Articles de revues : « JHMC »

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Moreno, Sindy C., Justin To, Hajoon Chun et Ivan M. Ngai. « Vertical Transmission of COVID-19 to the Neonate ». Infectious Diseases in Obstetrics and Gynecology 2020 (12 novembre 2020) : 1–5. http://dx.doi.org/10.1155/2020/8460672.

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Objective. To estimate the incidence rate of vertical transmission of coronavirus disease 2019 (COVID-19) to the neonate during the third trimester. Study Design. We conducted a retrospective observational study of pregnant women diagnosed with COVID-19 during the third trimester, who delivered at Flushing Hospital Medical Centre (FHMC) or Jamaica Hospital Medical Centre (JHMC) between March 20, 2020, and April 30, 2020. The study participants were symptomatic pregnant women diagnosed with COVID-19 via positive SARS-CoV-2 RNA, real-time reverse transcription-polymerase chain reaction (SARS-CoV-2 rRT-PCR) test. Evidence of vertical transmission was assessed in the neonate via a SARS-CoV-2 rRT-PCR test, with nasopharyngeal swab samples collected on the neonates after 24 hours of birth. The exclusion criteria for this study were maternal or neonate records without SARS-CoV-2 rRT-PCR test results, neonates not delivered at FHMC or JHMC, and foetuses with suspected foetal anomalies or incomplete medical records. Results. We identified 19 symptomatic pregnant women diagnosed with COVID-19, including two women with twin pregnancies. Seven patients (36.8%) were delivered via cesarean. 12 patients (63.1%) presented in spontaneous labour, and 8 (38.1%) had preterm delivery. No maternal intensive care unit admission, maternal sepsis, or maternal mortality was observed. Twenty-one neonates were evaluated for COVID-19 after birth. SARS-CoV-2 rRT-PCR test results were negative in 100% of the neonates. Thirteen neonates (61.9%) were admitted to the neonatal intensive care unit. Prematurity was the most common cause of NICU admission 6 (46.1%), with a length of stay of 5.5 ± 6.4 days. No invasive mechanical ventilation, neonatal sepsis, or neonatal mortality was observed. Conclusion. In our cohort, symptomatic COVID-19 during the third trimester of pregnancy was not associated with vertical transmission to the neonate.

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Kyuwa, Shigeru, Yoh-ichi Tagawa, Shinwa Shibata, Kunio Doi, Kenji Machii et Yoichiroh Iwakura. « Murine Coronavirus-Induced Subacute Fatal Peritonitis in C57BL/6 Mice Deficient in Gamma Interferon ». Journal of Virology 72, n^o 11 (1 novembre 1998) : 9286–90. http://dx.doi.org/10.1128/jvi.72.11.9286-9290.1998.

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ABSTRACT Gamma interferon-deficient (IFN-γ−/−) mice with a C57BL/6 background were infected intraperitoneally with mouse hepatitis virus strain JHM (JHMV). In contrast to IFN-γ-+/− and IFN-γ+/+ mice, JHMV persisted in IFN-γ−/− mice and induced death during the subacute phase of the infection. Unexpectedly, infected IFN-γ−/− mice showed severe peritonitis accompanying the accumulation of a viscous fluid in the abdominal and thoracic cavities in the subacute phase. Destructive changes of hepatocytes were not observed. Administration of recombinant IFN-γ protracted the survival time of IFN-γ−/− mice after JHMV infection. These results demonstrate that IFN-γ plays a critical role in viral clearance in JHMV infection. They also show that a resultant persistent JHMV infection induces another form of disease in IFN-γ−/− mice, which bears a resemblance to feline infectious peritonitis in cats.

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Walsh, Kevin B., Lewis L. Lanier et Thomas E. Lane. « NKG2D Receptor Signaling Enhances Cytolytic Activity by Virus-Specific CD8+ T Cells : Evidence for a Protective Role in Virus-Induced Encephalitis ». Journal of Virology 82, n^o 6 (26 décembre 2007) : 3031–44. http://dx.doi.org/10.1128/jvi.02033-07.

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ABSTRACT Inoculation with the neurotropic JHM strain of mouse hepatitis virus (JHMV) into the central nervous system (CNS) of mice results in an acute encephalitis associated with an immune-mediated demyelinating disease. During acute disease, infiltrating CD8+ T cells secrete gamma interferon (IFN-γ) that controls replication in oligodendrocytes, while infected astrocytes and microglia are susceptible to perforin-mediated lysis. The present study was undertaken to reveal the functional contributions of the activating NKG2D receptor in host defense and disease following JHMV infection. NKG2D ligands RAE-1, MULT1, and H60 were expressed within the CNS following JHMV infection. The immunophenotyping of infiltrating cells revealed that NKG2D was expressed on ∼90% of infiltrating CD8+ T cells during acute and chronic disease. Blocking NKG2D following JHMV infection resulted in increased mortality that correlated with increased viral titers within the CNS. Anti-NKG2D treatment did not alter T-cell infiltration into the CNS or the generation of virus-specific CD8+ T cells, and the expression of IFN-γ was not affected. However, cytotoxic T-lymphocyte (CTL) activity was dependent on NKG2D expression, because anti-NKG2D treatment resulted in a dramatic reduction in lytic activity by virus-specific CD8+ T cells. Blocking NKG2D during chronic disease did not affect either T-cell or macrophage infiltration or the severity of demyelination, indicating that NKG2D does not contribute to virus-induced demyelination. These findings demonstrate a functional role for NKG2D in host defense during acute viral encephalitis by selectively enhancing CTL activity by infiltrating virus-specific CD8+ T cells.

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Dickey, Laura L., Colleen Worne, Jessica Glover, Joshua Daugherty, Thomas Lane et Ryan M. O’Connell. « MicroRNA-155 enhances T-cell trafficking and antiviral effector function in a model of coronavirus-induced neurologic disease ». Journal of Immunology 196, n^o 1_Supplement (1 mai 2016) : 55.12. http://dx.doi.org/10.4049/jimmunol.196.supp.55.12.

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Abstract Micro-RNAs (miRNAs) are non-coding RNAs that modulate cellular gene expression at the post-transcriptional level. These molecules are becoming increasingly recognized as important in helping tailor T-cell responses following viral infection. We therefore sought to examine the functional role of miR-155 in a model of viral-induced demyelination. Intracranial injection with the neurotropic JHM strain of mouse hepatitis virus (JHMV) results in an acute encephalomyelitis followed by an immune-mediated demyelinating disease. Compared to wild-type mice, JHMV-infected mice deficient in miR-155 (miR-155−/−) developed delayed but exacerbated disease concomitant with increased morbidity/mortality, weight loss, and spinal cord demyelination. In addition, miR-155−/− mice had decreased total and virus-specific CD4+ and CD8+ T-cell accumulation within the CNS during the acute phase of disease. Furthermore, IFN-γ and TNF-α production, as well as and cytolytic function, were impaired in CD8+ cells from miR-155−/− mice. These results identify miR-155 as a key mediator of disease development and recovery in a model of virus-induced neurological disease.

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Grist, Jonathan Jeffrey, Brett S. Marro et Thomas Lane. « Inducible expression of CXCL1 within the CNS amplifies demyelination in pre-clinical models of multiple sclerosis ». Journal of Immunology 196, n^o 1_Supplement (1 mai 2016) : 139.13. http://dx.doi.org/10.4049/jimmunol.196.supp.139.13.

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Abstract The functional role of the ELR+ chemokine CXCL1 in host defense and disease in two pre-clinical mouse models of the human demyelinating disease multiple sclerosis (MS) was assessed. Mice in which expression of CXCL1 is under the control of a tetracycline-inducible promoter active within GFAP-positive cells were generated and infected intracranially with the neurotropic JHM strain of mouse hepatitis virus (JHMV) or immunized with myelin oligodendrocyte glycoprotein (MOG)35-55 to induce experimental autoimmune encephalomyelitis (EAE). In both JHMV-induced neurologic disease and EAE, overexpression of CXCL1 by astrocytes resulted in increased clinical disease severity. Immunophenotyping cells infiltrating into the central nervous system (CNS) revealed a selective increase in Ly6G+CD11b+ neutrophils (but not Ly6G−Ly6C+CD11b+ monocytes) present within the CNS. In JHMV infected mice and MOG35-55-immunized mice, the T cell response to antigen with regard to proliferation and cytokine production was not altered, nor was trafficking into the CNS affected. In both models, increased CXCL1 expression within the CNS resulted in increased morbidity that correlated with selectively elevated neutrophil infiltration, diminished numbers of mature oligodendrocytes, and an increase in the severity of demyelination. Neutrophil ablation in CXCL1-transgenic mice reduced the severity of demyelination in mice arguing a role for these cells in white matter damage. Collectively, these findings illustrate that sustained CXCL1 expression amplifies the severity of white matter damage and neutrophils can contribute to this process in two different mouse models of MS.

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Parra, Beatriz, David R. Hinton, Norman W. Marten, Cornelia C. Bergmann, Mark T. Lin, Camillia S. Yang et Stephen A. Stohlman. « IFN-γ Is Required for Viral Clearance from Central Nervous System Oligodendroglia ». Journal of Immunology 162, n^o 3 (1 février 1999) : 1641–47. http://dx.doi.org/10.4049/jimmunol.162.3.1641.

