamsters and to humans.

Animals↗
PubMed1994

Expression of the inducible nitric oxide synthase. Correlation with neuropathology and clinical features in mice with lymphocytic choriomeningitis.

Nitric oxide (NO) synthesized by the cytokine-inducible enzyme, nitric oxide synthase (iNOS), is thought to be a key mediator in the host immune response to infection, in which it may have protective, as well as injurious, actions. We sought evidence for a role of NO in the pathogenesis of lymphocytic choriomeningitis by examining the cerebral expression of the iNOS gene in mice after intracranial inoculation of lymphocytic choriomeningitis virus. In euthymic, but not athymic, mice, elevated expression of iNOS mRNA was observed in the brain by day 5 and increased further to high levels by day 6 postinfection. Of the peripheral organs, only the spleen showed significant increases in iNOS mRNA at day 3 postinfection. In situ hybridization revealed that iNOS RNA expression was restricted to cells within the inflammatory infiltrates and in proximity to areas of lymphocytic choriomeningitis virus infection in the brain. Immunostaining for iNOS protein identified numerous positive cells within the inflammatory infiltrates present in the meninges and choroid plexus. Phenotypic analysis revealed the majority of the iNOS containing cells to be Mac-1 positive. T lymphocytes that belonged to the CD8+ and CD4+ subsets were negative for iNOS expression. The kinetics and distribution of cerebral iNOS expression in lymphocytic choriomeningitis are consistent with a major role for the iNOS/NO pathway in the pathogenesis of this immune-mediated neurologic disease.

Amino Acid Oxidoreductases↗
PubMed1999

Single H2Kb, H2Db and double H2KbDb knockout mice: peripheral CD8+ T cell repertoire and anti-lymphocytic choriomeningitis virus cytolytic responses.

Single H2Kb, H2Db and double H2KbDb homozygous knockout (KO) mice were generated and their peripheral CD8+ T cell repertoires compared to that of C57BL/6 (B6) mice. Limited (10-20%, H2Db), substantial (30-50%, H2Kb) and profound (90%, H2KbDb) reduction of peripheral CD8+ T cells was observed in KO mice, without Vbeta diversity alteration. Classical class Ia molecules therefore ensure most but not all of the peripheral CD8+ T cell repertoire education. As expected, H2Kb but also H2Db KO mice developed choriomeningitis following intracranial infection by lymphocytic choriomeningitis virus with the same kinetics, lethality and CD8+ cell implication as wild-type B6 mice. By contrast, H2KbDb (class Ia-Ib+) KO mice survived. Choriomeningitis of H2Db KO mice was linked to the development of a subdominant (in normal B6 mice) H2Kb-restricted cytotoxic T lymphocyte response. Mice expressing a restricted set of histocompatibility class I molecules should represent useful tools to evaluate the immunological potentials of individual MHC class I molecules.

Animals↗
PubMed1997

Lymphocytic choriomeningitis virus in southern France: four case reports and a review of the literature.

Infections due to choriomeningitis virus have been only infrequently reported in humans. Most cases have been diagnosed during laboratory outbreaks in the USA and Germany. In this report, we describe 4 cases of acute meningitis due to choriomeningitis virus occurring after close contact with domestic syrian hamsters. Although the disease is usually mild, some fatal cases have been described. The purpose of this report is to alert physicians to the possibility of lymphocytic choriomeningitis in patients who have had close contact with Syrian hamsters.

Adult↗
PubMed1972

Immunopathogenesis of acute central nervous system disease produced by lymphocytic choriomeningitis virus. II. Adoptive immunization of virus carriers.

