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Artículos de revistas sobre el tema "LCMV"

Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 21 de febrero de 2023

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1

Ishii, Akihiro, Yuka Thomas, Ladslav Moonga, et al. "Molecular surveillance and phylogenetic analysis of Old World arenaviruses in Zambia." Journal of General Virology 93, no. 10 (2012): 2247–51. http://dx.doi.org/10.1099/vir.0.044099-0.

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In order to survey arenaviruses in the Republic of Zambia, we captured 335 rodents from three cities between 2010 and 2011. Eighteen Luna virus (LUNV) and one lymphocytic choriomeningitis virus (LCMV)-related virus RNAs were detected by one-step RT-PCR from Mastomys natalensis and Mus minutoides, respectively. Four LUNV strains and one LCMV-related virus were isolated, and the whole genome nucleotide sequence was determined by pyrosequencing. Phylogenetic analyses revealed that the LUNV clade consists of two branches that are distinguished by geographical location and that the LCMV-related vir

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2

Ceredig, R., J. E. Allan, Z. Tabi, F. Lynch, and P. C. Doherty. "Phenotypic analysis of the inflammatory exudate in murine lymphocytic choriomeningitis." Journal of Experimental Medicine 165, no. 6 (1987): 1539–51. http://dx.doi.org/10.1084/jem.165.6.1539.

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The massive inflammation of the cerebrospinal fluid (CSF) which occurs in adult mice injected with lymphocytic choriomeningitis virus (LCMV) has been analyzed by flow microfluorometry (FMF). The great majority of the T cells detected by direct examination of freshly obtained CSF were found to be Lyt-2+, with an almost total absence of L3T4+ lymphocytes. The Lyt-2/L3T4 ratio of lymphocytes in blood was within normal limits. Predominance of the Lyt-2+ subset was confirmed by culturing the CSF cells after mitogenic stimulation. In addition, the T lymphocytes in CSF of cyclophosphamide-suppressed,

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3

Sullivan, Brian, John Teijaro, Juan Carlos de la Torre, and Michael Oldstone. "Early events dependent on the suppression of IPS signaling are necessary for persistent viral infection (P6300)." Journal of Immunology 190, no. 1_Supplement (2013): 182.2. http://dx.doi.org/10.4049/jimmunol.190.supp.182.2.

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Abstract Persistent infections are characterized by evasion of innate and adaptive immune responses controlled by the upregulation of immunosuppressive cytokines. However, little is known whether events during the first day of infection form the environment necessary for the establishment of a persistent infection. Using a novel in vivo competition approach by priming a persistent lymphocytic choriomenengitis virus (LCMV) infection with a non-propagating LCM virus, we found that suppression of the intracellular RNA sensing pathway and not the TLR7 pathway is necessary for establishing a persis

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4

Martínez-Sobrido, Luis, Sébastien Emonet, Panagiotis Giannakas, Beatrice Cubitt, Adolfo García-Sastre, and Juan C. de la Torre. "Identification of Amino Acid Residues Critical for the Anti-Interferon Activity of the Nucleoprotein of the Prototypic Arenavirus Lymphocytic Choriomeningitis Virus." Journal of Virology 83, no. 21 (2009): 11330–40. http://dx.doi.org/10.1128/jvi.00763-09.

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ABSTRACT Lymphocytic choriomeningitis virus (LCVM) nucleoprotein (NP) counteracts the host type I interferon (IFN) response by inhibiting activation of the IFN regulatory factor 3 (IRF3). In this study, we have mapped the regions and specific amino acid residues within NP involved in its anti-IFN activity. We identified a region spanning residues 382 to 386 as playing a critical role in the IFN-counteracting activity of NP. Alanine substitutions at several positions within this region resulted in NP mutants that lacked the IFN-counteracting activity but retained their functions in virus RNA sy

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5

Oxenius, A., M. F. Bachmann, D. Mathis, C. Benoist, R. M. Zinkernagel, and H. Hengartner. "Functional in vivo MHC class II loading by endogenously synthesized glycoprotein during viral infection." Journal of Immunology 158, no. 12 (1997): 5717–26. http://dx.doi.org/10.4049/jimmunol.158.12.5717.

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Abstract MHC class II presentation of antigenic peptides derived from soluble proteins is usually preceded by antigenic uptake via (nonreceptor-mediated) endocytosis by professional APCs, followed by processing in endosomal compartments. Although in vitro alternative pathways for MHC class II loading have been described for certain intracellularly synthesized proteins, the importance of these pathways has not been assessed in vivo. We have shown previously that endogenously produced membrane-associated glycoprotein (GP) of lymphocytic choriomeningitis virus (LCMV), a noncytopathic virus, can b

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6

Beura, Lalit K., Mark J. Pierson, Sathi P. Wijeyesinghe, et al. "Pet shop mice are infected with a novel lymphocytic choriomeningitis virus strain that sustains an abundance of stem-like PD-1+ CD8 T cells." Journal of Immunology 204, no. 1_Supplement (2020): 95.11. http://dx.doi.org/10.4049/jimmunol.204.supp.95.11.

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Abstract Lymphocytic choriomeningitis virus (LCMV) is a natural mouse pathogen. LCMV Armstrong, an acutely resolved strain, and LCMV Clone13, a mutant that establishes chronic infection, have provided contrasting infection models that continue to inform the fundamental biology of T cell differentiation, regulation of exhaustion, and response to checkpoint blockade. Here, we describe LCMV Minnesota (LCMV-MN), which was transmitted to laboratory mice upon cohousing with pet shop mice and shares 80–95% amino acid homology with previously characterized LCMV strains. Infection of laboratory mice wi

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7

Lee, Ki Jeong, Mar Perez, Daniel D. Pinschewer, and Juan Carlos de la Torre. "Identification of the Lymphocytic Choriomeningitis Virus (LCMV) Proteins Required To Rescue LCMV RNA Analogs into LCMV-Like Particles." Journal of Virology 76, no. 12 (2002): 6393–97. http://dx.doi.org/10.1128/jvi.76.12.6393-6397.2002.

