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[PMID]: 29432596
[Au] Autor:Kuroda MJ; Sugimoto C; Cai Y; Merino KM; Mehra S; Araínga M; Roy CJ; Midkiff CC; Alvarez X; Didier ES; Kaushal D
[Ad] Address:Division of Immunology, Tulane National Primate Research Center, Covington, Louisiana.
[Ti] Title:High Turnover of Tissue Macrophages Contributes to Tuberculosis Reactivation in Simian Immunodeficiency Virus-Infected Rhesus Macaques.
[So] Source:J Infect Dis;, 2018 Feb 08.
[Is] ISSN:1537-6613
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Background: Tuberculosis (TB) and human immunodeficiency virus (HIV)/acquired immune deficiency syndrome (AIDS) profoundly affect the immune system and synergistically accelerate disease progression. It is believed that CD4+ T-cell depletion by HIV is the major cause of immunodeficiency and reactivation of latent TB. Previous studies demonstrated that blood monocyte turnover concurrent with tissue macrophage death from virus infection better predicted AIDS onset than CD4+ T-cell depletion in macaques infected with simian immunodeficiency virus (SIV). Methods: In this study, we describe the contribution of macrophages to the pathogenesis of Mycobacterium tuberculosis (Mtb)/SIV coinfection in a rhesus macaque model using in vivo BrdU labeling, immunostaining, flow cytometry, and confocal microscopy. Results: We found that increased monocyte and macrophage turnover and levels of SIV-infected lung macrophages correlated with TB reactivation. All Mtb/SIV-coinfected monkeys exhibited declines in CD4+ T cells regardless of reactivation or latency outcomes, negating lower CD4+ T-cell levels as a primary cause of Mtb reactivation. Conclusions: Results suggest that SIV-related damage to macrophages contributes to Mtb reactivation during coinfection. This also supports strategies to target lung macrophages for the treatment of TB.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:Publisher
[do] DOI:10.1093/infdis/jix625

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[PMID]: 29324751
[Au] Autor:Echebli N; Tchitchek N; Dupuy S; Bruel T; Peireira Bittencourt Passaes C; Bosquet N; Le Grand R; Bourgeois C; Favier B; Cheynier R; Lambotte O; Vaslin B
[Ad] Address:CEA, Université Paris Sud, INSERM U1184, Immunology of Viral Infections and Autoimmune Diseases (IMVA), IDMIT Department / IBFJ, Fontenay-aux-Roses, France.
[Ti] Title:Stage-specific IFN-induced and IFN gene expression reveal convergence of type I and type II IFN and highlight their role in both acute and chronic stage of pathogenic SIV infection.
[So] Source:PLoS One;13(1):e0190334, 2018.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Interferons (IFNs) play a major role in controlling viral infections including HIV/SIV infections. Persistent up-regulation of interferon stimulated genes (ISGs) is associated with chronic immune activation and progression in SIV/HIV infections, but the respective contribution of different IFNs is unclear. We analyzed the expression of IFN genes and ISGs in tissues of SIV infected macaques to understand the respective roles of type I and type II IFNs. Both IFN types were induced in lymph nodes during early stage of primary infection and to some extent in rectal biopsies but not in PBMCs. Induction of Type II IFN expression persisted during the chronic phase, in contrast to undetectable induction of type I IFN expression. Global gene expression analysis with a major focus on ISGs revealed that at both acute and chronic infection phases most differentially expressed ISGs were inducible by both type I and type II IFNs and displayed the highest increases, indicating strong convergence and synergy between type I and type II IFNs. The analysis of functional signatures of ISG expression revealed temporal changes in IFN expression patterns identifying phase-specific ISGs. These results suggest that IFN-γ strongly contribute to shape ISG upregulation in addition to type I IFN.