Lymphocytic choriomeningitis (LCM) virus carriers were established by intracerebral inoculation of adult BALB/c mice followed by a single dose of cyclophosphamide (CY) (150 mg/kg) 3 days after infection, and by intracerebral injection within 24 hr of birth. These carriers were then adoptively immunized with spleen cells or serum from immune or normal BALB/c donors. Transfer of immune spleen cells into drug-induced carriers consistently resulted in acutely fatal choriomeningitis, histologically strikingly similar to classical LCM. Normal spleen cells or immune serum failed to produce either central nervous system (CNS) pathology or illness with any regularity. In addition, focal necrosis of the cerebellum was seen after adoptive immunization of drug-induced carriers but only when mice received cells at least 3 wk after inoculation, which is probably explained by the gradual spread of infection from membranes to the neural parenchyma during the first month after establishment of the carrier state in adult mice. Immune spleen cells, when transferred to neonatal carriers, led to a decrease in virus titers in blood and brains and to development of antibody without acute CNS disease. It appears that the production of fatal choriomeningitis after LCM infection is determined in part by the distribution of viral antigen, and this is markedly different in neonatal and drug-induced carriers at the time of cell transfer. Another factor of potential importance is the much higher level of circulating viral antigen in the plasma of neonatal than in that of drug-induced LCM carriers. Classical LCM disease can only be transferred by immune lymphoid cells and not by antiserum. Furthermore, little or no complement-fixing (CF) antibody was found in the plasma of mice dying of acute choroiditis. These observations strongly suggest that acute choroiditis is dependent upon the cell-mediated immune response.

Animals↗
PubMed1982

Cytotoxic T cells are induced in mice infected with lymphocytic choriomeningitis virus strains of markedly different pathogenicities.

The ability of two lymphocytic choriomeningitis virus substrains to induce cytotoxic T-lymphocyte (CTL) responses in intracerebrally infected mice was examined. One strain, designated A (aggressive), provoked a convulsive type of death in 100% of the mice within 8 to 9 days, whereas the other strain, designated D (docile), killed less than 10% of the mice during 28-day observation periods. CTL activity was assessed by the capacity of partially purified splenocytes to lyse 51Cr-labeled L-cell targets infected with either type of lymphocytic choriomeningitis substrain. The CTL population was identified by its sensitivity to anti-Thy-1 serum and its inability to lyse uninfected target cells or infected target cells with which it differed at the level of antigens controlled by the major histocompatibility gene complex. A strong CTL response developed in mice infected with either lymphocytic choriomeningitis substrain, although the activity provoked by substrain D was somewhat less than that seen after substrain A infection. Peak CTL activities induced by both strains occurred at about the same time. Even though docile virus replicated more extensively in the brain than did aggressive virus and fluorescent antibody staining revealed similar distributions of viral antigen, no inflammatory response was noted in the brains of mice infected with docile virus. These results are discussed with regard to the role of CTLs in mediating classic central nervous system pathology.

Animals↗
PubMed1995

Immunobiology of cytotoxic T-cell escape mutants of lymphocytic choriomeningitis virus.

Infection with virus variants exhibiting changes in the peptide sequences defining immunodominant determinants that abolish recognition by antiviral cytotoxic T cells (CTL) presents a considerable challenge to the antiviral T-cell immune system and may enable some viruses to persist in hosts. The potential importance of such variants with respect to mechanisms of viral persistence and disease pathogenesis was assessed by infecting adult mice with variants of lymphocytic choriomeningitis virus (LCMV) strain WE. These variants were selected in vivo or in vitro for resistance to lysis by CD8+ H-2b-restricted antiviral CTL. The majority of anti-LCMV CTL in infected H-2b mice recognize epitopes defined by residues 32 to 42 and 275 to 289 (epitopes 32-42 and 275-289) of the LCMV glycoprotein or 397 to 407 of the viral nucleoprotein. The 8.7 variant exhibits a change in the epitope 32-42 (Val-35-->Leu), and variant CL1.2 exhibits a change in the epitope 275-289 (Asn-280-->Asp) of the wild-type LCMV-WE. The double-mutated 8.7-B23 variant had the variation of 8.7 and an additional change located in the epitope 275-289 (Asn-280-->Ser). The 8.7 variant peptide with unchanged anchor positions bound efficiently to H-2Db and H-2Kb molecules but induced only a very weak CTL response. CTL epitope 275-289 of CL1.2 and 8.7-B23 altered at predicted anchor residues were unable to bind Db molecules and were also not recognized by antiviral CTL. Infection of C57BL/6 mice (H-2b) with the variants exhibiting mutations of one of the CTL epitopes, i.e., 8.7 or CL1.2, induced CTL responses specific for the unmutated epitopes comparable with those induced by infection with WE, and these responses were sufficient to eliminate virus from the host. In contrast, infection with the double-mutated variant 8.7-B23 induced CTL activity that was reduced by a factor of about 50-fold compared with wild-type LCMV. Consequently, high doses (10(7) PFU intravenously) of this virus were eliminated slowly and only by about day 100 after infection. 8.7-B23 failed to cause lethal lymphocytic choriomeningitis after intracerebral infection with a dose of > 10(4) PFU in C57BL/6 mice (but not in mice of nonselecting H-2d haplotype); with the other variants or wild-type LCMV, doses greater than 10(6) to 10(7) PFU were necessary to avoid lethal choriomeningitis.(ABSTRACT TRUNCATED AT 400 WORDS)