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ABSTRACT We have used a reverse genetic approach to identify the viral proteins required for packaging and assembly of the prototypic arenavirus lymphocytic choriomeningitis virus (LCMV). Plasmids encoding individual LCMV proteins under the control of an RNA polymerase II promoter were cotransfected with a plasmid containing an LCMV minigenome (MG). Intracellular synthesis of the LCMV MG was driven by T7 RNA polymerase whose expression was also mediated by a Pol II promoter. The supernatant from transfected cells was passaged onto fresh cells that were subsequently infected with LCMV to provid

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8

Seiler, Peter, Ulrich Kalinke, Thomas Rülicke, et al. "Enhanced Virus Clearance by Early Inducible Lymphocytic Choriomeningitis Virus-Neutralizing Antibodies in Immunoglobulin-Transgenic Mice." Journal of Virology 72, no. 3 (1998): 2253–58. http://dx.doi.org/10.1128/jvi.72.3.2253-2258.1998.

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ABSTRACT Following infection of mice with lymphocytic choriomeningitis virus (LCMV), virus-neutralizing antibodies appear late, after 30 to 60 days. Such neutralizing antibodies play an important role in protection against reinfection. To analyze whether a neutralizing antibody response which developed earlier could contribute to LCMV clearance during the acute phase of infection, we generated transgenic mice expressing LCMV-neutralizing antibodies. Transgenic mice expressing the immunoglobulin μ heavy chain of the LCMV-neutralizing monoclonal antibody KL25 (H25 transgenic mice) mounted LCMV-n

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9

Riviere, Y., P. J. Southern, R. Ahmed, and M. B. Oldstone. "Biology of cloned cytotoxic T lymphocytes specific for lymphocytic choriomeningitis virus. V. Recognition is restricted to gene products encoded by the viral S RNA segment." Journal of Immunology 136, no. 1 (1986): 304–7. http://dx.doi.org/10.4049/jimmunol.136.1.304.

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Abstract Lymphocytic choriomeningitis virus (LCMV) Armstrong (ARM) strain-specific, H-2d-restricted CTL effectively lyse syngeneic targets infected by LCMV ARM, but show reduced killing of LCMV Pasteur (PAST) strain-infected H-2d cells. We have reassorted the two RNA segments, large (L) and small (S), of LCMV ARM and PAST to generate LCMV with genotypes of L ARM/S PAST and L PAST/S ARM. By using these reassortants and both LCMV primary CTL and CTL clones, we report that the induction, recognition, and lysis of LCMV-specific CTL depend on the S RNA segment and the genes it encodes.

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10

Cheng, Benson Yee Hin, Emilio Ortiz-Riaño, Aitor Nogales, Juan Carlos de la Torre, and Luis Martínez-Sobrido. "Development of Live-Attenuated Arenavirus Vaccines Based on Codon Deoptimization." Journal of Virology 89, no. 7 (2015): 3523–33. http://dx.doi.org/10.1128/jvi.03401-14.

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ABSTRACTArenaviruses have a significant impact on public health and pose a credible biodefense threat, but the development of safe and effective arenavirus vaccines has remained elusive, and currently, no Food and Drug Administration (FDA)-licensed arenavirus vaccines are available. Here, we explored the use of a codon deoptimization (CD)-based approach as a novel strategy to develop live-attenuated arenavirus vaccines. We recoded the nucleoprotein (NP) of the prototypic arenavirus lymphocytic choriomeningitis virus (LCMV) with the least frequently used codons in mammalian cells, which caused

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11

Selin, L. K., S. R. Nahill, and R. M. Welsh. "Cross-reactivities in memory cytotoxic T lymphocyte recognition of heterologous viruses." Journal of Experimental Medicine 179, no. 6 (1994): 1933–43. http://dx.doi.org/10.1084/jem.179.6.1933.

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Analyses of the relationships between different viruses and viral proteins have focused on homologies between linear amino acid sequences, but cross-reactivities at the level of T cell recognition may not be dependent on a conserved linear sequence of several amino acids. The CTL response to Pichinde virus (PV) and vaccinia virus (VV) in C57BL/6 mice previously immunized with lymphocytic choriomeningitis virus (LCMV) included the reactivation of memory cytotoxic T lymphocyte (CTL) specific to LCMV. Limiting dilution assays (LDA) demonstrated that at least part of this reactivation of memory ce

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12

Beyer, Winfried R., Manfred Westphal, Wolfram Ostertag, and Dorothee von Laer. "Oncoretrovirus and Lentivirus Vectors Pseudotyped with Lymphocytic Choriomeningitis Virus Glycoprotein: Generation, Concentration, and Broad Host Range." Journal of Virology 76, no. 3 (2002): 1488–95. http://dx.doi.org/10.1128/jvi.76.3.1488-1495.2002.

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ABSTRACT Lymphocytic choriomeningitis virus (LCMV) is a noncytopathic arenavirus shown to infect a broad range of different cell types. Here, we combined the beneficial characteristics of the LCMV glycoprotein (LCMV-GP) and those of retroviral vectors to generate a new, safe, and efficient gene transfer system. These LCMV-GP pseudotypes were systematically compared with vectors containing the widely used amphotropic murine leukemia virus envelope (A-MLVenv) or the vesicular stomatitis virus G protein (VSV-G). Production of LCMV-GP-pseudotyped oncoretroviral and lentiviral vectors by transient

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13

Ngo, Nhi, Beatrice Cubitt, Masaharu Iwasaki, and Juan C. de la Torre. "Identification and Mechanism of Action of a Novel Small-Molecule Inhibitor of Arenavirus Multiplication." Journal of Virology 89, no. 21 (2015): 10924–33. http://dx.doi.org/10.1128/jvi.01587-15.