[Mh] MeSH terms primary: Gene Expression
Interferon Type I/genetics
Interferon-gamma/genetics
Simian Acquired Immunodeficiency Syndrome/immunology
[Mh] MeSH terms secundary: Acute Disease
Animals
Chronic Disease
Macaca fascicularis
Simian Immunodeficiency Virus/immunology
Simian Immunodeficiency Virus/physiology
Transcriptome
Virus Replication
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Interferon Type I); 82115-62-6 (Interferon-gamma)
[Em] Entry month:1802
[Cu] Class update date: 180223
[Lr] Last revision date:180223
[Js] Journal subset:IM
[Da] Date of entry for processing:180112
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190334

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[PMID]: 29220358
[Au] Autor:Dorta-Estremera S; Nehete PN; Yang G; He H; Nehete BP; Shelton KA; Barry MA; Sastry KJ
[Ad] Address:The University of Texas MD Anderson Cancer Center, Department of Immunology, Houston, TX, United States of America.
[Ti] Title:Minimally invasive monitoring of CD4 T cells at multiple mucosal tissues after intranasal vaccination in rhesus macaques.
[So] Source:PLoS One;12(12):e0188807, 2017.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Studies in nonhuman primates (NHP) for prospective immune cell monitoring subsequent to infection and/or vaccination usually rely on periodic sampling of the blood samples with only occasional collections of biopsies from mucosal tissues because of safety concerns and practical constraints. Here we present evidence in support of cytobrush sampling of oral, rectal, and genital mucosal tissues as a minimally invasive approach for the phenotypic analyses of different T cells subsets de novo as well as prospectively after intranasal immunization in rhesus macaques. Significant percentages of viable lymphocytes were obtained consistently from both naïve and chronically SIV-infected rhesus macaques. The percentages of CD3+ T cells in the blood were significantly higher compared to those in the mucosal tissues analyzed in the naïve animals, while in the SIV+ animals the CD3+ T cells were significantly elevated in the rectal tissues, relative to all other sites analyzed. In the naïve, but not SIV+ macaques, the rectal and vaginal mucosal tissues, compared to oral mucosa and blood, showed higher diversity and percentages of CD4+ T cells expressing the HIV entry co-receptor CCR5 and mucosal specific adhesion (CD103) as well as activation (HLA-DR) and proliferation (Ki67) markers. Sequential daily cytobrush sampling from the oral, rectal, and genital mucosal tissues was performed in SIV+ animals from an ongoing study where they were administered intranasal immunization with adenoviral vectored vaccines incorporating the green fluorescent protein (GFP) reporter gene. We detected a transient increase in GFP+ CD4 T cells in only oral mucosa suggesting limited mucosal trafficking. In general, CD4+ and CD8+ T cells expressing Ki67 transiently increased in all mucosal tissues, but those expressing the CCR5, HLA-DR, and CD103 markers exhibited minor changes. We propose the minimally invasive cytobrush sampling as a practical approach for effective and prospective immune monitoring of the oral-genital mucosal tissues in NHP.
[Mh] MeSH terms primary: CD4 Lymphocyte Count
CD4-Positive T-Lymphocytes/immunology
Macaca mulatta/immunology
Mucous Membrane/immunology
Viral Vaccines/administration & dosage
[Mh] MeSH terms secundary: Administration, Intranasal
Animals
Female
Flow Cytometry
Male
Simian Acquired Immunodeficiency Syndrome/immunology
Viral Vaccines/immunology
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Viral Vaccines)
[Em] Entry month:1712
[Cu] Class update date: 180218
[Lr] Last revision date:180218
[Js] Journal subset:IM
[Da] Date of entry for processing:171209
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188807

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[PMID]: 28463876
[Au] Autor:Anderson DJ; Politch JA; Zeitlin L; Hiatt A; Kadasia K; Mayer KH; Ruprecht RM; Villinger F; Whaley KJ
[Ad] Address:aDepartments of Obstetrics and Gynecology Boston University School of Medicine, Boston, Massachusetts bMapp Biopharmaceutical, San Diego California cDepartment of Molecular Medicine, Boston University School of Medicine dFenway Health, Harvard Medical School, Boston, Massachusetts eTexas Biomedical Institute, Southwest National Primate Research Center, San Antonio, Texas fNew Iberia Primate Center, New Iberia, Louisiana, USA.
[Ti] Title:Systemic and topical use of monoclonal antibodies to prevent the sexual transmission of HIV.