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Abstract Infection of the central nervous system (CNS) by the JHM strain of mouse hepatitis virus (JHMV) is a rodent model of the human demyelinating disease multiple sclerosis. The inability of effective host immune responses to eliminate virus from the CNS results in a chronic infection associated with ongoing recurrent demyelination. JHMV infects a variety of CNS cell types during the acute phase of infection including ependymal cells, astrocytes, microglia, oligodendroglia, and rarely in neurons. Replication within the majority of CNS cell types is controlled by perforin-dependent virus-specific CTL. However, inhibition of viral replication in oligodendroglia occurs via a perforin-independent mechanism(s). The potential role for IFN-γ as mediator controlling JHMV replication in oligodendroglia was examined in mice deficient in IFN-γ secretion (IFN-γ0/0 mice). IFN-γ0/0 mice exhibited increased clinical symptoms and mortality associated with persistent virus, demonstrating an inability to control replication. Neither antiviral Ab nor CTL responses were diminished in the absence of IFN-γ, although increased IgG1 was detected in IFN-γ0/0 mice. Increased virus Ag in the absence of IFN-γ localized almost exclusively to oligodendroglia and was associated with increased CD8+ T cells localized within white matter. These data suggest that although perforin-dependent CTL control virus replication within astrocytes and microglia, which constitute the majority of infected CNS cells, IFN-γ is critical for control of viral replication in oligodendroglia. Therefore, different mechanisms are used by the host defenses to control virus replication within the CNS, dependent upon the phenotype of the targets of virus replication.

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Lin, Mark T., David R. Hinton, Norman W. Marten, Cornelia C. Bergmann et Stephen A. Stohlman. « Antibody Prevents Virus Reactivation Within the Central Nervous System ». Journal of Immunology 162, n^o 12 (15 juin 1999) : 7358–68. http://dx.doi.org/10.4049/jimmunol.162.12.7358.

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Abstract The neurotropic JHM strain of mouse hepatitis virus (JHMV) produces an acute CNS infection characterized by encephalomyelitis and demyelination. The immune response cannot completely eliminate virus, resulting in persistence associated with chronic ongoing CNS demyelination. The contribution of humoral immunity to viral clearance and persistent infection was investigated in mice homozygous for disruption of the Ig μ gene (IgM−/−). Acute disease developed with equal kinetics and severity in IgM−/− and syngeneic C57BL/6 (wt) mice. However, clinical disease progressed in IgM−/− mice, while wt mice recovered. Viral clearance during acute infection was similar in both groups, supporting a primary role of cell-mediated immunity in viral clearance. In contrast to wt mice, in which infectious virus was reduced to below detection following acute infection, increasing infectious virus was recovered from the CNS of the IgM−/− mice following initial clearance. No evidence was obtained for selection of variant viruses nor was there an apparent loss of cell-mediated immunity in the absence of Ab. Passive transfer of anti-JHMV Ab following initial clearance prevented reactivation of infectious virus within the CNS of IgM−/− mice. These data demonstrate the clearance of infectious virus during acute disease by cell-mediated immunity. However, immunologic control is not maintained in the absence of anti-viral Ab, resulting in recrudescence of infectious virus. These data suggest that humoral immunity plays no role in controlling virus during acute infection, but plays an important role in establishing and maintaining CNS viral persistence.

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Stohlman, Stephen A., David R. Hinton, Beatriz Parra, Roscoe Atkinson et Cornelia C. Bergmann. « CD4 T Cells Contribute to Virus Control and Pathology following Central Nervous System Infection with Neurotropic Mouse Hepatitis Virus ». Journal of Virology 82, n^o 5 (19 décembre 2007) : 2130–39. http://dx.doi.org/10.1128/jvi.01762-07.

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ABSTRACT Replication of the neurotropic mouse hepatitis virus strain JHM (JHMV) is controlled primarily by CD8+ T-cell effectors utilizing gamma interferon (IFN-γ) and perforin-mediated cytotoxicity. CD4+ T cells provide an auxiliary function(s) for CD8+ T-cell survival; however, their direct contribution to control of virus replication and pathology is unclear. To examine a direct role of CD4+ T cells in viral clearance and pathology, pathogenesis was compared in mice deficient in both perforin and IFN-γ that were selectively reconstituted for these functions via transfer of virus-specific memory CD4+ T cells. CD4+ T cells from immunized wild-type, perforin-deficient, and IFN-γ-deficient donors all initially reduced virus replication. However, prolonged viral control by IFN-γ-competent donors suggested that IFN-γ is important for sustained virus control. Local release of IFN-γ was evident by up-regulation of class II molecules on microglia in recipients of IFN-γ producing CD4+ T cells. CD4+ T-cell-mediated antiviral activity correlated with diminished clinical symptoms, pathology, and demyelination. Both wild-type donor CD90.1 and recipient CD90.2 CD4+ T cells trafficked into the central nervous system (CNS) parenchyma and localized to infected white matter, correlating with decreased numbers of virus-infected oligodendrocytes in the CNS. These data support a direct, if limited, antiviral role for CD4+ T cells early during acute JHMV encephalomyelitis. Although the antiviral effector mechanism is initially independent of IFN-γ secretion, sustained control of CNS virus replication by CD4+ T cells requires IFN-γ.

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Matsuyama, Shutoku, et Fumihiro Taguchi. « Receptor-Induced Conformational Changes of Murine Coronavirus Spike Protein ». Journal of Virology 76, n^o 23 (1 décembre 2002) : 11819–26. http://dx.doi.org/10.1128/jvi.76.23.11819-11826.2002.

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ABSTRACT Although murine coronavirus mouse hepatitis virus (MHV) enters cells by virus-cell membrane fusion triggered by its spike (S) protein, it is not well known how the S protein participates in fusion events. We reported that the soluble form of MHV receptor (soMHVR) transformed a nonfusogenic S protein into a fusogenic one (F. Taguchi and S. Matsuyama, J. Virol. 76:950-958, 2002). In the present study, we demonstrate that soMHVR induces the conformational changes of the S protein, as shown by the proteinase digestion test. A cl-2 mutant, srr7, of the MHV JHM virus (JHMV) was digested with proteinase K after treatment with soMHVR, and the resultant S protein was analyzed by Western blotting using monoclonal antibody (MAb) 10G, specific for the membrane-anchored S2 subunit. A 58-kDa fragment, encompassing the two heptad repeats in S2, was detected when srr7 was digested after soMHVR treatment, while no band was seen when the virus was untreated. The appearance of the proteinase-resistant fragment was dependent on the temperature and time of srr7 incubation with soMHVR and also on the concentration of soMHVR. Coimmunoprecipitation indicated that the direct binding of soMHVR to srr7 S protein induced these conformational changes; this was also suggested by the inhibition of the changes following pretreatment of soMHVR with anti-MHVR MAb CC1. soMHVR induced conformational changes of the S proteins of wild-type (wt) JHMV cl-2, as well as revertants from srr7, srr7A and srr7B; however, a major proportion of these S proteins were resistant to proteinase K even without soMHVR treatment. The implications of this proteinase-resistant fraction are discussed. This is the first report on receptor-induced conformational changes of the membrane-anchored fragment of the coronavirus S protein.

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Watanabe, Rie, Shutoku Matsuyama et Fumihiro Taguchi. « Receptor-Independent Infection of Murine Coronavirus : Analysis by Spinoculation ». Journal of Virology 80, n^o 10 (15 mai 2006) : 4901–8. http://dx.doi.org/10.1128/jvi.80.10.4901-4908.2006.

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ABSTRACT A highly neurovirulent murine coronavirus JHMV (wild-type [wt] JHMV) is known to spread from cells infected via the murine coronavirus mouse hepatitis virus receptor (MHVR) to cells without MHVR (MHVR-independent infection), whereas a mutant virus isolated from wt JHMV, srr7, spread only in an MHVR-dependent fashion. These observations were obtained by the overlay of JHMV-infected cells onto receptor-negative cells that are otherwise resistant to wt JHMV infection. MHVR-independent infection is hypothetically thought to be attributed to a naturally occurring fusion activation of the wt JHMV S protein, which did not occur in the case of srr7. Attachment of S protein on cells without MHVR during the S-protein activation process seems to be a key condition. Thus, in the present study, we tried to see whether wt JHMV virions that are attached on MHVR-negative cells are able to infect those cells. In order to make virions attach to the cell surface without MHVR, we have used spinoculation, namely, the centrifugation of cells together with inoculated virus at 3,000 rpm for 2 h. This procedure forces viruses to attach to the cell surface, as revealed by quantitative estimation of attached virions by real-time PCR and also facilitated wt JHMV infection to MHVR-negative cells, but failed to do so for srr7. Virions of both wt and srr7 attached on MHVR-negative cells by spinoculation were facilitated for infection in the presence of a soluble form of MHVR that induces conformational changes of both wt and srr7. It was further revealed that wt JHMV S1, but not srr7, was released from the cell surface when S protein was expressed on cells. These observations support the hypothesis that attachment of the virion to MHVR-negative cells is a critical step and that a unique feature of wt JHMV S1 to be released from S2 in a naturally occurring event is involved in an MHVR-independent infection.

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Bergmann, Cornelia C., John D. Altman, David Hinton et Stephen A. Stohlman. « Inverted Immunodominance and Impaired Cytolytic Function of CD8+ T Cells During Viral Persistence in the Central Nervous System ». Journal of Immunology 163, n^o 6 (15 septembre 1999) : 3379–87. http://dx.doi.org/10.4049/jimmunol.163.6.3379.

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Abstract Mice infected with the neurotropic JHM strain of mouse hepatitis virus (JHMV) clear infectious virus; nevertheless, virus persists in the CNS as noninfectious RNA, resulting in ongoing primary demyelination. Phenotypic and functional analysis of CNS infiltrating cells during acute infection revealed a potent regional CD8+ T cell response comprising up to 50% virus-specific T cells. The high prevalence of virus-specific T cells correlated with ex vivo cytolytic activity and efficient reduction in viral titers. Progressive viral clearance coincided with the loss of cytolytic activity, but retention of IFN-γ secretion and increased expression of the early activation marker CD69, indicating differential regulation of effector function. Although the total number of infiltrating T cells declined following clearance of infectious virus, CD8+ T cells, both specific for the dominant viral epitopes and of unknown specificity, were retained within the CNS, suggesting an ongoing T cell response during persistent CNS infection involving a virus-independent component. Reversed immunodominance within the virus-specific CD8+ T cell population further indicated epitope-specific regulation, supporting ongoing T cell activation. Even in the absence of infectious virus, the CNS thus provides an environment that maintains both unspecific and Ag-specific CD8+ T cells with restricted effector function. Chronic T cell stimulation may thus play a role in preventing viral recrudescence, while increasing the risk of pathological conditions, such as demyelination.