Amino Acid Sequence↗
PubMed1989

[Lymphocytic choriomeningitis causing unilateral deafness].

Lymphocytic choriomeningitis is generally a benign disease passing off without complication. The authors describe a case where the disease appeared in the form of febrile infection and caused permanent unilateral deafness. In connection with this case the authors review briefly the clinical aspects, diagnostic difficulties of lymphocytic choriomeningitis virus infection and wish to draw the attention to the possibility of a lymphocytic choriomeningitis infection in the background of parainfluenza diseases occurring mainly in cold months.

Hearing Loss↗
PubMed1994

Altered tissue distribution of viral replication and T cell spreading is pivotal in the protection against fatal lymphocytic choriomeningitis in mice after neutralization of IFN-alpha/beta.

IFN-alpha/beta have been shown to play a central role in the development of lymphocytic choriomeningitis and increasing attention has been focused on this group of cytokines as early regulatory factors directing T lymphocyte responses. In the present study, injection of antiserum to IFN-alpha/beta prevented the development of lymphocytic choriomeningitis, was associated with the absence of detectable expression of early 2'-5' oligo-adenylate synthetase mRNA and coincided with viremia of lymphocytic choriomeningitis virus (LCMV) followed by establishment of a persistent infection. The LCMV-specific cytotoxic T lymphocyte response was unchanged in cervical lymph nodes but decreased in the spleen of anti-IFN-alpha/beta-treated animals. The expression of cytokine mRNA (particularly IFN-gamma) in organs of LCMV-infected mice treated with anti-IFN-alpha/beta coincided with infiltration of lymphocytes and tissue destruction. Furthermore, a reduced number of infiltrating leukocytes in the brain and cervical lymph nodes and a low expression of cytokine mRNA in the brain was observed in anti-IFN-alpha/beta-treated animals. In total, the findings support the view that neutralization of IFN-alpha/beta leads to extensive LCMV replication in the viscera. The therapeutic effects of anti-IFN-alpha/beta antiserum seem to be independent of the functional capacity of T cells but probably result in a dispersion of activated T cells throughout the body of LCMV-infected mice. Absence of IFN-alpha/beta expression in the central nervous system is proposed as the mechanism behind the IFN-alpha/beta-dependent targeting of T cells to the brain.

2',5'-Oligoadenylate Synthetase↗
PubMed1983

Evidence for cytotoxic T-lymphocyte-target cell interaction in brains of mice infected intracerebrally with lymphocytic choriomeningitis virus.

