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[PMID]: 28637388
[Au] Autor:Haley SA; Atwood WJ
[Ad] Address:Department of Molecular Biology, Cell Biology, and Biochemistry, Brown University, Providence, Rhode Island 02912; email: sheila_haley@brown.edu , walter_atwood@brown.edu.
[Ti] Title:Progressive Multifocal Leukoencephalopathy: Endemic Viruses and Lethal Brain Disease.
[So] Source:Annu Rev Virol;4(1):349-367, 2017 Sep 29.
[Is] ISSN:2327-0578
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:In 1971, the first human polyomavirus was isolated from the brain of a patient who died from a rapidly progressing demyelinating disease known as progressive multifocal leukoencephalopathy. The virus was named JC virus after the initials of the patient. In that same year a second human polyomavirus was discovered in the urine of a kidney transplant patient and named BK virus. In the intervening years it became clear that both viruses were widespread in the human population but only rarely caused disease. The past decade has witnessed the discovery of eleven new human polyomaviruses, two of which cause unusual and rare cancers. We present an overview of the history of these viruses and the evolution of JC polyomavirus-induced progressive multifocal leukoencephalopathy over three different epochs. We review what is currently known about JC polyomavirus, what is suspected, and what remains to be done to understand the biology of how this mostly harmless endemic virus gives rise to lethal disease.
[Mh] MeSH terms primary: JC Virus/pathogenicity
Leukoencephalopathy, Progressive Multifocal/virology
Polyomavirus/isolation & purification
[Mh] MeSH terms secundary: Acquired Immunodeficiency Syndrome/complications
Acquired Immunodeficiency Syndrome/virology
Animals
Autoimmune Diseases/virology
BK Virus/isolation & purification
BK Virus/pathogenicity
Humans
JC Virus/isolation & purification
Leukoencephalopathy, Progressive Multifocal/etiology
Mice
Multiple Sclerosis/complications
Polyomavirus/classification
Polyomavirus/pathogenicity
Polyomavirus Infections/virology
Tumor Virus Infections/virology
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1710
[Cu] Class update date: 171027
[Lr] Last revision date:171027
[Js] Journal subset:IM
[Da] Date of entry for processing:170623
[St] Status:MEDLINE
[do] DOI:10.1146/annurev-virology-101416-041439

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[PMID]: 28282446
[Au] Autor:Mühle M; Lehmann M; Hoffmann K; Stern D; Kroniger T; Luttmann W; Denner J
[Ad] Address:Robert Koch Institute, Berlin, Germany.
[Ti] Title:Antigenic and immunosuppressive properties of a trimeric recombinant transmembrane envelope protein gp41 of HIV-1.
[So] Source:PLoS One;12(3):e0173454, 2017.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The transmembrane envelope (TM) protein gp41 of the human immunodeficiency virus-1 (HIV-1) plays an important role during virus infection inducing the fusion of the viral and cellular membranes. In addition, there are indications that the TM protein plays a role in the immunopathogenesis leading to the acquired immunodeficiency syndrome (AIDS). Inactivated virus particles and recombinant gp41 have been reported to inhibit lymphocyte proliferation, as well as to alter cytokine release and gene expression. The same was shown for a peptide corresponding to a highly conserved domain of all retroviral TM proteins, the immunosuppressive domain. Due to its propensity to aggregate and to be expressed at low levels, studies comprising authentic gp41 produced in eukaryotic cells are extremely rare. Here we describe the production of a secreted, soluble recombinant gp41 in 293 cells. The antigen was purified to homogeneity and characterised thoroughly by various biochemical and immunological methods. It was shown that the protein was glycosylated and assembled into trimers. Binding studies by ELISA and surface plasmon resonance using conformation-specific monoclonal antibodies implied a six-helix bundle conformation. The low binding of broadly neutralising antibodies (bnAb) directed against the membrane proximal external region (MPER) suggested that this gp41 is probably not suited as vaccine to induce such bnAb. Purified gp41 bound to monocytes and to a lesser extent to lymphocytes and triggered the production of specific cytokines when added to normal peripheral blood mononuclear cells. In addition, gp41 expressed on target cells inhibited the antigen-specific response of murine CD8+ T cells by drastically impairing their IFNγ production. To our knowledge, this is the first comprehensive analysis of a gp41 produced in eukaryotic cells including its immunosuppressive properties. Our data provide another line of evidence that gp41 might be directly involved in HIV-1 immunopathogenesis through modulation of the cytokine release and active inhibition of immune responses.