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Nakagaki, Keiko, Kazuhide Nakagaki et Fumihiro Taguchi. « Receptor-Independent Spread of a Highly Neurotropic Murine Coronavirus JHMV Strain from Initially Infected Microglial Cells in Mixed Neural Cultures ». Journal of Virology 79, n^o 10 (15 mai 2005) : 6102–10. http://dx.doi.org/10.1128/jvi.79.10.6102-6110.2005.

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ABSTRACT Although neurovirulent mouse hepatitis virus (MHV) strain JHMV multiplies in a variety of brain cells, expression of its receptor carcinoembryonic antigen cell adhesion molecule 1 (CEACAM 1) (MHVR) is restricted only in microglia. The present study was undertaken to clarify the mechanism of an extensive JHMV infection in the brain by using neural cells isolated from mouse brain. In contrast to wild-type (wt) JHMV, a soluble-receptor-resistant mutant (srr7) infects and spreads solely in an MHVR-dependent fashion (F. Taguchi and S. Matsuyama, J. Virol. 76:950-958, 2002). In mixed neural cell cultures, srr7 infected a limited number of cells and infection did not spread, although wt JHMV induced syncytia in most of the cells. srr7-infected cells were positive for GS-lectin, a microglia marker. Fluorescence-activated cell sorter analysis showed that about 80% of the brain cells stained with anti-MHVR antibody (CC1) were also positive for GS-lectin. Pretreatment of those cells with CC1 prevented virus attachment to the cell surface and also blocked virus infection. These results show that microglia express functional MHVR that mediates JHMV infection. As expected, in microglial cell-enriched cultures, both srr7and wt JHMV produced syncytia in a majority of cells. Treatment with CC1 of mixed neural cell cultures and microglia cultures previously infected with wt virus failed to block the spread of infection, indicating that wt infection spreads in an MHVR-independent fashion. Thus, the present study indicates that microglial cells are the major population of the initial target for MHV infection and that the wt spreads from initially infected microglia to a variety of cells in an MHVR-independent fashion.

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Taguchi, Fumihiro, et Shutoku Matsuyama. « Soluble Receptor Potentiates Receptor-Independent Infection by Murine Coronavirus ». Journal of Virology 76, n^o 3 (1 février 2002) : 950–58. http://dx.doi.org/10.1128/jvi.76.3.950-958.2002.

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ABSTRACT Mouse hepatitis virus (MHV) infection spreads from MHV-infected DBT cells, which express the MHV receptor CEACAM1 (MHVR), to BHK cells, which are devoid of the receptor, by intercellular membrane fusion (MHVR-independent fusion). This mode of infection is a property of wild-type (wt) JHMV cl-2 virus but is not seen in cultures infected with the mutant virus JHMV srr7. In this study, we show that soluble MHVR (soMHVR) potentiates MHVR-independent fusion in JHMV srr7-infected cultures. Thus, in the presence of soMHVR, JHMV srr7-infected DBT cells overlaid onto BHK cells induce BHK cell syncytia and the spread of JHMV srr7 infection. This does not occur in the absence of soMHVR. soMHVR also enhanced wt virus MHVR-independent fusion. These effects were dependent on the concentration of soMHVR in the culture and were specifically blocked by the anti-MHVR monoclonal antibody CC1. Together with these observations, direct binding of soMHVR to the virus spike (S) glycoprotein as revealed by coimmunoprecipitation demonstrated that the effect is mediated by the binding of soMHVR to the S protein. Furthermore, fusion of BHK cells expressing the JHMV srr7 S protein was also induced by soMHVR. These results indicated that the binding of soMHVR to the S protein expressed on the DBT cell surface potentiates the fusion of MHV-infected DBT cells with nonpermissive BHK cells. We conclude that the binding of soMHVR to the S protein converts the S protein to a fusion-active form competent to mediate cell-cell fusion, in a fashion similar to the fusion of virus and cell membranes.

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Ayazi, Maryam, Kayla T. Johnson, Marcellus M. Merritt, Michelle R. Di Paolo, Christopher L. Edwards, Harold G. Koenig, Gary G. Bennett, Keith A. Whitfield et Camela S. Barker. « Religiosity, Education, John Henryism Active Coping, and Cardiovascular Responses to Anger Recall for African American Men ». Journal of Black Psychology 44, n^o 4 (mai 2018) : 295–321. http://dx.doi.org/10.1177/0095798418765859.

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The present study examined if high levels of religious attendance (ORG), private religious activity (NOR), or intrinsic religiosity (SUB) buffer cardiovascular responses to active speech and anger recall lab stressors alone and by John Henryism Active Coping (JHAC) and educational attainment. A sample of 74 healthy African American males, aged 23 to 47 years, completed psychosocial surveys and a lab reactivity protocol involving active speech and anger recall with a 5-minute baseline and ensuing recovery periods. Measures of religiosity, JHAC, and education were related to continuous measures of systolic and diastolic blood pressure (BP), for each task and rest period with repeated measures ANOVA tests. The period by education by JHAC interaction effect was significant for diastolic BP responses at low but not higher NOR. At low education and low NOR, diastolic BP levels increased significantly during anger recall and ensuing recovery for high but not low JHAC persons. Thus, being deprived of education and private religious activity may put these African American men in a vulnerable situation where higher effort coping may exacerbate their cardiovascular reactivity and recovery to anger induction.

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Isenberg, Sarina R., Chunhua Lu, John McQuade, Kelvin K. W. Chan, Natasha Gill, Michael Cardamone, Deirdre Torto, Terry Langbaum, Rab Razzak et Thomas J. Smith. « Impact of a New Palliative Care Program on Health System Finances : An Analysis of the Palliative Care Program Inpatient Unit and Consultations at Johns Hopkins Medical Institutions ». Journal of Oncology Practice 13, n^o 5 (mai 2017) : e421-e430. http://dx.doi.org/10.1200/jop.2016.014860.

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Purpose: Palliative care inpatient units (PCUs) can improve symptoms, family perception of care, and lower per-diem costs compared with usual care. In March 2013, Johns Hopkins Medical Institutions (JHMI) added a PCU to the palliative care (PC) program. We studied the financial impact of the PC program on JHMI from March 2013 to March 2014. Methods: This study considered three components of the PC program: PCU, PC consultations, and professional fees. Using 13 months of admissions data, the team calculated the per-day variable cost pre-PCU (ie, in another hospital unit) and after transfer to the PCU. These fees were multiplied by the number of patients transferred to the PCU and by the average length of stay in the PCU. Consultation savings were estimated using established methods. Professional fees assumed a collection rate of 50%. Results: The total positive financial impact of the PC program was $3,488,863.17. There were 153 transfers to the PCU, 60% with cancer, and an average length of stay of 5.11 days. The daily loss pretransfer to the PCU of $1,797.67 was reduced to $1,345.34 in the PCU (−25%). The PCU saved JHMI $353,645.17 in variable costs, or $452.33 per transfer. Cost savings for PC consultations in the hospital, 60% with cancer, were estimated at $2,765,218. $370,000 was collected in professional fees savings. Conclusion: The PCU and PC program had a favorable impact on JHMI while providing expert patient-centered care. As JHMI moves to an accountable care organization model, value-based patient-centered care and increased intensive care unit availability are desirable.

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Zhou, Haixia, et Stanley Perlman. « Preferential Infection of Mature Dendritic Cells by Mouse Hepatitis Virus Strain JHM ». Journal of Virology 80, n^o 5 (1 mars 2006) : 2506–14. http://dx.doi.org/10.1128/jvi.80.5.2506-2514.2006.

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ABSTRACT Mouse hepatitis virus strain JHM (MHV-JHM) causes acute encephalitis and acute and chronic demyelinating diseases in mice. Dendritic cells (DCs) are key cells in the initiation of innate and adaptive immune responses, and infection of these cells could potentially contribute to a dysregulated immune response; consistent with this, recent results suggest that DCs are readily infected by another strain of mouse hepatitis virus, the A59 strain (MHV-A59). Herein, we show that the JHM strain also productively infected DCs. Moreover, mature DCs were at least 10 times more susceptible than immature DCs to infection with MHV-JHM. DC function was impaired after MHV-JHM infection, resulting in decreased stimulation of CD8 T cells in vitro. Preferential infection of mature DCs was not due to differential expression of the MHV-JHM receptor CEACAM-1a on mature or immature cells or to differences in apoptosis. Although we could not detect infected DCs in vivo, both CD8+ and CD11b+ splenic DCs were susceptible to infection with MHV-JHM directly ex vivo. This preferential infection of mature DCs may inhibit the development of an efficient immune response to the virus.

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Navas, Sonia, et Susan R. Weiss. « Murine Coronavirus-Induced Hepatitis : JHM Genetic Background Eliminates A59 Spike-Determined Hepatotropism ». Journal of Virology 77, n^o 8 (15 avril 2003) : 4972–78. http://dx.doi.org/10.1128/jvi.77.8.4972-4978.2003.

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ABSTRACT Recombinant murine coronaviruses, differing only in the spike gene and containing the strain A59 (moderately hepatotropic) and JHM (neurotropic) spike genes in the background of the JHM genome, were compared for the ability to replicate in the liver and induce hepatitis in weanling C57BL/6 mice. Interestingly, expression of the A59 spike glycoprotein within the background of the neurotropic JHM strain does not reproduce the A59 hepatotropic phenotype. Thus, the JHM genetic background plays a dominant role over the spike in the determination of hepatotropism.

