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Michael B. A. Oldstone - One of the best experts on this subject based on the ideXlab platform.
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Is the TAM Receptor Axl a Receptor for Lymphocytic Choriomeningitis Virus
Journal of virology, 2013Co-Authors: Brian M. Sullivan, Megan J. Welch, Greg Lemke, Michael B. A. OldstoneAbstract:A recent publication indicated that overexpression of Axl, a cellular receptor that negatively regulates Toll-like receptor signaling, enhanced the entry of Viruses pseudotyped with the glycoprotein of Lymphocytic Choriomeningitis Virus (LCMV) in vitro. In testing the biological relevance of these observations, we found differences in neither viral kinetics between LCMV infections of Axl(-/-) and wild-type mice nor T-cell responses prior to spontaneous viral clearance. Thus, Axl is not required for productive LCMV infection of mice.
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Biology and Pathogenesis of Lymphocytic Choriomeningitis Virus Infection
Current topics in microbiology and immunology, 2002Co-Authors: Michael B. A. OldstoneAbstract:The strength of the Lymphocytic Choriomeningitis Virus (LCMV) model rests on the following five foundations. First, the Virus in vivo in its natural host, the mouse, or in vitro in cultured cells is non-cytolytic. This quality allows clear separation of effects caused by the Virus from those caused by the host immune system. Consequently, the host cell control of viral infection as opposed to how Virus interacts with cells to distort their functions without killing them can be decoded. Second, reactions to LCMV infection can encompass a widely diverse range of immune responses (Fig. 1). Usually when immunocompetent adult mice are injected with LCMV, they generate a marked immune response to eliminate the infectious agent. Although their innate responses include the production of interferon (IFN), macrophages and natural killer (NK) cells (Muller et al. 1994; see reviews Buchmeier et al. 1980; Borrow and Oldstone 1997; see chapter by Biron et al., this volume), it is the adoptive immune response — primarily the Virus-specific CD8+ CTL response — that is responsible for Virus clearance.
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Mechanism of Lymphocytic Choriomeningitis Virus Entry into Cells
Virology, 1994Co-Authors: Persephone Borrow, Michael B. A. OldstoneAbstract:Abstract The path that the arenaVirus Lymphocytic Choriomeningitis Virus (LCMV) uses to enter rodent fibroblastic cell lines was dissected by infectivity and inhibition studies and immunoelectron microscopy. Lysosomotropic weak bases (chloroquine and ammonium chloride) and carboxylic ionophores (monensin and nigericin) inhibited Virus entry, assessed as Virus nucleoprotein expression at early times post-infection, indicating that the entry process involved a pH-dependent fusion step in intracellular vesicles. That entry occurred in vesicles rather than by direct fusion of virions with the plasma membrane was confirmed by immunoelectron microscopy. The vesicles involved were large (150-300 nm diameter), smooth-walled, and not associated with clathrin. Unlike classical phagocytosis, Virus uptake in these vesicles was a microfilament-independent process, as it was not blocked by cytochalasins. LCMV entry into rodent fibroblast cell lines thus involves viropexis in large smooth-walled vesicles, followed by a pH-dependent fusion event inside the cell.
Marilyn B. Mets - One of the best experts on this subject based on the ideXlab platform.
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Congenital Lymphocytic Choriomeningitis Virus-an underdiagnosed fetal teratogen.
Journal of AAPOS : the official publication of the American Association for Pediatric Ophthalmology and Strabismus, 2017Co-Authors: Michael Kinori, Hal R. Schwartzstein, Janice Lasky Zeid, Sudhi P. Kurup, Marilyn B. MetsAbstract:Congenital Lymphocytic Choriomeningitis Virus (LCMV) infection is associated with high mortality and morbidity. Although the number of cases reported in the literature has been increasing, it might still be clinically an underdiagnosed human fetal teratogen. We report 2 more cases of serologically proven congenital LCMV infection. One case presented with Aicardi-like syndrome features. Since congenital LCMV infection may mimic Aicardi syndrome, serologic testing should be considered in the workup of patients with Aicardi syndrome to rule out LCMV infection.
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Lymphocytic Choriomeningitis Virus: emerging fetal teratogen.
American journal of obstetrics and gynecology, 2002Co-Authors: Leslie L. Barton, Marilyn B. Mets, Cynthia L. BeauchampAbstract:Lymphocytic Choriomeningitis Virus (LCMV), a rodent-borne arenaVirus, is an often undiagnosed human fetal teratogen. We describe a neonate born with hydrocephalus and chorioretinitis after maternal second-trimester symptomatic LCMV infection. Previously reported affected infants are reviewed. We strongly suggest that obstetricians counsel their pregnant patients regarding the potential hazard that contact with infected pet, laboratory, and household mice and hamsters poses to pregnant women and their unborn children.