[Mh] MeSH terms primary: Antigens, Viral/pharmacology
CD8-Positive T-Lymphocytes/immunology
HIV Envelope Protein gp41/pharmacology
HIV-1/immunology
Immune Tolerance/drug effects
Protein Multimerization
[Mh] MeSH terms secundary: Animals
Antigens, Viral/genetics
Antigens, Viral/immunology
HEK293 Cells
HIV Envelope Protein gp41/genetics
HIV Envelope Protein gp41/immunology
HIV-1/genetics
Humans
Interferon-gamma
Mice
Mice, Transgenic
Recombinant Proteins/genetics
Recombinant Proteins/immunology
Recombinant Proteins/pharmacology
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Antigens, Viral); 0 (HIV Envelope Protein gp41); 0 (IFNG protein, mouse); 0 (Recombinant Proteins); 0 (gp41 protein, Human immunodeficiency virus 1); 82115-62-6 (Interferon-gamma)
[Em] Entry month:1708
[Cu] Class update date: 170817
[Lr] Last revision date:170817
[Js] Journal subset:IM
[Da] Date of entry for processing:170311
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0173454

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[PMID]: 28216434
[Au] Autor:Liu X; Pichulik T; Wolz OO; Dang TM; Stutz A; Dillen C; Delmiro Garcia M; Kraus H; Dickhöfer S; Daiber E; Münzenmayer L; Wahl S; Rieber N; Kümmerle-Deschner J; Yazdi A; Franz-Wachtel M; Macek B; Radsak M; Vogel S; Schulte B; Walz JS; Hartl D; Latz E; Stilgenbauer S; Grimbacher B; Miller L; Brunner C; Wolz C; Weber ANR
[Ad] Address:Interfaculty Institute for Cell Biology, Department of Immunology, University of Tübingen, Tübingen, Germany.
[Ti] Title:Human NACHT, LRR, and PYD domain-containing protein 3 (NLRP3) inflammasome activity is regulated by and potentially targetable through Bruton tyrosine kinase.
[So] Source:J Allergy Clin Immunol;140(4):1054-1067.e10, 2017 Oct.
[Is] ISSN:1097-6825
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: The Nod-like receptor NACHT, LRR, and PYD domain-containing protein 3 (NLRP3) and Bruton tyrosine kinase (BTK) are protagonists in innate and adaptive immunity, respectively. NLRP3 senses exogenous and endogenous insults, leading to inflammasome activation, which occurs spontaneously in patients with Muckle-Wells syndrome; BTK mutations cause the genetic immunodeficiency X-linked agammaglobulinemia (XLA). However, to date, few proteins that regulate NLRP3 inflammasome activity in human primary immune cells have been identified, and clinically promising pharmacologic targeting strategies remain elusive. OBJECTIVE: We sought to identify novel regulators of the NLRP3 inflammasome in human cells with a view to exploring interference with inflammasome activity at the level of such regulators. METHODS: After proteome-wide phosphoproteomics, the identified novel regulator BTK was studied in human and murine cells by using pharmacologic and genetic BTK ablation. RESULTS: Here we show that BTK is a critical regulator of NLRP3 inflammasome activation: pharmacologic (using the US Food and Drug Administration-approved inhibitor ibrutinib) and genetic (in patients with XLA and Btk knockout mice) BTK ablation in primary immune cells led to reduced IL-1ß processing and secretion in response to nigericin and the Staphylococcus aureus toxin leukocidin AB (LukAB). BTK affected apoptosis-associated speck-like protein containing a CARD (ASC) speck formation and caspase-1 cleavage and interacted with NLRP3 and ASC. S aureus infection control in vivo and IL-1ß release from cells of patients with Muckle-Wells syndrome were impaired by ibrutinib. Notably, IL-1ß processing and release from immune cells isolated from patients with cancer receiving ibrutinib therapy were reduced. CONCLUSION: Our data suggest that XLA might result in part from genetic inflammasome deficiency and that NLRP3 inflammasome-linked inflammation could potentially be targeted pharmacologically through BTK.