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ABSTRACTSeveral arenaviruses cause hemorrhagic fever disease in humans and represent important public health problems in the regions where these viruses are endemic. In addition, evidence indicates that the worldwide-distributed prototypic arenavirus lymphocytic choriomeningitis virus (LCMV) is an important neglected human pathogen. There are no licensed arenavirus vaccines and current antiarenavirus therapy is limited to the use of ribavirin that is only partially effective. Therefore, there is an unmet need for novel antiarenaviral therapeutics. Here, we report the generation of a novel reco

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14

Oehen, S., H. Waldner, T. M. Kündig, H. Hengartner, and R. M. Zinkernagel. "Antivirally protective cytotoxic T cell memory to lymphocytic choriomeningitis virus is governed by persisting antigen." Journal of Experimental Medicine 176, no. 5 (1992): 1273–81. http://dx.doi.org/10.1084/jem.176.5.1273.

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The basis of antiviral protection by memory cytotoxic T lymphocytes (CTL) was investigated in vivo and in vitro using lymphocytic choriomeningitis virus (LCMV) and recombinant vaccinia viruses expressing the LCMV-glycoprotein (vacc-GP) or -nucleoprotein (vacc-NP). The widely replicating LCMV with a tendency to persist induced solid long-term protective memory. The poorly replicating vaccinia recombinant viruses revealed in the vaccinated host that the antiviral capacity of the secondary immune T cell response and the protection against lethal LCM was dependent upon the immunizing antigen and i

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15

Seiler, Peter, Beatrice M. Senn, Marie-Anne Bründler, Rolf M. Zinkernagel, Hans Hengartner, and Ulrich Kalinke. "In Vivo Selection of Neutralization-Resistant Virus Variants But No Evidence of B Cell Tolerance in Lymphocytic Choriomeningitis Virus Carrier Mice Expressing a Transgenic Virus-Neutralizing Antibody." Journal of Immunology 162, no. 8 (1999): 4536–41. http://dx.doi.org/10.4049/jimmunol.162.8.4536.

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Abstract B cell tolerance is maintained by active deletion and functional anergy of self-reactive B cells depending on the time, amount, and site of the self-antigen expression. To study B cell tolerance toward a transplacentally transmitted viral Ag, we crossed transgenic mice expressing the μ heavy and the κ light chain of the lymphocytic choriomeningitis virus (LCMV)-neutralizing mAb KL25 (HL25-transgenic mice) with persistently infected LCMV carrier mice. Although HL25-transgenic LCMV carrier mice exhibited the same high virus titers as nontransgenic LCMV carrier mice, no evidence for B ce

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16

Zhou, Shenghua, Anna M. Cerny, An Zacharia, Katherine A. Fitzgerald, Evelyn A. Kurt-Jones, and Robert W. Finberg. "Induction and Inhibition of Type I Interferon Responses by Distinct Components of Lymphocytic Choriomeningitis Virus." Journal of Virology 84, no. 18 (2010): 9452–62. http://dx.doi.org/10.1128/jvi.00155-10.

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ABSTRACT Type I interferons (IFNs) play a critical role in the host defense against viruses. Lymphocytic choriomeningitis virus (LCMV) infection induces robust type I IFN production in its natural host, the mouse. However, the mechanisms underlying the induction of type I IFNs in response to LCMV infection have not yet been clearly defined. In the present study, we demonstrate that IRF7 is required for both the early phase (day 1 postinfection) and the late phase (day 2 postinfection) of the type I IFN response to LCMV, and melanoma differentiation-associated gene 5 (MDA5)/mitochondrial antivi

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17

Zinkernagel, Martin S., Beatrice Bolinger, Philippe Krebs, Lucas Onder, Simone Miller, and Burkhard Ludewig. "Immunopathological Basis of Lymphocytic Choriomeningitis Virus-Induced Chorioretinitis and Keratitis." Journal of Virology 83, no. 1 (2008): 159–66. http://dx.doi.org/10.1128/jvi.01211-08.

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ABSTRACT The infection of humans with the rodent-borne lymphocytic choriomeningitis virus (LCMV) can lead to central nervous system disease in adults or severe neurological disease with hydrocephalus and chorioretinitis in children infected congenitally. Although LCMV-induced meningitis and encephalitis have been studied extensively, the immunopathological mechanisms underlying LCMV infection-associated ocular disease remain elusive. We report here that the intraocular administration of the neurotropic LCMV strain Armstrong (Arm) elicited pronounced chorioretinitis and keratitis and that infec

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18

Byrne, J. A., and M. B. Oldstone. "Biology of cloned cytotoxic T lymphocytes specific for lymphocytic choriomeningitis virus. VI. Migration and activity in vivo in acute and persistent infection." Journal of Immunology 136, no. 2 (1986): 698–704. http://dx.doi.org/10.4049/jimmunol.136.2.698.