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Fehr, Anthony R., Jeremiah Athmer, Rudragouda Channappanavar, Judith M. Phillips, David K. Meyerholz et Stanley Perlman. « The nsp3 Macrodomain Promotes Virulence in Mice with Coronavirus-Induced Encephalitis ». Journal of Virology 89, n^o 3 (26 novembre 2014) : 1523–36. http://dx.doi.org/10.1128/jvi.02596-14.

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ABSTRACTAll coronaviruses encode a macrodomain containing ADP-ribose-1″-phosphatase (ADRP) activity within the N terminus of nonstructural protein 3 (nsp3). Previous work showed that mouse hepatitis virus strain A59 (MHV-A59) with a mutated catalytic site (N1348A) replicated similarly to wild-type virus but was unable to cause acute hepatitis in mice. To determine whether this attenuated phenotype is applicable to multiple disease models, we mutated the catalytic residue in the JHM strain of MHV (JHMV), which causes acute and chronic encephalomyelitis, using a newly developed bacterial artificial chromosome (BAC)-based MHV reverse genetics system. Infection of mice with the macrodomain catalytic point mutant virus (N1347A) resulted in reductions in lethality, weight loss, viral titers, proinflammatory cytokine and chemokine expression, and immune cell infiltration in the brain compared to mice infected with wild-type virus. Specifically, macrophages were most affected, with approximately 2.5-fold fewer macrophages at day 5 postinfection in N1347A-infected brains. Tumor necrosis factor (TNF) and interferon (IFN) signaling were not required for effective host control of mutant virus as all N1347A virus-infected mice survived the infection. However, the adaptive immune system was required for protection since N1347A virus was able to cause lethal encephalitis in RAG1−/−(recombination activation gene 1 knockout) mice although disease onset was modestly delayed. Overall, these results indicate that the BAC-based MHV reverse genetics system will be useful for studies of JHMV and expand upon previous studies, showing that the macrodomain is critical for the ability of coronaviruses to evade the immune system and promote viral pathogenesis.IMPORTANCECoronaviruses are an important cause of human and veterinary diseases worldwide. Viral processes that are conserved across a family are likely to be good targets for the development of antiviral therapeutics and vaccines. The macrodomain is a ubiquitous structural domain and is also conserved among all coronaviruses. The coronavirus macrodomain has ADP-ribose-1″-phosphatase activity; however, its function during infection remains unclear as does the reason that coronaviruses have maintained this enzymatic activity throughout evolution. For MHV, this domain has now been shown to promote multiple types of disease, including hepatitis and encephalitis. These data indicate that this domain is vital for the virus to replicate and cause disease. Understanding the mechanism used by this enzyme to promote viral pathogenesis will open up novel avenues for therapies and may give further insight into the role of macrodomain proteins in the host cell since these proteins are found in all living organisms.

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Pandit, Ram Deo, Ashwani Upadhayaya, Chandni Gupta et Sunil Sharma. « Review on Reverse Pharmacology of Jawarhar Mahakashaya Drugs for Anti-pyretic Activity in Momoherbal and Polyherbal Form ». Journal of Ayurvedic and Herbal Medicine 8, n^o 1 (25 mars 2022) : 32–39. http://dx.doi.org/10.31254/jahm.2022.8109.

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Ayurvedic Jawarahara Mahakashaya (JhMh) includes Sariva, Sharkara, Patha, Manjishtha, Draksha, Pilu, Parushaka, Abhaya, Amalaka and Bibhitaka drugs as a set of ten herbal drugs, means this set of drug is effective in countering Jawar (fever) in single drug form or combined formulation. Globally the most accepted drugs which are used to cure pyrexia are NSAIDS. It is reported that most of these chemical antipyretic formulations has been associated with gastrointestinal, renal, hepatic, CNS and dermatological side effects. Extensive literature searches both electronic online databases on concerning issues. Drugs of Jawarhar Mahakashaya in monoherbal and polyherbal form have shown significant antipyretic activity in pre-clinical set up as mentioned in Ayurvedic literatures. The main aim of this paper is to review reverse pharmacology of JhMh drugs is described in terms of Ayurveda and is supported parallelly with the facts and findings of scientific researches done in modern science. JhMh can replace the side effects of chemical drugs and stand as sustainable antipyretics if used judicious.

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Miura, Tanya A., Emily A. Travanty, Lauren Oko, Helle Bielefeldt-Ohmann, Susan R. Weiss, Nicole Beauchemin et Kathryn V. Holmes. « The Spike Glycoprotein of Murine Coronavirus MHV-JHM Mediates Receptor-Independent Infection and Spread in the Central Nervous Systems of Ceacam1a−/− Mice ». Journal of Virology 82, n^o 2 (14 novembre 2007) : 755–63. http://dx.doi.org/10.1128/jvi.01851-07.

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ABSTRACT The MHV-JHM strain of the murine coronavirus mouse hepatitis virus is much more neurovirulent than the MHV-A59 strain, although both strains use murine CEACAM1a (mCEACAM1a) as the receptor to infect murine cells. We previously showed that Ceacam1a −/− mice are completely resistant to MHV-A59 infection (E. Hemmila et al., J. Virol. 78:10156-10165, 2004). In vitro, MHV-JHM, but not MHV-A59, can spread from infected murine cells to cells that lack mCEACAM1a, a phenomenon called receptor-independent spread. To determine whether MHV-JHM could infect and spread in the brain independent of mCEACAM1a, we inoculated Ceacam1a −/− mice. Although Ceacam1a −/− mice were completely resistant to i.c. inoculation with 106 PFU of recombinant wild-type MHV-A59 (RA59) virus, these mice were killed by recombinant MHV-JHM (RJHM) and a chimeric virus containing the spike of MHV-JHM in the MHV-A59 genome (SJHM/RA59). Immunohistochemistry showed that RJHM and SJHM/RA59 infected all neural cell types and induced severe microgliosis in both Ceacam1a −/− and wild-type mice. For RJHM, the 50% lethal dose (LD50) is <101.3 in wild-type mice and 103.1 in Ceacam1a −/− mice. For SJHM/RA59, the LD50 is <101.3 in wild-type mice and 103.6 in Ceacam1a −/− mice. This study shows that infection and spread of MHV-JHM in the brain are dependent upon the viral spike glycoprotein. RJHM can initiate infection in the brains of Ceacam1a −/− mice, but expression of mCEACAM1a increases susceptibility to infection. The spread of infection in the brain is mCEACAM1a independent. Thus, the ability of the MHV-JHM spike to mediate mCEACAM1a-independent spread in the brain is likely an important factor in the severe neurovirulence of MHV-JHM in wild-type mice.

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Okuda, Masumi, Toshiro Sugiyama, Kenichi Fukunaga, Masaru Kondou, Eikichi Miyashiro et Teruko Nakazawa. « A Strain-Specific Antigen in Japanese Helicobacter pylori Recognized in Sera of Japanese Children ». Clinical Diagnostic Laboratory Immunology 12, n^o 11 (novembre 2005) : 1280–84. http://dx.doi.org/10.1128/cdli.12.11.1280-1284.2005.

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ABSTRACT An enzyme immuno assay (EIA) test based on Japanese strain-derived high-molecular-weight cell-associated proteins (JHM-CAP) was evaluated by comparing with a previously developed EIA test based on a U.S. strain-derived high-molecular-weight cell-associated proteins (HM-CAP). Serum samples of 131 Japanese asymptomatic children (mean age, 5.5 years; range, 0 to 21 years) were tested that include 43 positive and 88 negative children as judged by Helicobacter pylori stool antigen test (HpSA test). Both tests showed comparable and reliable specificities, but the sensitivity of JHM-CAP EIA, at 93.0%, was much higher than that of HM-CAP EIA, at 67.4%. More false-negative results of HM-CAP were obtained in children under 10 years of age. Immunoblot analysis revealed that the JHM-CAP but not the HM-CAP preparation had a 100-kDa antigen recognized by JHM-CAP positive sera. It was concluded that JHM-CAP EIA is highly accurate for the serodiagnosis of H. pylori infection in Japanese young children and that the high sensitivity of JHM-CAP EIA in contrast to HM-CAP EIA is due to the presence of a 100-kDa antigen in Japanese strains that may be recognized by the host immune system at an early stage of infection.

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Zirk, Anna, Rebecca Wiczorek et Dietrich Manzey. « Do We Really Need More Stages ? Comparing the Effects of Likelihood Alarm Systems and Binary Alarm Systems ». Human Factors : The Journal of the Human Factors and Ergonomics Society 62, n^o 4 (19 juin 2019) : 540–52. http://dx.doi.org/10.1177/0018720819852023.

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Objective This research investigates the potential behavioral and performance benefits of a four-stage likelihood alarm system (4-LAS) contrasting a 3-LAS, a binary alarm system with a liberal threshold (lib-BAS), and a BAS with a conservative threshold (con-BAS). Background Prior research has shown performance benefits of 3-LASs over conventional lib-BASs due to more distinct response strategies and better discriminating true from false alerts. This effect might be further enhanced using 4-LASs. However, the increase in stages could cause users to reduce cognitive complexity by responding in the same way to the two lower and the two higher stages, thus treating the 4-LAS like a con-BAS. Method All systems were compared using a dual-task paradigm. Response strategies, number of joint human machine (JHM) false alarms (FAs), misses, and sensitivity were regarded. Results Compared with the lib-BAS, JHM sensitivity only improved with the 4-LAS and the con-BAS. However, the number of JHM misses was lowest for the con-BAS compared with all other systems. Conclusion JHM sensitivity improvements can be achieved by using a 4-LAS, as well as a con-BAS. However, only the latter one may also reduce the number of JHM misses, which is remarkable considering that BASs with conservative thresholds a priori commit more inbuilt misses than other systems. Application Results suggest implementing conservative BASs in multi-task working environments to improve JHM sensitivity and reduce the number of JHM misses. When refraining from designing systems which are miss prone, 4-LASs represent a suitable compromise.