[Mh] MeSH terms primary: Agammaglobulinemia/genetics
Cryopyrin-Associated Periodic Syndromes/genetics
Genetic Diseases, X-Linked/genetics
Inflammasomes/metabolism
NLR Family, Pyrin Domain-Containing 3 Protein/metabolism
Protein-Tyrosine Kinases/metabolism
Staphylococcal Infections/immunology
Staphylococcus aureus/immunology
[Mh] MeSH terms secundary: Adaptive Immunity
Adaptor Proteins, Signal Transducing
Animals
Apoptosis Regulatory Proteins
Bacterial Proteins/immunology
Cells, Cultured
Humans
Immunity, Innate
Leukocidins/immunology
Mice
Mice, Inbred C57BL
Mice, Knockout
Molecular Targeted Therapy
Nigericin/immunology
Protein-Tyrosine Kinases/genetics
Proteomics
Pyrin Domain/genetics
Receptors, Cytoplasmic and Nuclear/metabolism
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Adaptor Proteins, Signal Transducing); 0 (Apoptosis Regulatory Proteins); 0 (Bacterial Proteins); 0 (Inflammasomes); 0 (Leukocidins); 0 (NLR Family, Pyrin Domain-Containing 3 Protein); 0 (NLRP1 protein, human); 0 (NLRP3 protein, human); 0 (Receptors, Cytoplasmic and Nuclear); 0 (lamin B receptor); 0 (leukocidin AB, Staphylococcus aureus); EC 2.7.10.1 (Agammaglobulinaemia tyrosine kinase); EC 2.7.10.1 (Protein-Tyrosine Kinases); RRU6GY95IS (Nigericin)
[Em] Entry month:1710
[Cu] Class update date: 171023
[Lr] Last revision date:171023
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:170221
[St] Status:MEDLINE

  4 / 2487 MEDLINE  
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[PMID]: 28093272
[Au] Autor:Mallard J; Papazian E; Soulas C; Nolan DJ; Salemi M; Williams KC
[Ad] Address:Department of Biology, Boston College, Chestnut Hill, MA, USA.
[Ti] Title:A method for obtaining simian immunodeficiency virus RNA sequences from laser capture microdissected and immune captured CD68+ and CD163+ macrophages from frozen tissue sections of bone marrow and brain.
[So] Source:J Immunol Methods;442:59-63, 2017 Mar.
[Is] ISSN:1872-7905
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Laser capture microdissection (LCM) is used to extract cells or tissue regions for analysis of RNA, DNA or protein. Several methods of LCM are established for different applications, but a protocol for consistently obtaining lentiviral RNA from LCM captured immune cell populations is not described. Obtaining optimal viral RNA for analysis of viral genes from immune-captured cells using immunohistochemistry (IHC) and LCM is challenging. IHC protocols have long antibody incubation times that increase risk of RNA degradation. But, immune capture of specific cell populations like macrophages without staining for virus cannot result in obtaining only a fraction of cells which are productively lentivirally infected. In this study we sought to obtain simian immunodeficiency virus (SIV) RNA from SIV gp120+ and CD68+ monocyte/macrophages in bone marrow (BM) and CD163+ perivascular macrophages in brain of SIV-infected rhesus macaques. Here, we report an IHC protocol with RNase inhibitors that consistently results in optimal quantity and yield of lentiviral RNA from LCM-captured immune cells.