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Abstract Cloned cytotoxic T lymphocytes (CTL) specific for lymphocytic choriomeningitis virus (LCMV) were adoptively transferred to syngeneic mice acutely or persistently (carrier mice) infected with LCMV. Although infectious virus was cleared from the spleens during acute LCMV infection begun 24 hr earlier and the spleens remained clear of virus for the 4 days of testing, there was no concomitant reduction of viral titers in lymph nodes. In contrast, adoptive transfer of cloned CTL into animals with persistent rather than acute LCMV infection resulted in deaths of syngeneic but not allogeneic

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19

Martínez-Sobrido, Luis, Elina I. Zúñiga, Debralee Rosario, Adolfo García-Sastre, and Juan Carlos de la Torre. "Inhibition of the Type I Interferon Response by the Nucleoprotein of the Prototypic Arenavirus Lymphocytic Choriomeningitis Virus." Journal of Virology 80, no. 18 (2006): 9192–99. http://dx.doi.org/10.1128/jvi.00555-06.

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ABSTRACT The prototypic arenavirus lymphocytic choriomeningitis virus (LCMV) is a formidable battle horse for the study of viral immunology, as well as viral persistence and associated diseases. Investigations with LCMV have uncovered basic mechanisms by which viruses avoid elimination by the host adaptive immune response. In this study we show that LCMV also disables the host innate defense by interfering with beta interferon (IFN-β) production in response to different stimuli, including infection with Sendai virus and liposome-mediated DNA transfection. Inhibition of IFN production in LCMV-i

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20

Zarozinski, Christopher C., and Raymond M. Welsh. "Minimal Bystander Activation of CD8 T Cells during the Virus-induced Polyclonal T Cell Response." Journal of Experimental Medicine 185, no. 9 (1997): 1629–40. http://dx.doi.org/10.1084/jem.185.9.1629.

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Acute infections with viruses such as lymphocytic choriomeningitis virus (LCMV) are associated with a massive polyclonal T cell response, but the specificities of only a small percentage of these activated T cells are known. To determine if bystander stimulation of T cells not specific to the virus plays a role in this T cell response, we examined two different systems, HY-specific T cell receptor (TCR)-transgenic mice, which have a restricted TCR repertoire, and LCMVcarrier mice, which are tolerant to LCMV. LCMV infection of HY-transgenic C57BL/6 mice induced antiviral CTLs that lysed target

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21

Zinkernagel, R. M., T. Leist, H. Hengartner, and A. Althage. "Susceptibility to lymphocytic choriomeningitis virus isolates correlates directly with early and high cytotoxic T cell activity, as well as with footpad swelling reaction, and all three are regulated by H-2D." Journal of Experimental Medicine 162, no. 6 (1985): 2125–41. http://dx.doi.org/10.1084/jem.162.6.2125.

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The lymphocytic choriomeningitis virus (LCMV) isolates Docile (D) and Aggressive (A) of Pfau et al. were studied in various strains of mice. Disease susceptibility, assessed as mortality and time to death to LCMV-D or -A varied greatly amongst mouse strains, and all four possible susceptibility patterns were observed: susceptibility to both (e.g. SWR/J), resistance to both (e.g. DBA/2), susceptibility to A but resistance to D (C57BL/6), or vice versa (CBA/J). Irrespective of the virus isolate or the mouse strain tested, susceptibility correlated with both early and high cytotoxic T cell activi

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22

Kägi, D., B. Odermatt, P. S. Ohashi, R. M. Zinkernagel, and H. Hengartner. "Development of insulitis without diabetes in transgenic mice lacking perforin-dependent cytotoxicity." Journal of Experimental Medicine 183, no. 5 (1996): 2143–52. http://dx.doi.org/10.1084/jem.183.5.2143.

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It is widely accepted that T cells play an important role in the destruction of beta cells leading to autoimmune type I diabetes, but the involved effector mechanisms have remained unclear. We addressed this issue by testing the role of perforin-dependent cytotoxicity in a disease model involving transgenic mice expressing glycoprotein of lymphocytic choriomeningitis virus (LCMV-GP) in the beta cells of the endocrine pancreas. In such mice, LCMV infection leads to a potent LCMV-GP-specific T cell response resulting in rapid development of diabetes. We report here that in perforin-deficient LCM

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23

Vilibic-Cavlek, Tatjana, Vladimir Savic, Thomas Ferenc, et al. "Lymphocytic Choriomeningitis—Emerging Trends of a Neglected Virus: A Narrative Review." Tropical Medicine and Infectious Disease 6, no. 2 (2021): 88. http://dx.doi.org/10.3390/tropicalmed6020088.

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Lymphocytic choriomeningitis virus (LCMV) is a neglected rodent-borne zoonotic virus distributed worldwide. Since serologic assays are limited to several laboratories, the disease has been underreported, often making it difficult to determine incidence and seroprevalence rates. Although human clinical cases are rarely recorded, LCMV remains an important cause of meningitis in humans. In addition, a fatal donor-derived LCMV infection in several clusters of solid organ transplant recipients further highlighted a pathogenic potential and clinical significance of this virus. In the transplant popu

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Leist, T. P., E. Rüedi, and R. M. Zinkernagel. "Virus-triggered immune suppression in mice caused by virus-specific cytotoxic T cells." Journal of Experimental Medicine 167, no. 5 (1988): 1749–54. http://dx.doi.org/10.1084/jem.167.5.1749.

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Normal mice infected with 10(5) infectious doses of lymphocytic choriomeningitis virus (LCMV, WE isolate) generated a reduced or no T cell-independent IgM and/or T cell-dependent IgG response to a subsequent vesicular stomatitis virus Indiana (VSV-IND) injection; this transient immune suppression lasted for weeks to months. Connatally infected LCMV-carrier mice or acutely infected T cell-deficient nude mice had normal anti-VSV IgM and IgG or IgM responses respectively. LCMV-infected nude mice transfused with helper cell-depleted LCMV-specific immune spleen cells were immunosuppressed. Normal m

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Darzi, Soodabeh, Tiong Sieh Kiong, Mohammad Tariqul Islam, Mahamod Ismail, Salehin Kibria, and Balasem Salem. "Null Steering of Adaptive Beamforming Using Linear Constraint Minimum Variance Assisted by Particle Swarm Optimization, Dynamic Mutated Artificial Immune System, and Gravitational Search Algorithm." Scientific World Journal 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/724639.