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congenital Lymphocytic Choriomeningitis Virus infection decade of rediscovery
Clinical Infectious Diseases, 2001Co-Authors: Leslie L. Barton, Marilyn B. MetsAbstract:Lymphocytic Choriomeningitis Virus (LCMV) is an underdiagnosed fetal teratogen. This diagnosis should be considered for infants and children with unexplained hydrocephalus, micro- or macrocephaly, intracranial calcifications, chorioretinitis, and nonimmune hydrops. The immunofluorescent antibody test is the only reasonable, commercially available, screening diagnostic tool. The differential diagnosis of congenital LCMV infection includes toxoplasmosis, rubella, cytomegaloVirus, herpes simplex Virus, enteroViruses, human parvoVirus B12, and syphilis. The infection has also been misdiagnosed as various neurologic, ophthalmologic, and chromosomal syndromes. Further research, to determine the prevalence of this infection in human and rodent populations, and prospective studies, to delineate the clinical spectrum of congenital infection, are needed. The public and members of the medical profession should be made aware of the hazard that wild, pet, and laboratory rodents pose to pregnant women.
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Lymphocytic Choriomeningitis Virus: an underdiagnosed cause of congenital chorioretinitis.
American journal of ophthalmology, 2000Co-Authors: Marilyn B. Mets, Leslie L. Barton, Ali S. Khan, Thomas G. KsiazekAbstract:Abstract 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.
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Lymphocytic Choriomeningitis Virus chorioretinitis mimicking ocular toxoplasmosis in two otherwise normal children
American journal of ophthalmology, 2000Co-Authors: Antoine P. Brézin, Marilyn B. Mets, Philippe Thulliez, Bruno Cisneros, Marie Françoise SaronAbstract:Abstract 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.
Leslie L. Barton - One of the best experts on this subject based on the ideXlab platform.
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Human Infection with Lymphocytic Choriomeningitis Virus
Emerging infectious diseases, 2010Co-Authors: Leslie L. BartonAbstract:To the Editor: I read with great interest the article regarding Lymphocytic Choriomeningitis Virus (LCMV) meningitis in a New York City resident (1). The authors’ conclusion that there is a need to ascertain the true incidence of LCMV infection is worthy of underscoring. Nearly 15 years ago, in this same journal, we described congenital LCMV as an unrecognized teratogen and recommended further “research to define the frequency of LCMV” (2). Five years later, we reiterated that recommendation when reporting acquired LCMV meningoencephalitis in an adolescent from Tucson, Arizona (3). Despite, or because of, the lack of prospective studies, the fact that this author has accrued data regarding >60 congenitally infected infants from all geographic areas in the United States during the past 15 years reinforces the concept that LCMV is a neglected pathogen whose time for more extensive study has indeed come.
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Lymphocytic Choriomeningitis Virus: emerging fetal teratogen.
American journal of obstetrics and gynecology, 2002Co-Authors: Leslie L. Barton, Marilyn B. Mets, Cynthia L. BeauchampAbstract:Lymphocytic Choriomeningitis Virus (LCMV), a rodent-borne arenaVirus, is an often undiagnosed human fetal teratogen. We describe a neonate born with hydrocephalus and chorioretinitis after maternal second-trimester symptomatic LCMV infection. Previously reported affected infants are reviewed. We strongly suggest that obstetricians counsel their pregnant patients regarding the potential hazard that contact with infected pet, laboratory, and household mice and hamsters poses to pregnant women and their unborn children.
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congenital Lymphocytic Choriomeningitis Virus infection decade of rediscovery
Clinical Infectious Diseases, 2001Co-Authors: Leslie L. Barton, Marilyn B. MetsAbstract:Lymphocytic Choriomeningitis Virus (LCMV) is an underdiagnosed fetal teratogen. This diagnosis should be considered for infants and children with unexplained hydrocephalus, micro- or macrocephaly, intracranial calcifications, chorioretinitis, and nonimmune hydrops. The immunofluorescent antibody test is the only reasonable, commercially available, screening diagnostic tool. The differential diagnosis of congenital LCMV infection includes toxoplasmosis, rubella, cytomegaloVirus, herpes simplex Virus, enteroViruses, human parvoVirus B12, and syphilis. The infection has also been misdiagnosed as various neurologic, ophthalmologic, and chromosomal syndromes. Further research, to determine the prevalence of this infection in human and rodent populations, and prospective studies, to delineate the clinical spectrum of congenital infection, are needed. The public and members of the medical profession should be made aware of the hazard that wild, pet, and laboratory rodents pose to pregnant women.
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Lymphocytic Choriomeningitis Virus: reemerging central nervous system pathogen.