[Mh] MeSH terms primary: Antigens, CD/analysis
Antigens, Differentiation, Myelomonocytic/analysis
Bone Marrow/immunology
Brain/immunology
Immunohistochemistry
Laser Capture Microdissection
Macrophages/immunology
RNA, Viral/genetics
Receptors, Cell Surface/analysis
Sequence Analysis, RNA
Simian Acquired Immunodeficiency Syndrome/genetics
Simian Immunodeficiency Virus/genetics
[Mh] MeSH terms secundary: Animals
Biomarkers/analysis
Bone Marrow/virology
Brain/virology
Macaca mulatta
Macrophages/virology
Membrane Glycoproteins/genetics
Membrane Glycoproteins/immunology
RNA, Viral/isolation & purification
Reverse Transcriptase Polymerase Chain Reaction
Simian Acquired Immunodeficiency Syndrome/immunology
Simian Acquired Immunodeficiency Syndrome/virology
Simian Immunodeficiency Virus/immunology
Simian Immunodeficiency Virus/isolation & purification
Viral Envelope Proteins/genetics
Viral Envelope Proteins/immunology
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Antigens, CD); 0 (Antigens, Differentiation, Myelomonocytic); 0 (Biomarkers); 0 (CD163 antigen); 0 (CD68 antigen, human); 0 (Membrane Glycoproteins); 0 (RNA, Viral); 0 (Receptors, Cell Surface); 0 (Viral Envelope Proteins); 0 (gp120 protein, Simian immunodeficiency virus)
[Em] Entry month:1707
[Cu] Class update date: 170713
[Lr] Last revision date:170713
[Js] Journal subset:IM
[Da] Date of entry for processing:170118
[St] Status:MEDLINE

  5 / 2487 MEDLINE  
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[PMID]: 27928002
[Au] Autor:Kasturi SP; Kozlowski PA; Nakaya HI; Burger MC; Russo P; Pham M; Kovalenkov Y; Silveira EL; Havenar-Daughton C; Burton SL; Kilgore KM; Johnson MJ; Nabi R; Legere T; Sher ZJ; Chen X; Amara RR; Hunter E; Bosinger SE; Spearman P; Crotty S; Villinger F; Derdeyn CA; Wrammert J; Pulendran B
[Ad] Address:Emory Vaccine Center/Yerkes National Primate Research Center at Emory University, Atlanta, Georgia, USA.
[Ti] Title:Adjuvanting a Simian Immunodeficiency Virus Vaccine with Toll-Like Receptor Ligands Encapsulated in Nanoparticles Induces Persistent Antibody Responses and Enhanced Protection in TRIM5α Restrictive Macaques.
[So] Source:J Virol;91(4), 2017 Feb 15.
[Is] ISSN:1098-5514
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Our previous work has shown that antigens adjuvanted with ligands specific for Toll-like receptor 4 (TLR4) and TLR7/8 encapsulated in poly(lactic-co-glycolic) acid (PLGA)-based nanoparticles (NPs) induce robust and durable immune responses in mice and macaques. We investigated the efficacy of these NP adjuvants in inducing protective immunity against simian immunodeficiency virus (SIV). Rhesus macaques (RMs) were immunized with NPs containing TLR4 and TLR7/8 agonists mixed with soluble recombinant SIVmac239-derived envelope (Env) gp140 and Gag p55 (protein) or with virus-like particles (VLPs) containing SIVmac239 Env and Gag. NP-adjuvanted vaccines induced robust innate responses, antigen-specific antibody responses of a greater magnitude and persistence, and enhanced plasmablast responses compared to those achieved with alum-adjuvanted vaccines. NP-adjuvanted vaccines induced antigen-specific, long-lived plasma cells (LLPCs), which persisted in the bone marrow for several months after vaccination. NP-adjuvanted vaccines induced immune responses that were associated with enhanced protection against repeated low-dose, intravaginal challenges with heterologous SIVsmE660 in animals that carried TRIM5α restrictive alleles. The protection induced by immunization with protein-NP correlated with the prechallenge titers of Env-specific IgG antibodies in serum and vaginal secretions. However, no such correlate was apparent for immunization with VLP-NP or alum as the adjuvant. Transcriptional profiling of peripheral blood mononuclear cells isolated within the first few hours to days after primary vaccination revealed that NP-adjuvanted vaccines induced a molecular signature similar to that induced by the live attenuated yellow fever viral vaccine. This systems approach identified early blood transcriptional signatures that correlate with Env-specific antibody responses in vaginal secretions and protection against infection. These results demonstrate the adjuvanticity of the NP adjuvant in inducing persistent and protective antibody responses against SIV in RMs with implications for the design of vaccines against human immunodeficiency virus (HIV). IMPORTANCE: The results of the RV144 HIV vaccine trial, which demonstrated a rapid waning of protective immunity with time, have underscored the need to develop strategies to enhance the durability of protective immune responses. Our recent work in mice has highlighted the capacity of nanoparticle-encapsulated TLR ligands (NP) to induce potent and durable antibody responses that last a lifetime in mice. In the present study, we evaluated the ability of these NP adjuvants to promote robust and durable protective immune responses against SIV in nonhuman primates. Our results demonstrate that immunization of rhesus macaques with NP adjuvants mixed with soluble SIV Env or a virus-like particle form of Env (VLP) induces potent and durable Env-specific antibody responses in the serum and in vaginal secretions. These responses were superior to those induced by alum adjuvant, and they resulted in enhanced protection against a low-dose intravaginal challenge with a heterologous strain of SIV in animals with TRIM5a restrictive alleles. These results highlight the potential for such NP TLR L adjuvants in promoting robust and durable antibody responses against HIV in the next generation of HIV immunogens currently being developed.