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Linear constraint minimum variance (LCMV) is one of the adaptive beamforming techniques that is commonly applied to cancel interfering signals and steer or produce a strong beam to the desired signal through its computed weight vectors. However, weights computed by LCMV usually are not able to form the radiation beam towards the target user precisely and not good enough to reduce the interference by placing null at the interference sources. It is difficult to improve and optimize the LCMV beamforming technique through conventional empirical approach. To provide a solution to this problem, arti

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Djavani, Mahmoud, Juan Rodas, Igor S. Lukashevich, et al. "Role of the Promyelocytic Leukemia Protein PML in the Interferon Sensitivity of Lymphocytic Choriomeningitis Virus." Journal of Virology 75, no. 13 (2001): 6204–8. http://dx.doi.org/10.1128/jvi.75.13.6204-6208.2001.

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ABSTRACT Lymphocytic choriomeningitis virus (LCMV) induces type I interferon (alpha and beta interferon [IFN-α and IFN-β]) upon infection and yet is sensitive to the addition of type II interferon (gamma interferon [IFN-γ]) to the culture media. This sensitivity is biologically important because it correlates inversely with the ability of certain LCMV strains to persist in mice (D. Moskophidis, M. Battegay, M. A. Bruendler, E. Laine, I. Gresser, and R. M. Zinkernagel, J. Virol. 68:1951-1955, 1994). The cellular oncoprotein PML is induced by both IFN-α/β and IFN-γ, and PML binds the LCMV Z prot

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Kotturi, Maya, Bjoern Peters, Fernando Buendia-Laysa, et al. "The L Antigen of the LCM Virus is a Target of Dominant CD8+ Responses (43.47)." Journal of Immunology 178, no. 1_Supplement (2007): S45. http://dx.doi.org/10.4049/jimmunol.178.supp.43.47.

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Abstract CD8+ T cell responses control lymphocytic choriomeningitis virus (LCMV) infection in H-2b mice. Although antigen-specific responses against LCMV infection are well studied, we found that up to one third of the CD8+CD44hi response to LCMV in H-2b mice was not accounted for by known epitopes. We screened peptides predicted to bind MHC Class I, and overlapping 15-mer peptides spanning the complete LCMV proteome for their capacity to induce interferon-γ (IFNγ) production from CD8+ T cells derived from LCMV-infected H-2b mice. We identified thirteen novel epitopes. These together with the

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Koutrouvelis, Andreas I., Richard Christian Hendriks, Richard Heusdens, and Jesper Jensen. "Relaxed Binaural LCMV Beamforming." IEEE/ACM Transactions on Audio, Speech, and Language Processing 25, no. 1 (2017): 137–52. http://dx.doi.org/10.1109/taslp.2016.2628642.

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Kim, Sung-Kwon, Markus Cornberg, Xiaoting Z. Wang, Hong D. Chen, Liisa K. Selin, and Raymond M. Welsh. "Private specificities of CD8 T cell responses control patterns of heterologous immunity." Journal of Experimental Medicine 201, no. 4 (2005): 523–33. http://dx.doi.org/10.1084/jem.20041337.

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CD8 T cell cross-reactivity between viruses can play roles in protective heterologous immunity and damaging immunopathology. This cross-reactivity is sometimes predictable, such as between lymphocytic choriomeningitis virus (LCMV) and Pichinde virus, where cross-reactive epitopes share six out of eight amino acids. Here, however, we demonstrate more subtle and less predictable cross-reactivity between LCMV and the unrelated vaccinia virus (VV). Epitope-specific T cell receptor usage differed between individual LCMV-infected C57BL/6 mice, even though the mice had similar epitope-specific T cell

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Kotturi, Maya F., Bjoern Peters, Fernando Buendia-Laysa, et al. "The CD8+ T-Cell Response to Lymphocytic Choriomeningitis Virus Involves the L Antigen: Uncovering New Tricks for an Old Virus." Journal of Virology 81, no. 10 (2007): 4928–40. http://dx.doi.org/10.1128/jvi.02632-06.

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ABSTRACT CD8+ T-cell responses control lymphocytic choriomeningitis virus (LCMV) infection in H-2b mice. Although antigen-specific responses against LCMV infection are well studied, we found that a significant fraction of the CD8+ CD44hi T-cell response to LCMV in H-2b mice was not accounted for by known epitopes. We screened peptides predicted to bind major histocompatibility complex class I and overlapping 15-mer peptides spanning the complete LCMV proteome for gamma interferon (IFN-γ) induction from CD8+ T cells derived from LCMV-infected H-2b mice. We identified 19 novel epitopes. Together

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Enninga, Elizabeth Ann L., and Regan N. Theiler. "Lymphocytic Choriomeningitis Virus Infection Demonstrates Higher Replicative Capacity and Decreased Antiviral Response in the First-Trimester Placenta." Journal of Immunology Research 2019 (February 7, 2019): 1–8. http://dx.doi.org/10.1155/2019/7375217.

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Lymphocytic choriomeningitis virus (LCMV) is a rodent disease that can be transmitted to humans. A majority of persons infected with LCMV have only minor symptoms; however, it can cross the placental barrier during pregnancy and cause congenital defects in the fetus. Some viral infections early in gestation are hypothesized to lead to worse outcomes compared to those acquired during late gestation; however, LCMV has not been studied in this context. In the present study, differences in immunomodulation between the first- and third-trimester placental explants infected with LCMV were measured.