[So] Source:AIDS;31(11):1505-1517, 2017 Jul 17.
[Is] ISSN:1473-5571
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:: Passive immunization, the transfer of antibodies to a nonimmune individual to provide immunological protection, has been used for over 100 years to prevent and treat human infectious diseases. The introduction of techniques to produce human mAbs has revolutionized the field, and a large number of human mAbs have been licensed for the treatment of cancer, autoimmune and inflammatory diseases. With the recent discovery and production of highly potent broadly neutralizing and other multifunctional antibodies to HIV, mAbs are now being considered for HIV therapy and prophylaxis. In this review, we briefly present recent advances in the anti-HIV mAb field and outline strategies for the selection, engineering and production of human mAbs, including the modification of their structure for optimized stability and function. We also describe results from nonhuman primate studies and phase 1 clinical trials that have tested the safety, tolerability, pharmacokinetics, and efficacy of mAb-based HIV prevention strategies, and discuss the future of parenteral and topical mAb administration for the prevention of HIV transmission.
[Mh] MeSH terms primary: Antibodies, Monoclonal/immunology
Antibodies, Monoclonal/pharmacology
HIV Antibodies/drug effects
HIV Antibodies/immunology
HIV Infections/prevention & control
Immunization, Passive
Pre-Exposure Prophylaxis/methods
Simian Acquired Immunodeficiency Syndrome/prevention & control
[Mh] MeSH terms secundary: Administration, Topical
Animals
Antibodies, Monoclonal/administration & dosage
Female
HIV Infections/transmission
HIV-1/drug effects
Humans
Immunization, Passive/methods
Rectum/virology
Simian Acquired Immunodeficiency Syndrome/transmission
Simian Immunodeficiency Virus/drug effects
Treatment Outcome
Vagina/virology
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:0 (Antibodies, Monoclonal); 0 (HIV Antibodies)
[Em] Entry month:1802
[Cu] Class update date: 180208
[Lr] Last revision date:180208
[Js] Journal subset:IM; X
[Da] Date of entry for processing:170503
[St] Status:MEDLINE
[do] DOI:10.1097/QAD.0000000000001521

  5 / 5588 MEDLINE  
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[PMID]: 29229308
[Au] Autor:Mangus LM; Beck SE; Queen SE; Brill SA; Shirk EN; Metcalf Pate KA; Muth DC; Adams RJ; Gama L; Clements JE; Mankowski JL
[Ad] Address:Department of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
[Ti] Title:Lymphocyte-Dominant Encephalitis and Meningitis in Simian Immunodeficiency Virus-Infected Macaques Receiving Antiretroviral Therapy.
[So] Source:Am J Pathol;188(1):125-134, 2018 01.
[Is] ISSN:1525-2191
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:A retrospective neuropathologic review of 30 SIV-infected pigtailed macaques receiving combination antiretroviral therapy (cART) was conducted. Seventeen animals with lymphocyte-dominant inflammation in the brain and/or meninges that clearly was morphologically distinct from prototypic SIV encephalitis and human immunodeficiency virus encephalitis were identified. Central nervous system (CNS) infiltrates in cART-treated macaques primarily comprised CD20 B cells and CD3 T cells with fewer CD68 macrophages. Inflammation was associated with low levels of SIV RNA in the brain as shown by in situ hybridization, and generally was observed in animals with episodes of cerebrospinal fluid (CSF) viral rebound or sustained plasma and CSF viremia during treatment. Although the lymphocytic CNS inflammation in these macaques shared morphologic characteristics with uncommon immune-mediated neurologic disorders reported in treated HIV patients, including CNS immune reconstitution inflammatory syndrome and neurosymptomatic CSF escape, the high prevalence of CNS lesions in macaques suggests that persistent adaptive immune responses in the CNS also may develop in neuroasymptomatic or mildly impaired HIV patients yet remain unrecognized given the lack of access to CNS tissue for histopathologic evaluation. Continued investigation into the mechanisms and outcomes of CNS inflammation in cART-treated, SIV-infected macaques will advance our understanding of the consequences of residual CNS HIV replication in patients on cART, including the possible contribution of adaptive immune responses to HIV-associated neurocognitive disorders.