[Mh] MeSH terms primary: Adjuvants, Immunologic
Antibodies, Viral/immunology
Nanoparticles
SAIDS Vaccines/immunology
Simian Acquired Immunodeficiency Syndrome/immunology
Simian Immunodeficiency Virus/immunology
[Mh] MeSH terms secundary: Animals
Antigens, Viral/immunology
CD4-Positive T-Lymphocytes/immunology
CD4-Positive T-Lymphocytes/metabolism
Carrier Proteins/metabolism
Cluster Analysis
Female
Gene Expression Profiling
Immunization Schedule
Immunoglobulin G/immunology
Ligands
Lymphocyte Count
Plasma Cells/immunology
Plasma Cells/metabolism
SAIDS Vaccines/administration & dosage
Simian Acquired Immunodeficiency Syndrome/metabolism
Simian Acquired Immunodeficiency Syndrome/mortality
Simian Acquired Immunodeficiency Syndrome/prevention & control
Toll-Like Receptor 4/metabolism
Viral Envelope Proteins/immunology
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Adjuvants, Immunologic); 0 (Antibodies, Viral); 0 (Antigens, Viral); 0 (Carrier Proteins); 0 (Immunoglobulin G); 0 (Ligands); 0 (SAIDS Vaccines); 0 (Toll-Like Receptor 4); 0 (Viral Envelope Proteins)
[Em] Entry month:1705
[Cu] Class update date: 170731
[Lr] Last revision date:170731
[Js] Journal subset:IM
[Da] Date of entry for processing:161209
[St] Status:MEDLINE

  6 / 2487 MEDLINE  
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[PMID]: 27903799
[Au] Autor:Wetzel KS; Yi Y; Elliott ST; Romero D; Jacquelin B; Hahn BH; Muller-Trutwin M; Apetrei C; Pandrea I; Collman RG
[Ad] Address:Department of Medicine and Penn Center for AIDS Research, University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania, USA.
[Ti] Title:CXCR6-Mediated Simian Immunodeficiency Virus SIVagmSab Entry into Sabaeus African Green Monkey Lymphocytes Implicates Widespread Use of Non-CCR5 Pathways in Natural Host Infections.
[So] Source:J Virol;91(4), 2017 Feb 15.