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Iacono, Kathryn T., Lubna Kazi et Susan R. Weiss. « Both Spike and Background Genes Contribute to Murine Coronavirus Neurovirulence ». Journal of Virology 80, n^o 14 (15 juillet 2006) : 6834–43. http://dx.doi.org/10.1128/jvi.00432-06.

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ABSTRACT Various strains of mouse hepatitis virus (MHV) exhibit different pathogenic phenotypes. Infection with the A59 strain of MHV induces both encephalitis and hepatitis, while the highly neurovirulent JHM strain induces a fatal encephalitis with little, if any, hepatitis. The pathogenic phenotype for each strain is determined by the genetic composition of the viral genome, as well as the host immune response. Using isogenic recombinant viruses with A59 background genes differing only in the spike gene, we have previously shown that high neurovirulence is associated with the JHM spike protein, the protein responsible for attachment to the host cell receptor (J. J. Phillips, M. M. Chua, G. F. Rall, and S. R. Weiss, Virology 301:109-120, 2002). Using another set of isogenic recombinant viruses with JHM background genes expressing either the JHM or A59 spike, we have further investigated the roles of viral genes in pathogenesis. Here, we demonstrate that the high neurovirulence of JHM is associated with accelerated spread through the brain and a heightened innate immune response that is characterized by high numbers of infiltrating neutrophils and macrophages, suggesting an immunopathogenic component to neurovirulence. While expression of the JHM spike is sufficient to confer a neurovirulent phenotype, as well as increased macrophage infiltration, background genes contribute to virulence as well, at least in part, by dictating the extent of the T-cell immune response.

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Kolb, Andreas F., Lecia Pewe, John Webster, Stanley Perlman, C. Bruce A. Whitelaw et Stuart G. Siddell. « Virus-Neutralizing Monoclonal Antibody Expressed in Milk of Transgenic Mice Provides Full Protection against Virus-Induced Encephalitis ». Journal of Virology 75, n^o 6 (15 mars 2001) : 2803–9. http://dx.doi.org/10.1128/jvi.75.6.2803-2809.2001.

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ABSTRACT Neutralizing antibodies represent a major host defense mechanism against viral infections. In mammals, passive immunity is provided by neutralizing antibodies passed to the offspring via the placenta or the milk as immunoglobulin G and secreted immunoglobulin A. With the long-term goal of producing virus-resistant livestock, we have generated mice carrying transgenes that encode the light and heavy chains of an antibody that is able to neutralize the neurotropic JHM strain of murine hepatitis virus (MHV-JHM). MHV-JHM causes acute encephalitis and acute and chronic demyelination in susceptible strains of mice and rats. Transgene expression was targeted to the lactating mammary gland by using the ovine β-lactoglobulin promoter. Milk from these transgenic mice contained up to 0.7 mg of recombinant antibody/ml. In vitro analysis of milk derived from different transgenic lines revealed a linear correlation between antibody expression and virus-neutralizing activity, indicating that the recombinant antibody is the major determinant of MHV-JHM neutralization in murine milk. Offspring of transgenic and control mice were challenged with a lethal dose of MHV-JHM. Litters suckling nontransgenic dams succumbed to fatal encephalitis, whereas litters suckling transgenic dams were fully protected against challenge, irrespective of whether they were transgenic. This demonstrates that a single neutralizing antibody expressed in the milk of transgenic mice is sufficient to completely protect suckling offspring against MHV-JHM-induced encephalitis.

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Zidany, H., M. Waterman, K. Toledano, Y. Chowers, D. Markovits, A. Karban, A. Balbir-Gurman et Y. Braun-Moscovici. « THU0458 HIGH PREVALENCE OF JOINT HYPERMOBILITY IN INFLAMMATORY BOWEL DISEASE PATIENTS WITH PAIN UNRESPONSIVE TO BOWEL-TARGETED THERAPY ». Annals of the Rheumatic Diseases 79, Suppl 1 (juin 2020) : 466.2–466. http://dx.doi.org/10.1136/annrheumdis-2020-eular.4767.

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Background:Musculoskeletal manifestations occur in 20-50% of patients (pts) with inflammatory bowel disease (IBD). A substantial number of patients complain of non-inflammatory musculoskeletal pain.Objectives:To assess the incidence of joint hypermobility (JHM), benign joint hypermobility syndrome (BJHS) among patients with inflammatory bowel disease (IBD) examined in the inter-disciplinary rheumatology service at a tertiary referral center and the impact on IBD manifestations and outcome.Methods:Medical records of 180 consecutive IBD pts referred to the inter-disciplinary clinic were retrospectively reviewed. Data regarding age, gender, diagnosis, disease duration, clinical and laboratory features, previous and current therapy, Harvey-Brandshaw Index were entered into a database and analyzed. Beighton’s scoring of ≥4/9 was used to define patients with JHM. The 1998 Brighton’s criteria were used to identify patients with BJHS. Outcome was defined as improvement of joint pain. The statistical methods used included descriptive statistics, T test, Spearman’s correlation and multiple logistic regression analysis.Results:Forty-six patients (mean(SD) age 36.2(12.4), disease duration 13.9(8.8) years) out of 180 IBD patients (mean(SD) age 40.4(14.3), disease duration 15.7(9.1) years) fulfilled the criteria for JHM. Twelve patients had active inflammatory joint disease (2 with axial involvement, 10 with peripheral joint disease and 2 with axial and peripheral joint involvement). The other 32 answered both major criteria for BJHS. The median Beighton scoring was 7 (range 5-9). Most of them were on biological treatment. Patients with JHM suffered frequently of arthralgia and abdominal pain, in spite of endoscopic remission and normal levels of calprotectin and inflammatory markers (p=0.02, r=0.17). JHM and BJHS were associated with poorer outcome (p=0.004, r=0.2). In a multiple logistic regression analysis, only JHM reached borderline significance for predicting worse outcome.Conclusion:Joint and abdominal pain did not improve with immunomodulatory therapy in IBD patients with JHM. JHM may have a negative impact on achievement of clinical remission, in a significant subset of IBD patients. Rheumatologists and gastroenterologists should be aware of this.Disclosure of Interests: :Haya Zidany: None declared, Matti Waterman: None declared, Kohava Toledano: None declared, Yehuda Chowers: None declared, Doron Markovits: None declared, Amir Karban: None declared, Alexandra Balbir-Gurman Consultant of: Novartis, Yolanda Braun-Moscovici: None declared

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Hasibuan, Anggi Praya, et Dian Anubhakti. « IMPLEMENTASI E-COMMERCE MENGGUNAKAN CONTENT MANAGEMENT SYSTEM (CMS) UNTUK MENINGKATKAN PENJUALAN PADA TOKO JHM HERBAL ». IDEALIS : InDonEsiA journaL Information System 3, n^o 1 (5 février 2020) : 157–63. http://dx.doi.org/10.36080/idealis.v3i1.2135.

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Toko JHM Herbal adalah toko yang menjual beraneka ragam produk untuk kesehatan tubuh berupa produk herbal seperti kurma, madu, susu kambing dan lain sebagainya. Toko JHM Herbal masih menggunakan sistem manual dalam proses penjualan produk yaitu pelanggan harus datang langsung ke toko untuk melihat, membeli dan melakukan transaksi pembayaran. Hal ini membuat penjualan produk kurang optimal karena penjualan produk terbatas pada pelanggan yang berada di sekitar toko saja. Oleh sebab itu, penulis membuat suatu sistem E-Commerce menggunakan Content Management System (CMS) dengan metode Business Model Canvas (BMC) untuk diterapkan pada toko JHM Herbal. Hadirnya E-Commerce sebagai media transaksi jual beli pada Toko JHM Herbal memberikan keuntungan antara lain: memperluas pemasaran produk karena dapat diakses oleh siapa saja, dimana saja dan kapan saja, memudahkan dalam memberikan informasi produk yang dipasarkan, memudahan proses transaksi pembayaran, meningkatkan penjualan produk, dan mempermudah dalam pembuatan laporan penjualan toko.

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Indrawan, Andry Nor, Pardi Affandi et Oni Soesanto. « PENGGUNAAN JUMAN & ; HOQUE METHOD (JHM) PADA PENENTUAN SOLUSI AWAL MASALAH TRANSPORTASI ». EPSILON : JURNAL MATEMATIKA MURNI DAN TERAPAN 15, n^o 1 (16 juillet 2021) : 27. http://dx.doi.org/10.20527/epsilon.v15i1.2876.

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Transportation problems are related to the efficient process of distributing goods by a company or industry. The purpose of solving transportation problems is to minimize the costs incurred in the process of distributing goods from several sources (supply) to several destinations (demand). One way to solve transportation problems is to find an initial feasible solution, continued by finding the optimal solution. This research was done by finding an initial feasible solution using the JHM (Juman & Hoque Method) for both the case of solving balanced transportation problems and unbalanced transportation problems. The method has the characteristic in the initial allocation process starting at the cell with the smallest cost in each column as much as the quantity of each demand. In addition, identification of whether the row if occupied or not was done based on the allocation for each row to the quantity of each inventory. This research aimed to explain about solving transportation problems by determining the initial feasible solution using JHM and performing optimality test using potential method. The methods of this research was to identify categories of transportation problems, determine the initial solution using JHM, and test the optimality using potential method. Based on the results of this research, JHM model may be used to solve transportation problems. In the steps of JHM there are explanations of some theorem regarding the selection of the column and row which will be the first to be processed to determine the value of intial solution of transportation problems. The initial solution by using JHM tends to approach the value of optimal solution after test of optimality was done by using the potential method.