[Mh] MeSH terms primary: Anti-Retroviral Agents/therapeutic use
Brain/pathology
Encephalitis/pathology
Lymphocytes/pathology
Meningitis/pathology
Simian Acquired Immunodeficiency Syndrome/pathology
[Mh] MeSH terms secundary: Animals
Encephalitis/complications
Inflammation/pathology
Macaca nemestrina
Male
Meningitis/complications
Simian Acquired Immunodeficiency Syndrome/complications
Simian Acquired Immunodeficiency Syndrome/drug therapy
Simian Immunodeficiency Virus
Viral Load
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Name of substance:0 (Anti-Retroviral Agents)
[Em] Entry month:1801
[Cu] Class update date: 180131
[Lr] Last revision date:180131
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:171213
[St] Status:MEDLINE

  6 / 5588 MEDLINE  
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[PMID]: 28465428
[Au] Autor:Jiang G; Santos Rocha C; Hirao LA; Mendes EA; Tang Y; Thompson GR; Wong JK; Dandekar S
[Ad] Address:Department of Medical Microbiology and Immunology, University of California, Davis, California, USA.
[Ti] Title:HIV Exploits Antiviral Host Innate GCN2-ATF4 Signaling for Establishing Viral Replication Early in Infection.
[So] Source:MBio;8(3), 2017 May 02.
[Is] ISSN:2150-7511
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Antiviral innate host defenses against acute viral infections include suppression of host protein synthesis to restrict viral protein production. Less is known about mechanisms by which viral pathogens subvert host antiviral innate responses for establishing their replication and dissemination. We investigated early innate defense against human immunodeficiency virus (HIV) infection and viral evasion by utilizing human CD4 T cell cultures and a simian immunodeficiency virus (SIV) model of AIDS Our data showed that early host innate defense against the viral infection involves GCN2-ATF4 signaling-mediated suppression of global protein synthesis, which is exploited by the virus for supporting its own replication during early viral infection and dissemination in the gut mucosa. Suppression of protein synthesis and induction of protein kinase GCN2-ATF4 signaling were detected in the gut during acute SIV infection. These changes diminished during chronic viral infection. HIV replication induced by serum deprivation in CD4 T cells was linked to the induction of ATF4 that was recruited to the HIV long terminal repeat (LTR) to promote viral transcription. Experimental inhibition of GCN2-ATF4 signaling either by a specific inhibitor or by amino acid supplementation suppressed the induction of HIV expression. Enhancing ATF4 expression through selenium administration resulted in reactivation of latent HIV as well as in the primary CD4 T cells isolated from patients receiving suppressive antiretroviral therapy (ART). In summary, HIV/SIV exploits the early host antiviral response through GCN2-ATF4 signaling by utilizing ATF4 for activating the viral LTR transcription to establish initial viral replication and is a potential target for HIV prevention and therapy. Understanding how HIV overcomes host antiviral innate defense response in order to establish infection and dissemination is critical for developing prevention and treatment strategies. Most investigations focused on the viral pathogenic mechanisms leading to immune dysfunction following robust viral infection and dissemination. Less is known about mechanisms that enable HIV to establish its presence despite rapid onset of host antiviral innate response. Our novel findings provide insights into the viral strategy that hijacks the host innate response of the suppression of protein biosynthesis to restrict the virus production. The virus leverages transcription factor ATF4 expression during the GCN2-ATF4 signaling response and utilizes it to activate viral transcription through the LTR to support viral transcription and production in both HIV and SIV infections. This unique viral strategy is exploiting the innate response and is distinct from the mechanisms of immune dysfunction after the critical mass of viral loads is generated.