[Is] ISSN:1098-5514
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:African green monkeys (AGM) and sooty mangabeys (SM) are well-studied natural hosts of simian immunodeficiency virus (SIV) that do not progress to AIDS when infected with their species-specific viruses. Natural hosts of SIV express very low levels of the canonical entry coreceptor CCR5, and recent studies have shown that CCR5 is dispensable for SIV infection of SM in vivo and that blocking of CCR5 does not prevent ex vivo infection of peripheral blood mononuclear cells (PBMC) from SM or vervet AGM. In both hosts, CXCR6 is an efficient entry pathway in vitro Here we investigated the use of species-matched CXCR6 and other alternative coreceptors by SIVagmSab, which infects sabaeus AGM. We cloned sabaeus CD4 and 10 candidate coreceptors. Species-matched CXCR6, CCR5, and GPR15 mediated robust entry into transfected cells by pseudotypes carrying SIVagmSab92018ivTF Env, with lower-level entry through GPR1 and APJ. We cloned genetically divergent env genes from the plasma of two wild-infected sabaeus AGM and found similar patterns of coreceptor use. Titration experiments showed that CXCR6 and CCR5 were more efficient than other coreceptors when tested at limiting CD4/coreceptor levels. Finally, blocking of CXCR6 with its ligand CXCL16 significantly inhibited SIVagmSab replication in sabaeus PBMC and had a greater impact than did the CCR5 blocker maraviroc, confirming the use of CXCR6 in primary lymphocyte infection. These data suggest a new paradigm for SIV infection of natural host species, whereby a shared outcome of virus-host coevolution is the use of CXCR6 or other alternative coreceptors for entry, which may direct SIV toward CD4 T cell subsets and anatomical sites that support viral replication without disrupting immune homeostasis and function. IMPORTANCE: Natural hosts of SIV do not progress to AIDS, in stark contrast to pathogenic human immunodeficiency virus type 1 (HIV-1)-human and SIVmac-macaque infections. Identifying how natural hosts avoid immunodeficiency can elucidate key mechanisms of pathogenesis. It is known that despite high viral loads, natural hosts have a low frequency of CD4 cells expressing the SIV coreceptor CCR5. In this study, we demonstrate the efficient use of the coreceptor CXCR6 by SIVagmSab to infect sabaeus African green monkey lymphocytes. In conjunction with studies of SIVsmm, which infects sooty mangabeys, and SIVagmVer, which infects vervet monkeys, our data suggest a unifying model whereby in natural hosts, in which the CCR5 expression level is low, the use of CXCR6 or other coreceptors to mediate infection may target SIV toward distinct cell populations that are able to support high-level viral replication without causing a loss of CD4 T cell homeostasis and lymphoid tissue damage that lead to AIDS in HIV-1 and SIVmac infections.
[Mh] MeSH terms primary: Lymphocytes/metabolism
Lymphocytes/virology
Receptors, CCR5/metabolism
Receptors, CCR6/metabolism
Simian Acquired Immunodeficiency Syndrome/metabolism
Simian Acquired Immunodeficiency Syndrome/virology
Simian Immunodeficiency Virus/physiology
Virus Internalization
[Mh] MeSH terms secundary: Animals
CD4-Positive T-Lymphocytes/immunology
CD4-Positive T-Lymphocytes/metabolism
CD4-Positive T-Lymphocytes/virology
Cercopithecus aethiops
Cloning, Molecular
Host-Pathogen Interactions
Lymphocytes/immunology
Phylogeny
Receptors, CCR5/genetics
Receptors, CCR6/genetics
Receptors, Virus/metabolism
Sequence Analysis, DNA
Simian Acquired Immunodeficiency Syndrome/immunology
Simian Immunodeficiency Virus/classification
Viral Envelope Proteins/genetics
Viral Envelope Proteins/metabolism
Viral Tropism
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Receptors, CCR5); 0 (Receptors, CCR6); 0 (Receptors, Virus); 0 (Viral Envelope Proteins)
[Em] Entry month:1705
[Cu] Class update date: 170902
[Lr] Last revision date:170902
[Js] Journal subset:IM
[Da] Date of entry for processing:161202
[St] Status:MEDLINE

  7 / 2487 MEDLINE  
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[PMID]: 27895171
[Au] Autor:Cecchinato V; Bernasconi E; Speck RF; Proietti M; Sauermann U; D'Agostino G; Danelon G; Rezzonico Jost T; Grassi F; Raeli L; Schöni-Affolter F; Stahl-Hennig C; Uguccioni M; Swiss HIV Cohort Study
[Ad] Address:Institute for Research in Biomedicine, University of Italian Switzerland, 6500 Bellinzona, Switzerland; mariagrazia.uguccioni@irb.usi.ch valentina.cecchinato@irb.usi.ch.
[Ti] Title:Impairment of CCR6+ and CXCR3+ Th Cell Migration in HIV-1 Infection Is Rescued by Modulating Actin Polymerization.