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Safeer, Richard Scott, Meg Mia Lucik et Katherine Claire Christel. « Using the CDC Worksite Health ScoreCard to Promote Organizational Change ». American Journal of Health Promotion 35, n^o 7 (7 juin 2021) : 997–1001. http://dx.doi.org/10.1177/08901171211012948.

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Purpose: To measure the impact of tying adoption of evidence-based worksite health promotion (WHP) interventions to annual organizational strategic objectives, as measured by the Centers for Disease Control and Prevention (CDC) Worksite Health ScoreCard (ScoreCard). Design: A prospective cohort study following Johns Hopkins Medicine (JHM) affiliates against industry-specific and large employer benchmarks from 2016-2020. Settings: JHM, the largest private employer in Maryland with facilities in Florida and the District of Columbia. Subjects: Twelve JHM affiliates representing over 40,000 employees. Intervention: A strategic objective was established annually based on the ScoreCard and organizational priorities. Measures: JHM affiliates measured their WHP efforts annually using the ScoreCard. CDC industry-specific and large employer benchmarks were collected for comparison. Analysis: ScoreCard data was assessed annually to measure deviations from CDC benchmarks, determine whether strategic objectives were met, and inform additional annual objectives. Results: JHM demonstrated improvement from 8.9 percentage points above industry-specific and 3.4 percentage points below large employer benchmarks in 2016, to 26.4 percentage points above industry-specific and 21.8 percentage points above large employer benchmarks in 2020. Conclusion: Large employers face unique challenges in implementing WHP programs. Our study suggests embedding health promotion in annual strategic objectives may alleviate these challenges by prioritizing the goal and ensuring adequate resources to be successful. There are however, some limitations on using benchmarking data for comparison.

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Tennakoon, Nipuna, Jihoon Ryu, Makoto Ujike, Fumihiro Taguchi et Hyun-Jin Shin. « Reduction of Cell Fusion by Deletion in the Hypervariable Region of the Spike Protein of Mouse Hepatitis Virus ». Viruses 14, n^o 2 (15 février 2022) : 398. http://dx.doi.org/10.3390/v14020398.

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Deletions in the spike gene of mouse hepatitis virus (MHV) produce several variants with diverse biological characteristics, highlighting the significance of the spike gene in viral pathogenesis. In this study, we characterized the JHM-X strain, which has a deletion in the hypervariable region (HVR) of the spike gene, compared with the cl-2 strain, which has a full spike gene. Cytopathic effects (CPEs) induced by the two strains revealed that the size of the CPE produced by cl-2 is much greater than that produced by JHM-X in delayed brain tumor (DBT) cells. Thus, this finding explains the greater fusion activity of cl-2 than JHM-X in cultured cells, and we speculate that the deletion region of the spike protein is involved in the fusion activity differences. In contrast with the fusion activity, a comparison of the virus growth kinetics revealed that the titer of JHM-X was approximately 100 times higher than that of cl-2. We found that the deletion region of the spike protein was involved in fusion activity differences, whereas cl-2 produced significantly higher luciferase activity than JHM-X upon similar expression levels of the spike protein. However, the reason behind the growth difference is still unknown. Overall, we discovered that deletion in the HVR of the spike gene could be involved in the fusion activity differences between the two strains.

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Smith, A. L., K. Bottomly et D. F. Winograd. « Altered splenic T cell function of BALB/cByJ mice infected with mouse hepatitis virus or Sendai virus. » Journal of Immunology 138, n^o 10 (15 mai 1987) : 3426–30. http://dx.doi.org/10.4049/jimmunol.138.10.3426.

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Abstract Mouse hepatitis virus and Sendai virus are among the most common viruses naturally infecting laboratory mice. Concanavalin A-stimulated in vitro proliferative responses of splenocytes were examined after infection of BALB/cByJ mice with the JHM strain of mouse hepatitis virus (MHV-JHM) or Sendai virus. Mice were exposed to these viruses by presumed natural routes (per os or intranasally). Immunodepression was marked but transient among BALB/cByJ mice exposed to MHV-JHM. Among mice exposed to Sendai virus and examined over a 21-day period, spleen cells from only one mouse, sacrificed 10 days postinoculation, exhibited a severely impaired ability to respond to concanavalin A. Lymphokine production by spleen cells from control and infected mice was then assessed. IL 2 was either absent or present at very low levels in culture supernates of concanavalin A-unresponsive spleen cells from MHV-JHM-infected mice. Spleen cells from the single Sendai virus-infected mouse also produced very low levels of IL 2. In contrast, IL 1 was detected in supernatants of all spleen cell cultures derived from control, MHV-JHM-infected, or Sendai virus-infected mice. There was not a clear correlation between concanavalin A responsiveness and the ability of spleen cells to produce interferon-gamma. These results stress the importance of using laboratory mice of known microbiological status for immunologic experiments.

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Shin, Hyun-Jin. « Reduction of cell fusion by deletion in the hypervariable region of the spike protein of mouse hepatitis virus ». Journal of Immunology 210, n^o 1_Supplement (1 mai 2023) : 235.05. http://dx.doi.org/10.4049/jimmunol.210.supp.235.05.

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Abstract Deletions in the spike gene of mouse hepatitis virus (MHV) produce several variants with diverse biological characteristics, highlighting the significance of the spike gene in viral pathogenesis. In this study, we characterized the JHM-X strain, which has a deletion in the hypervariable region (HVR) of the spike gene, compared with the cl-2 strain, which has a full spike gene. Cytopathic effects (CPEs) induced by the two strains revealed that the size of the CPE produced by cl-2 is much greater than that produced by JHM-X in delayed brain tumor (DBT) cells. Thus, this finding explains the greater fusion activity of cl-2 than JHM-X in cultured cells, and we speculate that the deletion region of the spike protein is involved in the fusion activity differences. In contrast with the fusion activity, comparison of the virus growth kinetics revealed that the titer of JHM-X was approximately 100 times higher than that of cl-2. We found that the deletion region of the spike protein was involved in fusion activity differences, whereas cl-2 produced significantly higher luciferase activity than JHM-X upon similar expression levels of the spike protein. However, the reason behind the growth difference is still unknown. Overall, we discovered that deletion in the HVR of the spike gene could be involved in the fusion activity differences between the two strains.

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Massa, P. T., R. Brinkmann et V. ter Meulen. « Inducibility of Ia antigen on astrocytes by murine coronavirus JHM is rat strain dependent. » Journal of Experimental Medicine 166, n^o 1 (1 juillet 1987) : 259–64. http://dx.doi.org/10.1084/jem.166.1.259.

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Inducibility of Ia molecules on cultivated astrocytes by JHM virus correlates with demyelinating disease susceptibility of animals from which these astrocytes are derived. On the contrary, class I induction of both astrocytes and oligodendrocytes occurs as a consequence of normal cultivation procedures in both susceptible and resistant strains. Increased expression of class I antigens on rat astrocytes and oligodendrocytes is not related to JHM viral infection as it is in the mouse. These data indicate that strain differences in Ia inducibility, rather than inducibility of class I antigens, by JHM virus may explain higher levels of T cell-mediated damage to myelin during infection in susceptible rat strains compared with resistant strains.

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Huynh, Melissa, Chirag Vyas, Kathryn L. Penney et Adam S. Kibel. « Associations of cell cycle genetic variants with aggressive prostate cancer in the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial. » Journal of Clinical Oncology 37, n^o 7_suppl (1 mars 2019) : 175. http://dx.doi.org/10.1200/jco.2019.37.7_suppl.175.

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175 Background: The need to differentiate patients at risk for developing aggressive prostate cancer (CaP) from those at risk for less aggressive disease has led to efforts to identify genetic markers to predict disease course and personalize treatment. A study with participants from Johns Hopkins Medical Institutions (JHMI) and Washington University (WU) found single nucleotide polymorphisms (SNPs) in cell cycle genes were associated with risk of aggressive CaP. We sought to replicate those results in the European-American population of the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial. Methods: We focused on variants associated with aggressive CaP in the JHMI and WU cohorts, which included 13 SNPs in 12 genes ( CCNC, CCND3, CCNG1, CCNT2, CDK2, CDK6, MDM2, SKP2, TERF2, WEE1, YWHAB, YWHAH). Variants were genotyped using the Pyrosequencing assay. Patients were classified into high risk (Gleason≥8, pT3b, N+, M+), low risk (Gleason≤7, ≤pT3a, N0, M0) or non-cancer control groups based on clinicopathologic characteristics. Logistic regression analysis was used to compare genotype frequencies of each variant between groups using the dominant model. Results: There were 108 aggressive and 1080 non-aggressive CaP patients, and 1155 controls . CDK6 ( rs8) was associated with increased risk of any CaP (OR 1.2, 95% CI 1.02-1.42; p = 0.032) and high risk disease (OR 1.63, 95% CI 1.09-2.42; p = 0.017) vs. controls. In contrast, the JHMI and WU cohort found CDK6 variants to be protective against aggressive CaP. CCNG1 ( rs11541970) approached significance (p = 0.052) between high risk and control groups, and CCNC conferred a protective effect consistent with the prior study, but did not reach significance (p = 0.101). No associations with any cell cycle gene variants were detected when comparing high and low risk patients. Conclusions: Our study did not replicate the results from the JHMI and WU cohorts. CDK6 predicted an increased risk of developing any CaP and high risk CaP. However, directionality was opposite to the prior study, indicating that this variant is unlikely to be a true predictor of increased risk of or protection from aggressive CaP.

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Haas, Robert. « JHM Contents Word Puzzle ». Journal of Humanistic Mathematics 4, n^o 2 (juillet 2014) : [146]—147. http://dx.doi.org/10.5642/jhummath.201402.18.

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Cowley, Timothy J., Simon Y. Long et Susan R. Weiss. « The Murine Coronavirus Nucleocapsid Gene Is a Determinant of Virulence ». Journal of Virology 84, n^o 4 (9 décembre 2009) : 1752–63. http://dx.doi.org/10.1128/jvi.01758-09.