[Mh] MeSH terms primary: Activating Transcription Factor 4/metabolism
CD4-Positive T-Lymphocytes/virology
HIV-1/physiology
Host-Pathogen Interactions
Immunity, Innate
Protein-Serine-Threonine Kinases/metabolism
Virus Replication
[Mh] MeSH terms secundary: Activating Transcription Factor 4/genetics
Animals
CD4-Positive T-Lymphocytes/drug effects
Cells, Cultured
Disease Models, Animal
Gastrointestinal Tract/virology
HIV Infections/drug therapy
HIV Infections/immunology
HIV Infections/virology
HIV-1/immunology
HIV-1/pathogenicity
Humans
Immune Evasion
Macaca mulatta
Protein-Serine-Threonine Kinases/genetics
Selenium/pharmacology
Signal Transduction
Simian Acquired Immunodeficiency Syndrome/immunology
Simian Acquired Immunodeficiency Syndrome/virology
Simian Immunodeficiency Virus
Viral Load
Virus Latency
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (ATF4 protein, human); 145891-90-3 (Activating Transcription Factor 4); EC 2.7.11.1 (EIF2AK4 protein, human); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); H6241UJ22B (Selenium)
[Em] Entry month:1801
[Cu] Class update date: 180126
[Lr] Last revision date:180126
[Js] Journal subset:IM
[Da] Date of entry for processing:170504
[St] Status:MEDLINE

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[PMID]: 29267382
[Au] Autor:Zhang Z; Gu Q; de Manuel Montero M; Bravo IG; Marques-Bonet T; Häussinger D; Münk C
[Ad] Address:Clinic for Gastroenterology, Hepatology, and Infectiology, Medical Faculty, Heinrich-Heine-Universität Düsseldorf, Düsseldorf, Germany.
[Ti] Title:Stably expressed APOBEC3H forms a barrier for cross-species transmission of simian immunodeficiency virus of chimpanzee to humans.
[So] Source:PLoS Pathog;13(12):e1006746, 2017 12.
[Is] ISSN:1553-7374
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:APOBEC3s (A3s) are potent restriction factors of human immunodeficiency virus type 1/simian immunodeficiency viruses (HIV-1/SIV), and can repress cross-species transmissions of lentiviruses. HIV-1 originated from a zoonotic infection of SIV of chimpanzee (SIVcpz) to humans. However, the impact of human A3s on the replication of SIVcpz remains unclear. By using novel SIVcpz reporter viruses, we identified that human APOBEC3B (A3B) and APOBEC3H (A3H) haplotype II strongly reduced the infectivity of SIVcpz, because both of them are resistant to SIVcpz Vifs. We further demonstrated that human A3H inhibited SIVcpz by deaminase dependent as well independent mechanisms. In addition, other stably expressed human A3H haplotypes and splice variants showed strong antiviral activity against SIVcpz. Moreover, most SIV and HIV lineage Vif proteins could degrade chimpanzee A3H, but no Vifs from SIVcpz and SIV of gorilla (SIVgor) lineages antagonized human A3H haplotype II. Expression of human A3H hapII in human T cells efficiently blocked the spreading replication of SIVcpz. The spreading replication of SIVcpz was also restricted by stable A3H in human PBMCs. Thus, we speculate that stably expressed human A3H protects humans against the cross-species transmission of SIVcpz and that SIVcpz spillover to humans may have started in individuals that harbor haplotypes of unstable A3H proteins.
[Mh] MeSH terms primary: Aminohydrolases/metabolism
Disease Transmission, Infectious
Simian Acquired Immunodeficiency Syndrome/transmission
Simian Immunodeficiency Virus
Zoonoses
[Mh] MeSH terms secundary: Animals
Humans
Pan troglodytes
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:EC 3.5.4.- (APOBEC3H protein, human); EC 3.5.4.- (Aminohydrolases)
[Em] Entry month:1801
[Cu] Class update date: 180111
[Lr] Last revision date:180111
[Js] Journal subset:IM
[Da] Date of entry for processing:171222
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006746

  8 / 5588 MEDLINE  
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[PMID]: 29261677
[Au] Autor:Steele AK; Carrasco-Medina L; Sodora DL; Crawley AM
[Ad] Address:Center for Infectious Disease Research, Seattle, WA, United States of America.
[Ti] Title:Increased soluble IL-7 receptor concentrations associate with improved IL-7 therapy outcomes in SIV-infected ART-treated Rhesus macaques.