[So] Source:J Immunol;198(1):184-195, 2017 Jan 01.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:CD4 T cell repopulation of the gut is rarely achieved in HIV-1-infected individuals who are receiving clinically effective antiretroviral therapy. Alterations in the integrity of the mucosal barrier have been indicated as a cause for chronic immune activation and disease progression. In this study, we present evidence that persistent immune activation causes impairment of lymphocytes to respond to chemotactic stimuli, thus preventing their trafficking from the blood stream to peripheral organs. CCR6 and CXCR3 Th cells accumulate in the blood of aviremic HIV-1-infected patients on long-term antiretroviral therapy, and their frequency in the circulation positively correlates to levels of soluble CD14 in plasma, a marker of chronic immune activation. Th cells show an impaired response to chemotactic stimuli both in humans and in the pathogenic model of SIV infection, and this defect is due to hyperactivation of cofilin and inefficient actin polymerization. Taking advantage of a murine model of chronic immune activation, we demonstrate that cytoskeleton remodeling, induced by okadaic acid, restores lymphocyte migration in response to chemokines, both in vitro and in vivo. This study calls for novel pharmacological approaches in those pathological conditions characterized by persistent immune activation and loss of trafficking of T cell subsets to niches that sustain their maturation and activities.
[Mh] MeSH terms primary: Actins/metabolism
Chemotaxis, Leukocyte/immunology
HIV Infections/immunology
T-Lymphocytes, Helper-Inducer/immunology
[Mh] MeSH terms secundary: Animals
Cell Separation
Cytoskeleton/metabolism
Enzyme-Linked Immunosorbent Assay
Flow Cytometry
HIV-1
Humans
Immunohistochemistry
Macaca mulatta
Mice
Mice, Inbred C57BL
Polymerization
Real-Time Polymerase Chain Reaction
Receptors, CCR6/immunology
Receptors, CXCR3/immunology
Simian Acquired Immunodeficiency Syndrome/immunology
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Actins); 0 (CCR6 protein, human); 0 (CXCR3 protein, human); 0 (Receptors, CCR6); 0 (Receptors, CXCR3)
[Em] Entry month:1708
[Cu] Class update date: 170808
[Lr] Last revision date:170808
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:161130
[St] Status:MEDLINE

  8 / 2487 MEDLINE  
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[PMID]: 27807233
[Au] Autor:Wrensch F; Hoffmann M; Gärtner S; Nehlmeier I; Winkler M; Pöhlmann S
[Ad] Address:Infection Biology Unit, German Primate Center, Göttingen, Germany.
[Ti] Title:Virion Background and Efficiency of Virion Incorporation Determine Susceptibility of Simian Immunodeficiency Virus Env-Driven Viral Entry to Inhibition by IFITM Proteins.
[So] Source:J Virol;91(2), 2017 Jan 15.
[Is] ISSN:1098-5514
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Interferon-induced transmembrane proteins (IFITMs) can inhibit the cellular entry of several enveloped viruses, including simian immunodeficiency virus (SIV). The blockade of SIV by IFITMs is isolate specific, raising the question of which parameters impact sensitivity to IFITM. We show that the virion context in which SIV-Env is presented and the efficiency of virion incorporation determine Env susceptibility to inhibition by IFITMs. Thus, determinants other than the nature of the envelope protein can impact the IFITM sensitivity of viral entry. IMPORTANCE: The host cell-encoded IFITM proteins can block viral entry and are an important component of the innate defenses against viral infection. However, the determinants controlling whether a virus is susceptible to blockade by IFITM proteins are incompletely understood. Our study shows that the amount of envelope proteins incorporated into virions as well as the nature of the virion particle itself can impact the sensitivity of viral entry to IFITMs. These results show for the first time that determinants other than the viral envelope protein can impact sensitivity to IFITM and have implications for the interpretation of previously published data on inhibition of viruses by IFITM proteins. Moreover, our findings might help to define the mechanism underlying the antiviral activity of IFITM proteins.
[Mh] MeSH terms primary: Disease Susceptibility
Host-Pathogen Interactions
Simian Acquired Immunodeficiency Syndrome/virology
Virion
Virus Assembly
Virus Internalization
[Mh] MeSH terms secundary: Animals
Cell Line
Gene Knockdown Techniques
Genetic Vectors/genetics
Genome, Viral
Humans
Simian Immunodeficiency Virus/physiology
Transduction, Genetic
Viral Envelope Proteins/metabolism
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Viral Envelope Proteins)
[Em] Entry month:1705
[Cu] Class update date: 170515
[Lr] Last revision date:170515
[Js] Journal subset:IM
[Da] Date of entry for processing:161104
[St] Status:MEDLINE

  9 / 2487 MEDLINE  
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[PMID]: 27682074
[Au] Autor:Auvinen E
[Ad] Address:Department of Virology, University of Helsinki and Helsinki University Hospital, Haartmaninkatu 3, POB 21, 00014, Helsinki, Finland. Eeva.auvinen@helsinki.fi.