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ABSTRACT The murine coronavirus, mouse hepatitis virus (MHV) strain A59, causes acute encephalitis and chronic demyelinating disease as well as hepatitis in mice. The JHM strain (also called MHV-4 or JHM.SD) causes fatal encephalitis and only minimal hepatitis. Previous analysis of chimeric recombinant MHVs in which the spike gene, encoding the protein that mediates viral entry and cell-to-cell fusion, was exchanged between JHM and A59 showed that the spike plays a major role in determining organ tropism and neurovirulence but that other genes also play important roles in pathogenic outcome. Here, we have investigated the role of the nucleocapsid protein in MHV-induced disease. The multifunctional nucleocapsid protein is complexed with the genomic RNA, interacts with the viral membrane protein during virion assembly, and plays an import role in enhancing the efficiency of transcription. A pair of chimeric recombinant viruses in which the nucleocapsid gene was exchanged between JHM and A59 was selected and compared to wild-type parental strains in terms of virulence. Importantly, expression of the JHM nucleocapsid in the context of the A59 genome conferred increased mortality and spread of viral antigen in the mouse central nervous system compared to the parental A59 strain, while having little effect on the induction of hepatitis. While the JHM nucleocapsid did not appear to enhance neuron-to-neuron spread in primary neuronal cultures, the increased neurovirulence it conferred may be due in part to the induction of a less robust T-cell response than that induced by strain A59.

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Tallis, Jason, Rhys O. Morris, Michael J. Duncan, Emma L. J. Eyre et Lucas Guimaraes-Ferreira. « Agreement between Force Platform and Smartphone Application-Derived Measures of Vertical Jump Height in Youth Grassroots Soccer Players ». Sports 11, n^o 6 (13 juin 2023) : 117. http://dx.doi.org/10.3390/sports11060117.

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Given the importance of vertical jump assessments as a performance benchmarking tool, the assessment of neuromuscular function and indicator of health status, accurate assessment is essential. This study compared countermovement jump (CMJ) height assessed using MyJump2 (JHMJ) to force-platform-derived jump height calculated from time in the air (JHTIA) and take-off velocity (JHTOV) in youth grassroots soccer players. Thirty participants (Age: 8.7 ± 0.42 yrs; 9 females) completed bilateral CMJs on force platforms whilst jump height was simultaneously evaluated using MyJump2. Intraclass correlation coefficients (ICC), Standard error of measurement (SEM), coefficient of variance (CV) and Bland–Altman analysis were used to compare performance of MyJump2 to force-platform-derived measures of CMJ height. The median jump height was 15.5 cm. Despite a high level of agreement between JHTIA and JHTOV (ICC = 0.955), CV (6.6%), mean bias (1.33 ± 1.62 cm) and 95% limits of agreement (LoA −1.85–4.51 cm) were greater than in other comparisons. JHMJ performed marginally better than JHTIA when compared to JHTOV (ICC = 0.971; 95% CI’s = 0.956–0.981; SEM = 0.3 cm; CV = 5.7%; mean bias = 0.36 ± 1.61 cm; LoA = −3.52–2.80 cm). Irrespective of method, jump height did not differ between males and females (p > 0.381; r < 0.093), and the comparison between assessment tools was not affected by sex. Given low jump heights achieved in youth, JHTIA and JHMJ should be used with caution. JHTOV should be used to guarantee accuracy in the calculation of jump height.

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Lemarchand, Yannick, et Souad Seboui. « Les JHCM 1995-2008. Rétrospective et perspectives ». Revue française de gestion 34, n^o 188-189 (30 décembre 2008) : 31–52. http://dx.doi.org/10.3166/rfg.188-189.31-52.

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Krueger, Dawn K., Sean M. Kelly, Daniel N. Lewicki, Rosanna Ruffolo et Thomas M. Gallagher. « Variations in Disparate Regions of the Murine Coronavirus Spike Protein Impact the Initiation of Membrane Fusion ». Journal of Virology 75, n^o 6 (15 mars 2001) : 2792–802. http://dx.doi.org/10.1128/jvi.75.6.2792-2802.2001.

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ABSTRACT The prototype JHM strain of murine hepatitis virus (MHV) is an enveloped, RNA-containing coronavirus that has been selected in vivo for extreme neurovirulence. This virus encodes spike (S) glycoproteins that are extraordinarily effective mediators of intercellular membrane fusion, unique in their ability to initiate fusion even without prior interaction with the primary MHV receptor, a murine carcinoembryonic antigen-related cell adhesion molecule (CEACAM). In considering the possible role of this hyperactive membrane fusion activity in neurovirulence, we discovered that the growth of JHM in tissue culture selected for variants that had lost murine CEACAM-independent fusion activity. Among the collection of variants, mutations were identified in regions encoding both the receptor-binding (S1) and fusion-inducing (S2) subunits of the spike protein. Each mutation was separately introduced into cDNA encoding the prototype JHM spike, and the set of cDNAs was expressed using vaccinia virus vectors. The variant spikes were similar to that of JHM in their assembly into oligomers, their proteolysis into S1 and S2 cleavage products, their transport to cell surfaces, and their affinity for a soluble form of murine CEACAM. However, these tissue culture-adapted spikes were significantly stabilized as S1-S2 heteromers, and their entirely CEACAM-dependent fusion activity was delayed or reduced relative to prototype JHM spikes. The mutations that we have identified therefore point to regions of the S protein that specifically regulate the membrane fusion reaction. We suggest that cultured cells, unlike certain in vivo environments, select for S proteins with delayed, CEACAM-dependent fusion activities that may increase the likelihood of virus internalization prior to the irreversible uncoating process.

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Monchaux, Georges. « Risk of fatal versus incidental lung cancer in radon-exposed rats : A reanalysis of French data ». Archive of Oncology 12, n^o 1 (2004) : 7–12. http://dx.doi.org/10.2298/aoo0401007m.

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This review summarizes data on lung cancer risk from radon experimental studies performed by our group in France with emphasis on the most recent findings and analyses on the influence of dose-rate and that of fatal versus incidental tumors. A dose-effect relationship was established in rats, which was very similar for medium and high cumulative exposures, to that observed in uranium miners. At low cumulative exposures in the range of 0.18 Jhm-3 (50 WLM) to 0.36 Jhm-3 (100 WLM), the proportion of fatal lung cancer is about 80% that of total lung cancers. In contrast, at cumulative exposures of 0.72 Jhm-3 (200 WLM) and higher, the proportion of fatal lung cancer is about half that of total lung cancers. The parameters that influence fatal lung cancer risk are cumulative exposure, potential alpha energy concentration (PAEC), exposure rate, and protraction of exposure. At high cumulative exposures up to 10.8 Jhm-3 (3,000 WLM), an inverse dose-rate effect similar to that observed in uranium miners was also found in rats. The inverse exposure- rate effect was observed mainly at the highest exposure-rates. In contrast, our recent results indicate that at relatively low cumulative exposures of 0.36 Jhm-3 (100 WLM), comparable to lifetime exposures in high-radon houses or current underground mining exposures, the risk of lung cancer in rats decreases with decreasing PAEC, i.e., exposure rate. These data suggest that the induction of lung cancer results from a complex inter- play between cumulative exposure and exposure rate, with an optimal combination of these two parameters that results in a maximum risk of lung cancer induction. They support the hypothesis that, at low doses, the risk of lung cancer is governed by the rate at which the dose is delivered, and not by the total cumulative dose alone. These data are also consistent with those of underground uranium miners showing an inverse dose-rate effect at high cumulative exposures, but an attenuation of this effect at cumulative exposures lower than 0.18 Jhm-3 (50 WLM). They support both an inverse dose-rate effect at high cumulative exposures, as well as its attenuation or disappearance at low cumulative exposures.

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Fitriana, Umiatul. « Dampak Keberadaan Pondok Pesantren Terhadap Perkembangan Ekonomi Masyarakat : Studi Kasus di Pondok Pesantren Ulil Al Baab NW Gegek Lombok Timur ». Jurnal Humanitas : Katalisator Perubahan dan Inovator Pendidikan 6, n^o 1 (30 décembre 2019) : 76–98. http://dx.doi.org/10.29408/jhm.v6i1.3751.

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Chen, Cheng-Hsu, Ming-Ju Wu et Shang-Feng Tsai. « The Feasibility of Japanese Histological Grade Classification for Predicting Renal Function Deterioration among Taiwanese Individuals with IgA Nephropathy ». Journal of Clinical Medicine 12, n^o 23 (27 novembre 2023) : 7339. http://dx.doi.org/10.3390/jcm12237339.

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Background: We aimed to validate the Japanese histological grading classification (JHGC) in our population of IgA immunoglobulin (IgAN) cases. Methods: We conducted a retrospective cohort study at Taichung Veterans General Hospital in Taiwan from January 2011 to December 2023. The process involved assessing JHGC’s clinical, histological, and merged grading system. Composite renal outcomes based on glomerular filtrate rate (eGFR) were considered. Results: The study included 359 IgAN by renal biopsies. Kidney function at the time of biopsy was suboptimal, with average SCr of 1.3 mg/dL, eGFR of 54.0 mL/min/1.732 m2, and urine protein–creatinine ratio (UPCR) of 1.2 mg/mg. JHGC effectively identified different severity levels of histological and clinical aspects in Taiwanese IgAN. Initial 4-histological classification showed significantly higher MEST-C scores (p < 0.001). Merging grade III and IV was reasonable in Japanese and Taiwanese populations. The clinical grading system (3C) was associated with histological status and proteinuria, but there was no significant trend with SCr, eGFR, and blood urea nitrogen. Significant differences were found among the three groups (log-rank p < 0.01), but C-grade I and II lacked significant difference in long-term renal outcomes. We separated UPCR < 0.5 mg/mg into two groups: eGFR≥ and <60 mL/min/1.732 m2. The new grading system effectively differentiated risk factors for renal outcomes (log-rank p < 0.01), suggesting the need for separation in Taiwanese IgAN. Conclusions: Our study externally validated JHGC in non-Japanese IgAN. Despite applicability to our population, we recommend a new classification specifically for Taiwanese IgAN patients with increased case numbers in eGFR ≥ 60 mL/min/1.732 m2 and UPCR < 0.5 g/day group.