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Lee, Ki Jeong, Isabel S. Novella, Michael N. Teng, Michael B. A. Oldstone, and Juan Carlos de la Torre. "NP and L Proteins of Lymphocytic Choriomeningitis Virus (LCMV) Are Sufficient for Efficient Transcription and Replication of LCMV Genomic RNA Analogs." Journal of Virology 74, no. 8 (2000): 3470–77. http://dx.doi.org/10.1128/jvi.74.8.3470-3477.2000.

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ABSTRACT The genome of lymphocytic choriomeningitis virus (LCMV) consists of two negative-sense single-stranded RNA segments, designated L and S. Both segments contain two viral genes in an ambisense coding strategy, with the genes being separated by an intergenic region (IGR). We have developed a reverse genetic system that allows the investigation ofcis-acting signals and trans-acting factors involved in transcription and replication of LCMV. To this end, we constructed an LCMV S minigenome consisting of a negative-sense copy of the chloramphenicol acetyltransferase (CAT) reporter gene flank

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33

Gallimore, Awen, Tilman Dumrese, Hans Hengartner, Rolf M. Zinkernagel, and Hans-Georg Rammensee. "Protective Immunity Does Not Correlate with the Hierarchy of Virus-specific Cytotoxic T Cell Responses to Naturally Processed Peptides." Journal of Experimental Medicine 187, no. 10 (1998): 1647—b—1657. http://dx.doi.org/10.1084/jem.187.10.1647-b.

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Infection of C57BL/6 mice with lymphocytic choriomeningitis virus (LCMV) stimulates major histocompatibility complex class I–restricted cytotoxic T cells (CTLs), which normally resolve the infection. Three peptide epitopes derived from LCMV have been shown to bind the mouse class I molecule H-2 Db and to stimulate CTL responses in LCMV-infected mice. This report describes the identity and abundance of each CTL epitope after their elution from LCMV-infected cells. Based on this information, peptide abundance was found to correlate with the magnitude of each CTL response generated after infectio

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Fung-Leung, W. P., T. M. Kündig, R. M. Zinkernagel, and T. W. Mak. "Immune response against lymphocytic choriomeningitis virus infection in mice without CD8 expression." Journal of Experimental Medicine 174, no. 6 (1991): 1425–29. http://dx.doi.org/10.1084/jem.174.6.1425.

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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 LCM

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Müller, Stefan, Lukas Hunziker, Susanne Enzler, et al. "Role of an Intact Splenic Microarchitecture in Early Lymphocytic Choriomeningitis Virus Production." Journal of Virology 76, no. 5 (2002): 2375–83. http://dx.doi.org/10.1128/jvi.76.5.2375-2383.2002.

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ABSTRACT An acute infection with lymphocytic choriomeningitis virus (LCMV) is efficiently controlled by the cytotoxic-T-cell (CTL) response of the host, and LCMV titers in the spleen and peripheral solid organs usually fall sharply after day 4 to 6 postinfection. Surprisingly, infection of immunodeficient recombination-activating gene 2-deficient (RAG2−/−) mice with 5 × 102 PFU of LCMV-WE causes about 80-fold-lower LCMV titers in the spleen on day 4 postinfection compared with C57BL/6 control mice. This could not be attributed to NK cell activity, since common gamma-chain-deficient RAG2−/− mic

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von Herrath, Matthias G., Bryan Coon, Hanna Lewicki, Honore Mazarguil, Jean Edouard Gairin, and Michael B. A. Oldstone. "In Vivo Treatment with a MHC Class I-Restricted Blocking Peptide Can Prevent Virus-Induced Autoimmune Diabetes." Journal of Immunology 161, no. 9 (1998): 5087–96. http://dx.doi.org/10.4049/jimmunol.161.9.5087.

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Abstract We tested the in vivo potential of a MHC class I-restricted blocking peptide to sufficiently lower an anti-viral CTL response for preventing virus-induced CTL-mediated autoimmune diabetes (insulin-dependent diabetes mellitus (IDDM)) in vivo without affecting systemic viral clearance. By designing and screening several peptides with high binding affinities to MHC class I H-2Db for best efficiency in blocking killing of target cells by lymphocytic choriomeningitis virus (LCMV) and other viral CTL, we identified the peptide for this study. In vitro, it selectively lowered CTL killing res

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McDermott, Daniel, Matthew Olson, and Steven Varga. "Virus-specific CD62L- memory CD8 T cells are preferentially retained in the draining lymph node following systemic viral infection (105.28)." Journal of Immunology 188, no. 1_Supplement (2012): 105.28. http://dx.doi.org/10.4049/jimmunol.188.supp.105.28.

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Abstract Lymphocytic choriomeningitis virus (LCMV) induces a systemic infection in mice with virus replication occurring in both peripheral tissues and secondary lymphoid organs. Because of the rapid dissemination of the virus, the secondary lymphoid organs responsible for the induction of the LCMV-specific CD8 T cell response are poorly defined. We show that the mediastinal lymph nodes (MedLN) serve as the primary draining lymph node following intraperitoneal LCMV infection and that the majority of the LCMV-specific CD8 T cells are primed within the MedLN. Following the resolution of the acut

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Abt, Michael C., Daniel Beiting, Dymtro Kobuley, et al. "The influence of commensal bacteria on anti-viral immunity (39.26)." Journal of Immunology 182, no. 1_Supplement (2009): 39.26. http://dx.doi.org/10.4049/jimmunol.182.supp.39.26.