[So] Source:PLoS One;12(12):e0188427, 2017.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The use of interleukin-7 (IL-7) as an immunorestorative therapeutic has proven effective in HIV infection, cancer and bone marrow transplantation. Mediating its activity through membrane-bound IL-7 receptor α (mCD127), IL-7 therapy increases T-cell numbers and survival. A soluble form, sCD127, is found in plasma, and we have previously identified increased plasma sCD127 concentrations in HIV infection. Furthermore, patients with high sCD127 exhibited the best viral control, implicating a role for IL-7 or sCD127 directly in improved virologic/immunologic outcomes. The role of the cytokine IL-7 in elevating sCD127 levels was addressed here through assessment of retrospective samples obtained from SIV-infected antiretroviral (ART)-treated Rhesus macaques. IL-7 was administered in clustered weekly doses, allowing for an assessment prior, during and following IL-7 administration. The levels of sCD127 remained relatively unchanged during both early SIV infection and following initiation of ART. However, treatment with IL-7 increased sCD127 concentrations in most animals, transiently or persistently, paralleling increased T-cell numbers, correlating significantly with CD8+ T-cell levels. In addition, proliferating CD4+ or CD8+ T-cells (measured by Ki67) increased in association with elevated sCD127 concentrations. Finally, a high concentration of sCD127 in IL7-treated animals was associated with increased retention of T-cells (measured by BrDU). In addition, a lack, or loss of viral control was associated with more pronounced and frequent elevations in plasma sCD127 concentrations with IL-7 therapy. In summary, plasma sCD127 levels in SIV-infected ART-treated macaques was associated with therapeutic IL-7 administration, with higher sCD127 levels in macaques demonstrating the best T-cell responses. This study furthers our knowledge regarding the interrelationship between increased IL-7 levels and elevated sCD127 levels that may have implications for future IL-7 immunotherapeutic approaches in HIV-infected patients.
[Mh] MeSH terms primary: Anti-Retroviral Agents/therapeutic use
Interleukin-7/therapeutic use
Receptors, Interleukin-7/metabolism
Simian Acquired Immunodeficiency Syndrome/drug therapy
Simian Acquired Immunodeficiency Syndrome/virology
Simian Immunodeficiency Virus/physiology
[Mh] MeSH terms secundary: Animals
Anti-Retroviral Agents/pharmacology
CD8-Positive T-Lymphocytes/immunology
Cell Survival/immunology
Interleukin-7/administration & dosage
Interleukin-7/pharmacology
Lymphocyte Activation/immunology
Lymphocyte Count
Macaca mulatta
Receptors, Interleukin-7/blood
Simian Acquired Immunodeficiency Syndrome/blood
Simian Acquired Immunodeficiency Syndrome/immunology
Simian Immunodeficiency Virus/drug effects
Solubility
Treatment Outcome
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Anti-Retroviral Agents); 0 (Interleukin-7); 0 (Receptors, Interleukin-7); 0 (interleukin-7 receptor, alpha chain)
[Em] Entry month:1801
[Cu] Class update date: 180108
[Lr] Last revision date:180108
[Js] Journal subset:IM
[Da] Date of entry for processing:171221
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188427

  9 / 5588 MEDLINE  
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[PMID]: 27779180
[Au] Autor:Kotb A; Klippert A; Daskalaki M; Sauermann U; Stahl-Hennig C; Neumann B
[Ad] Address:Unit of Infection Models, German Primate Center, Leibniz Institute for Primate Research, Goettingen, Germany.
[Ti] Title:Elevated granzyme B B-cell level in SIV-infection correlate with viral load and low CD4 T-cell count.
[So] Source:Immunol Cell Biol;95(3):316-320, 2017 03.