Pediatrics, 2000Co-Authors: Leslie L. Barton, N. Joanne HyndmanAbstract:Lymphocytic Choriomeningitis Virus (LCMV), a human zoonosis caused by a rodent-borne arenaVirus, has been associated with both postnatal and intrauterine human disease. Infection in man is acquired after inhalation, ingestion, or direct contact with Virus found in the urine, feces, and saliva of infected mice, hamsters, and guinea pigs. Congenital LCMV infection is a significant, often unrecognized cause of chorioretinitis, hydrocephalus, microcephaly or macrocephaly, and mental retardation. Acquired LCMV infection, asymptomatic in approximately one third of individuals, is productive of central nervous system manifestations in one half of the remaining cases. Aseptic meningitis or meningoencephalitis are the predominant syndromes, although transverse myelitis, a Guillain-Barre-type syndrome, as well as transient and permanent acquired hydrocephalus have also been reported. Fatalities are rare. We report a patient with meningoencephalitis attributable to LCMV and discuss the spectrum of central nervous system disease, newer diagnostic modalities, and preventive strategies. Lymphocytic Choriomeningitis Virus, aseptic meningitis, meningoencephalitis, zoonosis, hydrocephalus, arenaVirus.
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Lymphocytic Choriomeningitis Virus: an underdiagnosed cause of congenital chorioretinitis.
American journal of ophthalmology, 2000Co-Authors: Marilyn B. Mets, Leslie L. Barton, Ali S. Khan, Thomas G. KsiazekAbstract:Abstract 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.
Francis V Chisari - One of the best experts on this subject based on the ideXlab platform.
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human plasmacytoid dendritic cells sense Lymphocytic Choriomeningitis Virus infected cells in vitro
Journal of Virology, 2014Co-Authors: Stefan Wieland, Kenji Takahashi, Bryan Boyd, Christina Whittenbauer, Nhi Ngo, J C De La Torre, Francis V ChisariAbstract:We previously reported that exosomal transfer of hepatitis C Virus (HCV) positive-strand RNA from human Huh-7 hepatoma cells to human plasmacytoid dendritic cells (pDCs) triggers pDC alpha/beta interferon (IFN-α/β) production in a Toll-like receptor 7 (TLR7)-dependent, Virus-independent manner. Here we show that human pDCs are also activated by a TLR7-dependent, Virus-independent, exosomal RNA transfer mechanism by human and mouse hepatoma and nonhepatoma cells that replicate the negative-strand Lymphocytic Choriomeningitis Virus (LCMV).
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Noncytopathic clearance of Lymphocytic Choriomeningitis Virus from the hepatocyte.
The Journal of experimental medicine, 1999Co-Authors: Luca G. Guidotti, Persephone Borrow, Amy Brown, Heike Mcclary, Rick Koch, Francis V ChisariAbstract:We have previously shown that interferon and tumor necrosis factor noncytopathically abolish hepatitis B Virus (HBV) replication from the hepatocyte and kidney tubular epithelial cells in vivo. Here we show that a persistent Lymphocytic Choriomeningitis Virus (LCMV) infection is cleared from the hepatocyte noncytopathically when the same cytokines are induced in the liver by antigen-nonspecific stimuli. These results indicate that, like HBV, LCMV is also susceptible to intracellular inactivation by cytokine-induced antiviral mechanisms that are operative in the hepatocyte. In contrast, LCMV is not cleared from intrahepatic nonparenchymal cells or splenocytes, indicating that, unlike the hepatocyte, these cells do not produce the factors required to inactivate LCMV. Antiviral mechanisms like these may have evolved to maintain the functional integrity of vital organs in the face of massive infection.
Rémi N. Charrel - One of the best experts on this subject based on the ideXlab platform.
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Microcephaly Caused by Lymphocytic Choriomeningitis Virus
Emerging infectious diseases, 2017Co-Authors: Maia Delaine, A. S. Weingertner, Antoine Nougairede, Quentin Lepiller, Samira Fafi-kremer, Romain Favre, Rémi N. CharrelAbstract:We report congenital microencephaly caused by infection with Lymphocytic Choriomeningitis Virus in the fetus of a 29-year-old pregnant women at 23 weeks' gestation. The diagnosis was made by ultrasonography and negative results for other agents and confirmed by a positive PCR result for Lymphocytic Choriomeningitis Virus in an amniotic fluid sample.
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Mouse-to-Human Transmission of Variant Lymphocytic Choriomeningitis Virus
Emerging infectious diseases, 2007Co-Authors: Sébastien Emonet, Karine Retornaz, Jean-paul Gonzalez, Xavier De Lamballerie, Rémi N. CharrelAbstract:A case of Lymphocytic Choriomeningitis Virus (LCMV) infection led to investigation of the reservoir. LCMV was detected in mice trapped at the patient's home, and 12 isolates were recovered. Genetic analysis showed that human and mouse LCMVs were identical and that this LCMV strain was highly divergent from previously characterized LCMV.