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Abstract Alterations in the composition of intestinal commensal bacteria in humans are associated with enhanced susceptibility to multiple inflammatory diseases suggesting that signals derived from commensal bacteria may influence the development and/or function of the immune system. Supporting this, germ-free or gnotobiotic mice exhibit reduced numbers of lymphocytes in the intestinal intraepithelial compartment. However, whether alterations in the acquisition or composition of commensal bacteria influence immunity to infection remains poorly defined. To test this, mice housed under conventio

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Selin, Liisa, Priti Agarwal, Anke Kraft, and Myriam Wlodarczyk. "Crossreactive influenza A(IAV)-Specific CD4 memory cells enhance viral load during lymphocytic choriomeningitis (LCMV) infection (IRC5P.635)." Journal of Immunology 194, no. 1_Supplement (2015): 58.18. http://dx.doi.org/10.4049/jimmunol.194.supp.58.18.

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Abstract IAV is a common human respiratory pathogen with a strong association with heterotypic and heterologous immunity. IAV-immune mice challenged with LCMV develop detrimental effects with both increased virus titers and immunopathology. Crossreactive CD8 T cell responses between these two viruses mediate the enhanced lung pathology. Here, we questioned whether crossreactive CD4 memory cells in IAV-immune mice could play a role in increasing viral titers during the subsequent LCMV infection. Preferential depletion of memory CD4 but not CD8 cells in IAV-immune mice prevented the increase in

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Beyer, Winfried R., Hrvoje Miletic, Wolfram Ostertag, and Dorothee von Laer. "Recombinant Expression of Lymphocytic Choriomeningitis Virus Strain WE Glycoproteins: a Single Amino Acid Makes the Difference." Journal of Virology 75, no. 2 (2001): 1061–64. http://dx.doi.org/10.1128/jvi.75.2.1061-1064.2001.

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ABSTRACT Cytoplasmic vector systems are generally used for expression of lymphocytic choriomeningitis virus (LCMV) proteins. However, we achieved high levels of cell surface glycoproteins using a standard nuclear expression plasmid. Expression was independent of other LCMV proteins but was blocked by a missense mutation within the original LCMV(WE) glycoprotein cDNA.

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Vilibic-Cavlek, Tatjana, Tena Oreski, Misa Korva, et al. "Prevalence and Risk Factors for Lymphocytic Choriomeningitis Virus Infection in Continental Croatian Regions." Tropical Medicine and Infectious Disease 6, no. 2 (2021): 67. http://dx.doi.org/10.3390/tropicalmed6020067.

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Lymphocytic choriomeningitis virus (LCMV) is a neglected human pathogen associated with aseptic meningitis, severe systemic infections in immunocompromised persons, and congenital anomalies. Data on the prevalence of LCMV infections are scarce. We analyzed the seroprevalence of LCMV in continental Croatian regions. A total of 338 serum samples of professionally exposed (forestry workers, hunters, agriculture workers in contact with rodents) and non-exposed populations (general population, pregnant women) were tested for the presence of LCMV antibodies using indirect immunofluorescence assay. N

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Labudova, Martina, Jana Tomaskova, Ludovit Skultety, Jaromir Pastorek, and Silvia Pastorekova. "The Nucleoprotein of Lymphocytic Choriomeningitis Virus Facilitates Spread of Persistent Infection through Stabilization of the Keratin Network." Journal of Virology 83, no. 16 (2009): 7842–49. http://dx.doi.org/10.1128/jvi.00309-09.

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ABSTRACT Lymphocytic choriomeningitis virus (LCMV) is a prototypic arenavirus containing a bisegmented single-stranded RNA genome with an ambisense coding strategy. MX is a noncytolytic LCMV strain with an in vitro host range restricted to only few cell lines. MX LCMV spreads via cell-cell contacts and causes persistent infection with high production of viral nucleoprotein (NP). Using a proteomic approach, we identified keratin 1 (K1), an intermediate filament network component, as a binding partner of the viral NP. The functional significance of this interaction has been examined by chemical

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Zimmerman, C., K. Brduscha-Riem, C. Blaser, R. M. Zinkernagel, and H. Pircher. "Visualization, characterization, and turnover of CD8+ memory T cells in virus-infected hosts." Journal of Experimental Medicine 183, no. 4 (1996): 1367–75. http://dx.doi.org/10.1084/jem.183.4.1367.

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The cellular basis of T cell memory is a controversial issue and progress has been hampered by the inability to induce and to trace long-term memory T cells specific for a defined antigen in vivo. By using the murine model of lymphocytic choriomeningitis virus (LCMV) infection and an adoptive transfer system with CD8+ T cells from transgenic mice expressing an LCMV-specific T cell receptor, a population of authentic memory T cells specific for LCMV was generated and analyzed in vivo. The transgenic T cells that have expanded (1,000-fold) and then decreased (10-fold) in LCMV-infected C57BL/6 re

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Cornu, Tatjana I., and Juan Carlos de la Torre. "RING Finger Z Protein of Lymphocytic Choriomeningitis Virus (LCMV) Inhibits Transcription and RNA Replication of an LCMV S-Segment Minigenome." Journal of Virology 75, no. 19 (2001): 9415–26. http://dx.doi.org/10.1128/jvi.75.19.9415-9426.2001.

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ABSTRACT Arenaviruses have a bisegmented negative-strand RNA genome whose proteomic capability is limited to only four polypeptides, namely, nucleoprotein (NP), surface glycoprotein (GP) that is proteolytically processed into GP1+GP2, polymerase (L), and a small (11-kDa) RING finger protein (Z). The role of Z during the Lymphocytic choriomeningitis virus (LCMV) life cycle is poorly understood. We investigated the function of Z in virus transcription and replication by using a reverse genetic system for the prototypic arenavirus LCMV. This system involves an LCMV minigenome and the minimal vira

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Cheng, Benson Yee Hin, Emilio Ortiz-Riaño, Juan Carlos de la Torre, and Luis Martínez-Sobrido. "Arenavirus Genome Rearrangement for the Development of Live Attenuated Vaccines." Journal of Virology 89, no. 14 (2015): 7373–84. http://dx.doi.org/10.1128/jvi.00307-15.