[Is] ISSN:1440-1711
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Granzyme B-expressing (GrB ) B cells are thought to contribute to immune dysfunctions in HIV patients, but so far their exact role is unknown. This report demonstrates for the first time the existence of GrB B cells in SIV-infected rhesus macaques, which represent the most commonly used nonhuman primate model for HIV research. Similar to HIV patients, we found significantly higher frequencies of these cells in the blood of chronically SIV-infected rhesus monkeys compared with uninfected healthy ones. These frequencies correlated with plasma viral load and inversely with absolute CD4 T-cell counts. When investigating GrB B cells in different compartments, levels were highest in blood, spleen and bone marrow, but considerably lower in lymph nodes and tonsils. Analysis of expression of various surface markers on this particular B-cell subset in SIV-infected macaques revealed differences between the phenotype in macaques and in humans. GrB B cells in SIV-infected rhesus macaques exhibit an elevated expression of CD5, CD10, CD25 and CD27, while expression of CD19, CD185 and HLA-DR is reduced. In contrast to human GrB B cells, we did not observe a significantly increased expression of CD43 and CD86. B-cell receptor stimulation in combination with IL-21 of purified B cells from healthy animals led to the induction of GrB expression. Furthermore, initial functional analyses indicated a regulatory role on T-cell proliferation. Overall, our data pave the way for longitudinal analyses including studies on the functionality of GrB B cells in the nonhuman primate model for AIDS.
[Mh] MeSH terms primary: B-Lymphocytes/metabolism
CD4-Positive T-Lymphocytes/immunology
Granzymes/metabolism
Simian Acquired Immunodeficiency Syndrome/immunology
Simian Acquired Immunodeficiency Syndrome/virology
Simian Immunodeficiency Virus/physiology
Viral Load/immunology
[Mh] MeSH terms secundary: Animals
CD4 Lymphocyte Count
Disease Progression
Female
Humans
Interleukin-10/metabolism
Macaca mulatta
Male
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:130068-27-8 (Interleukin-10); EC 3.4.21.- (Granzymes)
[Em] Entry month:1711
[Cu] Class update date: 171216
[Lr] Last revision date:171216
[Js] Journal subset:IM
[Da] Date of entry for processing:161026
[St] Status:MEDLINE
[do] DOI:10.1038/icb.2016.96

  10 / 5588 MEDLINE  
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[PMID]: 29134258
[Au] Autor:Semler MR; Wiseman RW; Karl JA; Graham ME; Gieger SM; O'Connor DH
[Ad] Address:Department of Pathology and Laboratory Medicine, University of Wisconsin-Madison, 555 Science Drive, Madison, WI, 53705, USA.
[Ti] Title:Novel full-length major histocompatibility complex class I allele discovery and haplotype definition in pig-tailed macaques.
[So] Source:Immunogenetics;, 2017 Nov 13.
[Is] ISSN:1432-1211
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Pig-tailed macaques (Macaca nemestrina, Mane) are important models for human immunodeficiency virus (HIV) studies. Their infectability with minimally modified HIV makes them a uniquely valuable animal model to mimic human infection with HIV and progression to acquired immunodeficiency syndrome (AIDS). However, variation in the pig-tailed macaque major histocompatibility complex (MHC) and the impact of individual transcripts on the pathogenesis of HIV and other infectious diseases is understudied compared to that of rhesus and cynomolgus macaques. In this study, we used Pacific Biosciences single-molecule real-time circular consensus sequencing to describe full-length MHC class I (MHC-I) transcripts for 194 pig-tailed macaques from three breeding centers. We then used the full-length sequences to infer Mane-A and Mane-B haplotypes containing groups of MHC-I transcripts that co-segregate due to physical linkage. In total, we characterized full-length open reading frames (ORFs) for 313 Mane-A, Mane-B, and Mane-I sequences that defined 86 Mane-A and 106 Mane-B MHC-I haplotypes. Pacific Biosciences technology allows us to resolve these Mane-A and Mane-B haplotypes to the level of synonymous allelic variants. The newly defined haplotypes and transcript sequences containing full-length ORFs provide an important resource for infectious disease researchers as certain MHC haplotypes have been shown to provide exceptional control of simian immunodeficiency virus (SIV) replication and prevention of AIDS-like disease in nonhuman primates. The increased allelic resolution provided by Pacific Biosciences sequencing also benefits transplant research by allowing researchers to more specifically match haplotypes between donors and recipients to the level of nonsynonymous allelic variation, thus reducing the risk of graft-versus-host disease.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 171114
[Lr] Last revision date:171114
[St] Status:Publisher
[do] DOI:10.1007/s00251-017-1042-2


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