Murine lymphocytic choriomeningitis is a T-cell-mediated pathologic immune phenomenon. The name of this experimental illness was derived from the principal histopathologic alterations of the central nervous system (CNS) of adult mice infected intracerebrally with lymphocytic choriomeningitis virus, i.e., lymphocytic infiltrations of plexus choroidei and meninges. The general assumption that the main event in the pathogenesis is damage to virus-infected target cells by cytotoxic T-lymphocytes is plausible but direct evidence is scarce. We have studied the ultrastructural alterations of both types of cells that are thought to participate in this immunopathologic interaction. Lymphocytes with signs of T-cell transformation were first evident on day 4 after infection. One day later, lymphoblasts, often extending uropods and containing cytoplasmic dense and compound multivesicular bodies, predominated. They were sometimes seen in intimate contact with connective tissue cells of the leptomeninx and epithelial cells of the choroid plexuses which were shown to be infected by immunofluorescence procedure. Lymphoblasts occasionally invaginated the cytoplasm of the putative target cells with cytoplasmic processes, and were even found inside the latter, exhibiting the phenomenon of emperipolesis. Lymphocytic transformation was at its maximum 6 days after infection. At this time, individual leptomeningeal cells and groups of plexus epithelial cells showed signs of cytolysis, and in a few instances these damaged cells were in close spatial association with lymphoblasts. Similar observations have been reported by others who studied the interaction between cytotoxic T-lymphocytes and their appropriate targeted cells in vitro. We interpret our findings as providing direct evidence for the assumption that one link in the chain of events leading to the cerebral form of lymphocytic choriomeningitis of the mouse is damage to virus-infected leptomeningeal and plexus cells by cytotoxic T-lymphocytes.

Animals↗
PubMed1991

Immune response against lymphocytic choriomeningitis virus infection in mice without CD8 expression.

The immune response against lymphocytic choriomeningitis virus (LCMV) was studied in a mutant mouse strain that does not possess CD8+ T lymphocytes. Virus-specific cytotoxic T cell activity was generated in spleens of wild-type mice in an acute LCMV infection but was not measurable in mutant mice. Injection of replicating LCMV into footpads of wild-type mice induced a CD8+ T cell-mediated swelling that peaked on day 8, followed by a CD4+ T cell-mediated swelling that peaked on day 11, whereas mutant mice exhibited only the CD4+ T cell-mediated swelling. After intracerebral inoculation with LCMV-Armstrong, all wild-type mice died of classical CD8+ T cell-dependent choriomeningitis in 8-10 days. Mutant mice showed symptoms of general malaise but most of them survived. Mutant mice depleted of CD4+ T cells by monoclonal antibody treatment showed no clinical signs of sickness. On day 9 after intravenous infection with LCMV-WE, virus was detected at high titers in spleens and livers of mutant mice but not in those of wild-type mice. On day 70 after injection of LCMV-WE into footpads, virus was not detected in wild-type mice and in one of the three mutant mice tested, but was still measurable in kidneys of the other two mutant mice. These results confirm in a new animal model that CD8+ T cell-mediated immunity is crucial in LCMV clearance and in the immunopathological disease during LCMV infection. In addition, our results demonstrated a less severe form of choriomeningitis mediated by CD4+ T cells and slow clearance of LCMV by alternative pathways independent of CD8+ T cells.

Acute Disease↗
PubMed1985

Biology of cloned cytotoxic T lymphocytes specific for lymphocytic choriomeningitis virus: clearance of virus and in vitro properties.

We have generated lymphocytic choriomeningitis virus-specific, H-2-restricted cytotoxic thymus-derived lymphocyte (CTL) clones. By using these reagents in several in vitro assays with infected target cells, we show that CTLs by themselves prevent the release of infectious virus into culture fluids and significantly lower the titers of infectious virus previously produced. This ability of cloned CTLs is not influenced by monensin. However, monensin does abrogate the ability of CTLs from spleens of mice primed 6 to 8 days previously with virus to kill virus-infected syngeneic targets. When tested for the participation of lymphokines in this system, the CTLs proliferate when reacted with syngeneic lymphocytic choriomeningitis virus-infected macrophages but fail to make interleukin-2. These CTLs make gamma interferon when reacted with syngeneic virus-infected targets. However, the production of interferon does not directly correlate with CTL-mediated killing. The number of H-2K and D molecules expressed on the target cell surface is not altered during the course of lymphocytic choriomeningitis virus infection. Electron microscopy shows finger-like projections of the CTL clone thrust into the infected cell and lesions bearing an internal diameter of approximately 15 nm in those membranes, illustrating the lytic process.

Animals↗