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ABSTRACTSeveral members of theArenaviridaefamily cause hemorrhagic fever disease in humans and pose serious public health problems in their geographic regions of endemicity as well as a credible biodefense threat. To date, there have been no FDA-approved arenavirus vaccines, and current antiarenaviral therapy is limited to an off-label use of ribavirin that is only partially effective. Arenaviruses are enveloped viruses with a bisegmented negative-stranded RNA genome. Each genome segment uses an ambisense coding strategy to direct the synthesis of two viral polypeptides in opposite orientation

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von Herrath, Matthias G., та Michael B. A. Oldstone. "Interferon-γ Is Essential for Destruction of β Cells and Development of Insulin-dependent Diabetes Mellitus". Journal of Experimental Medicine 185, № 3 (1997): 531–40. http://dx.doi.org/10.1084/jem.185.3.531.

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Autoimmune mediated destruction of β cells of the islets of Langerhans leads to insulin-dependent diabetes mellitus (IDDM). Rat insulin promoter (RIP) lymphocytic choriomeningitis virus (LCMV) transgenic mice that express the nucleoprotein (NP) or glycoprotein (GP) of LCMV under control of the RIP in their β cells develop IDDM after infection with LCMV and serve as a model for virus-induced IDDM. Recently, Kagi et al. (Kagi, D., B. Odermatt, P. Ohashi, R.M. Zinkernagel, and H. Hengartner. 1996. J. Exp. Med. 183:2143–2149) showed, using RIP LCMV perforin-deficient mice, that IDDM does not occur

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Arthur, Connie Maridith, Andreas Weiland, Harold Clifford Sullivan, Rafi Ahmed, and Sean R. Stowell. "Clearance of Incompatible RBC Is Compromised during Persistent Viral Infection." Blood 126, no. 23 (2015): 1149. http://dx.doi.org/10.1182/blood.v126.23.1149.1149.

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Abstract Background: While immune-mediated destruction of red blood cells (RBCs) can occur following incompatible transfusion, the development of a hemolytic transfusion reaction is not the invariable outcome of an incompatible transfusion. Although a variety of factors may impact the likelihood of RBC clearance following incompatible RBC transfusion, chronic infection-induced immune complex formation may inhibit Fc gamma receptor-mediated removal of antibody coated RBCs. To examine this possibility, we tested the effect of persistent viral infection on the clearance of RBCs following incompat

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Peacock, Craig D., Meei Y. Lin, John R. Ortaldo, and Raymond M. Welsh. "The Virus-Specific and Allospecific Cytotoxic T-Lymphocyte Response to Lymphocytic Choriomeningitis Virus Is Modified in a Subpopulation of CD8+ T Cells Coexpressing the Inhibitory Major Histocompatibility Complex Class I Receptor Ly49G2." Journal of Virology 74, no. 15 (2000): 7032–38. http://dx.doi.org/10.1128/jvi.74.15.7032-7038.2000.

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ABSTRACT The role of negatively signaling NK cell receptors of the Ly49 family on the specificity of the acute CD8+ cytotoxic T-lymphocyte (CTL) response was investigated in lymphocytic choriomeningitis virus (LCMV)-infected C57BL/6 mice. Activated CD8+ T cells coexpressing Ly49G2 expanded during LCMV infection, and T-cell receptor analyses by flow cytometry and CDR3 spectratyping revealed a unique polyclonal T-cell population in the Ly49G2+ fraction. These cells lysed syngeneic targets infected with LCMV or coated with two of three LCMV immunodominant peptides examined. Transfection of these

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Belnoue, Elodie, Paola Fontannaz-Bozzotti, Stéphane Grillet, Paul-Henri Lambert, and Claire-Anne Siegrist. "Protracted Course of Lymphocytic Choriomeningitis Virus WE Infection in Early Life: Induction but Limited Expansion of CD8+ Effector T Cells and Absence of Memory CD8+ T Cells." Journal of Virology 81, no. 14 (2007): 7338–50. http://dx.doi.org/10.1128/jvi.00062-07.

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ABSTRACT Viral infections in human infants frequently follow a protracted course, with higher viral loads and delayed viral clearance compared to viral infections in older children. To identify the mechanisms responsible for this protracted pattern of infection, we developed an infant infection murine model using the well-characterized lymphocytic choriomeningitis virus (LCMV) WE strain in 2-week-old BALB/c mice. In contrast to adult mice, in which viral clearance occurred as expected 8 days after infection, LCMV titers persisted for several weeks after infection of infant mice. LCMV-specific

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Araki, Koichi, Shivaprakash Gangappa, Barry T. Rouse, Christian P. Larsen, and Rafi Ahmed. "Functionally impaired T cell-dependent immunopathology in FK506-treated mice with LCMV infection (46.10)." Journal of Immunology 178, no. 1_Supplement (2007): S62—S63. http://dx.doi.org/10.4049/jimmunol.178.supp.46.10.

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Abstract Lymphocytic choriomeningitis virus (LCMV) was recently shown to contaminate transplanted organs with lethal consequences in transplant recipients. The diagnosis of LCMV as a cause of death under circumstances of immunosuppression is somewhat paradoxical since LCMV is a non-cytolytic virus and is the classic example of immune-mediated disease. To understand how treatment with immunosuppressive drugs given to transplant recipients results in LCMV disease, we have initiated studies using the calcineurin inhibitor FK506. Surprisingly, FK506-treated LCMV-infected mice showed high lethality

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