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Dong, Yan, et Fu-Gui Shi. « On the disjoint sums of M-fuzzifying convex spaces ». Filomat 35, n^o 14 (2021) : 4675–90. http://dx.doi.org/10.2298/fil2114675d.

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In this paper, we first extend the concept of the arity in crisp convex spaces to the case of fuzzification and give some related properties. From the view of arity and hull operator, we study the relations between the disjoint sum of M-fuzzifying convex spaces and its factor spaces. We also examine the additivity of the degree of separability (S0,S1,S2,S3,S4). Finally, we show that every factor space is M-fuzzifying JHC iff the corresponding disjoint sum space is JHC.

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Ontiveros, Evelena, Taeg S. Kim, Thomas M. Gallagher et Stanley Perlman. « Enhanced Virulence Mediated by the Murine Coronavirus, Mouse Hepatitis Virus Strain JHM, Is Associated with a Glycine at Residue 310 of the Spike Glycoprotein ». Journal of Virology 77, n^o 19 (1 octobre 2003) : 10260–69. http://dx.doi.org/10.1128/jvi.77.19.10260-10269.2003.

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ABSTRACT The coronavirus, mouse hepatitis virus strain JHM, causes acute and chronic neurological diseases in rodents. Here we demonstrate that two closely related virus variants, both of which cause acute encephalitis in susceptible strains of mice, cause markedly different diseases if mice are protected with a suboptimal amount of an anti-JHM neutralizing antibody. One strain, JHM.SD, caused acute encephalitis, while infection with JHM.IA resulted in no acute disease. Using recombinant virus technology, we found that the differences between the two viruses mapped to the spike (S) glycoprotein and that the two S proteins differed at four amino acids. By engineering viruses that differed by only one amino acid, we identified a serine-to-glycine change at position 310 of the S protein (S310G) that recapitulated the more neurovirulent phenotype. The increased neurovirulence mediated by the virus encoding glycine at position S310 was not associated with a different tropism within the central nervous system (CNS) but was associated with increased lateral spread in the CNS, leading to significantly higher brain viral titers. In vitro studies revealed that S310G was associated with decreased S1-S2 stability and with enhanced ability to mediate infection of cells lacking the primary receptor for JHM (“receptor-independent spread”). These enhanced fusogenic properties of viruses encoding a glycine at position 310 of the S protein may contribute to spread within the CNS, a tissue in which expression of conventional JHM receptors is low.

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Navas-Martin, Sonia, Maarten Brom, Ming-Ming Chua, Richard Watson, Zhaozhu Qiu et Susan R. Weiss. « Replicase Genes of Murine Coronavirus Strains A59 and JHM Are Interchangeable : Differences in Pathogenesis Map to the 3′ One-Third of the Genome ». Journal of Virology 81, n^o 2 (1 novembre 2006) : 1022–26. http://dx.doi.org/10.1128/jvi.01944-06.

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ABSTRACT The important roles of the spike protein and other structural proteins in murine coronavirus (MHV) pathogenesis have been demonstrated; however, the role of the replicase gene remains unexplored. We assessed the influence of the replicase genes of the highly neurovirulent MHV-JHM strain and the hepatotropic and mildly neurovirulent A59 strain in acute infection of the mouse. Analysis of chimeric A59/JHM recombinant viruses indicates that the replicase genes are interchangeable and that it is the 3′ end of the genome, encoding the structural proteins, rather than the replicase gene, that determines the pathogenic properties of these chimeras.

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Sariol, Alan, Samantha Mackin, Merri-Grace Allred, Chen Ma, Yu Zhou, Qinran Zhang, Xiufen Zou, Juan E. Abrahante, David K. Meyerholz et Stanley Perlman. « Microglia depletion exacerbates demyelination and impairs remyelination in a neurotropic coronavirus infection ». Proceedings of the National Academy of Sciences 117, n^o 39 (14 septembre 2020) : 24464–74. http://dx.doi.org/10.1073/pnas.2007814117.

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Microglia are considered both pathogenic and protective during recovery from demyelination, but their precise role remains ill defined. Here, using an inhibitor of colony stimulating factor 1 receptor (CSF1R), PLX5622, and mice infected with a neurotropic coronavirus (mouse hepatitis virus [MHV], strain JHMV), we show that depletion of microglia during the time of JHMV clearance resulted in impaired myelin repair and prolonged clinical disease without affecting the kinetics of virus clearance. Microglia were required only during the early stages of remyelination. Notably, large deposits of extracellular vesiculated myelin and cellular debris were detected in the spinal cords of PLX5622-treated and not control mice, which correlated with decreased numbers of oligodendrocytes in demyelinating lesions in drug-treated mice. Furthermore, gene expression analyses demonstrated differential expression of genes involved in myelin debris clearance, lipid and cholesterol recycling, and promotion of oligodendrocyte function. The results also demonstrate that microglial functions affected by depletion could not be compensated by infiltrating macrophages. Together, these results demonstrate that microglia play key roles in debris clearance and in the initiation of remyelination following infection with a neurotropic coronavirus but are not necessary during later stages of remyelination.

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Rocha-Santos, Teresa, Wen Zhang et Guo-Ping Sheng. « JHM advances first volume and welcome ». Journal of Hazardous Materials Advances 2 (octobre 2021) : 100012. http://dx.doi.org/10.1016/j.hazadv.2021.100012.

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Eaton, Carrie, et Luz Bailey. « http://scholarship.claremont.edu/jhm/vol8/iss2/7/ ». Journal of Humanistic Mathematics 8, n^o 2 (juillet 2018) : 60–89. http://dx.doi.org/10.5642/jhummath.201802.08.

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Gilmore, W., J. Correale et L. P. Weiner. « Coronavirus induction of class I major histocompatibility complex expression in murine astrocytes is virus strain specific. » Journal of Experimental Medicine 180, n^o 3 (1 septembre 1994) : 1013–23. http://dx.doi.org/10.1084/jem.180.3.1013.

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Neurotropic strains of mouse hepatitis viruses (MHV) such as MHV-A59 (A59) and MHV-4 (JHMV) cause acute and chronic encephalomyelitis and demyelination in susceptible strains of mice and rats. They are widely used as models of human demyelinating diseases such as multiple sclerosis (MS), in which immune mechanisms are thought to participate in the development of lesions in the central nervous system (CNS). The effects of MHV infection on target cell functions in the CNS are not well understood, but A59 has been shown to induce the expression of MHC class I molecules in glial cells after in vivo and in vitro infection. Changes in class I expression in infected cells may contribute to the immunopathogenesis of MHV infection in the CNS. In this communication, a large panel of MHV strains was tested for their ability to stimulate class I expression in primary astrocytes in vitro. The data show that the more hepatotropic strains, such as MHV-A59, MHV-1, MHV-2, MHV-3, MHV-D, MHV-K, and MHV-NuU, were potent inducers of class I expression in astrocytes during acute infection, measured by radioimmunoassay. The Kb molecule was preferentially expressed over Db. By contrast, JHMV and several viral strains derived from it did not stimulate the expression of class I molecules. Assays of virus infectivity indicated that the class I-inducing activity did not correlate with the ability of the individual viral strain to replicate in astrocytes. However, exposure of the viruses or the supernatants from infected astrocytes to ultraviolet light abolished the class I-inducing activity, indicating that infectious virus is required for class I expression. These data also suggest that class I expression was induced directly by virus infection, and not by the secretion of a soluble substance into the medium by infected astrocytes. Finally, analyses of A59/JHMV recombinant viral strains suggest that class I-inducing activity resides in one of the A59 structural genes.

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Pewe, Lecia, Shurong Xue et Stanley Perlman. « Infection with Cytotoxic T-Lymphocyte Escape Mutants Results in Increased Mortality and Growth Retardation in Mice Infected with a Neurotropic Coronavirus ». Journal of Virology 72, n^o 7 (1 juillet 1998) : 5912–18. http://dx.doi.org/10.1128/jvi.72.7.5912-5918.1998.

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ABSTRACT C57BL/6 mice infected with mouse hepatitis virus strain JHM (MHV-JHM) develop a chronic demyelinating encephalomyelitis several weeks after inoculation. Previously, we showed that mutations in the immunodominant CD8 T-cell epitope (S-510-518) could be detected in nearly all samples of RNA and virus isolated from these mice. These mutations abrogated recognition by T cells harvested from the central nervous systems of infected mice in direct ex vivo cytotoxicity assays. These results suggested that cytotoxic T-lymphocyte (CTL) escape mutants contributed to virus amplification and the development of clinical disease in mice infected with wild-type virus. In the present study, the importance of these mutations was further evaluated by infecting naive mice with MHV-JHM variants isolated from infected mice and in which epitope S-510-518 was mutated. Compared to mice infected with wild-type virus, variant virus-infected animals showed higher mortality and morbidity manifested by decreased weight gain and neurological signs. Although a delay in the kinetics of virus clearance has been demonstrated in previous studies of CTL escape mutants, this is the first illustration of significant changes in clinical disease resulting from infection with viruses able to evade the CD8 T-cell immune response.

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TOMURO, Jinichi. « Hydrogen Refueling Stations for FCV's in the JHFC Project ». Journal of the Society of Mechanical Engineers 113, n^o 1098 (2010) : 376–79. http://dx.doi.org/10.1299/jsmemag.113.1098_376.

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