[Ti] Title:Diagnostic and Prognostic Value of MicroRNA in Viral Diseases.
[So] Source:Mol Diagn Ther;21(1):45-57, 2017 Feb.
[Is] ISSN:1179-2000
[Cp] Country of publication:New Zealand
[La] Language:eng
[Ab] Abstract:Virology is probably the most rapidly developing field within clinical laboratory medicine. Adequate diagnostic methods exist for the diagnostics of most acute viral infections. However, emergence of pathogenic viruses or virus strains and new disease associations of known viruses require the establishment of new diagnostic methods, sometimes very rapidly. In the field of chronic or persistent viral diseases, particularly those involving potential of malignant or fatal development, there is a constant need for improved differential diagnostics, monitoring, prognosis and risk assessment. Increasing understanding of disease pathogenesis also enables better patient management and personalized medicine, where companion diagnostics can offer precise and specific tools for individual care. Very often the new tools are offered by molecular diagnostic techniques, and this includes the detection of microRNAs (miRNAs). miRNAs are small regulatory RNA molecules, which regulate the expression of their target genes. They are encoded both by viruses and their host, and both can target either viral or cellular gene expression. In this review the diagnostic possibilities offered by miRNA will be discussed. The focus will be on selected viral and human miRNAs in viral diseases, and examples of miRNAs of putative diagnostic potential will be presented.
[Mh] MeSH terms primary: MicroRNAs/isolation & purification
RNA, Viral/isolation & purification
Virus Diseases/diagnosis
[Mh] MeSH terms secundary: Animals
Cardiomyopathies/diagnosis
Cardiomyopathies/virology
Disease Models, Animal
HIV/genetics
HIV/isolation & purification
Hepacivirus/genetics
Hepacivirus/isolation & purification
Hepatitis B virus/genetics
Hepatitis B virus/isolation & purification
Herpesviridae/genetics
Herpesviridae/isolation & purification
Human T-lymphotropic virus 1/genetics
Human T-lymphotropic virus 1/isolation & purification
Humans
Liver Neoplasms/diagnosis
Liver Neoplasms/virology
MicroRNAs/genetics
Picornaviridae/genetics
Picornaviridae/isolation & purification
Polyomavirus/genetics
Polyomavirus/isolation & purification
Prognosis
RNA, Viral/genetics
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Nm] Name of substance:0 (MicroRNAs); 0 (RNA, Viral)
[Em] Entry month:1710
[Cu] Class update date: 171114
[Lr] Last revision date:171114
[Js] Journal subset:IM
[Da] Date of entry for processing:160930
[St] Status:MEDLINE
[do] DOI:10.1007/s40291-016-0236-x

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[PMID]: 28185547
[Au] Autor:Pellin D; Di Serio C
[Ad] Address:University Center of Statistics for the Biomedical Sciences, Vita-Salute San Raffaele University, Via Olgettina 58, Milan, 20132, Italy. pellin.danilo@hsr.it.
[Ti] Title:A novel scan statistics approach for clustering identification and comparison in binary genomic data.
[So] Source:BMC Bioinformatics;17(Suppl 11):320, 2016 Sep 22.
[Is] ISSN:1471-2105
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: In biomedical research a relevant issue is to identify time intervals or portions of a n-dimensional support where a particular event of interest is more likely to occur than expected. Algorithms that require to specify a-priori number/dimension/length of clusters assumed for the data suffer from a high degree of arbitrariness whenever no precise information are available, and this may strongly affect final estimation on parameters. Within this framework, spatial scan-statistics have been proposed in the literature, representing a valid non-parametric alternative. RESULTS: We adapt the so called Bernoulli-model scan statistic to the genomic field and we propose a multivariate extension, named Relative Scan Statistics, for the comparison of two series of Bernoulli r.v. defined over a common support, with the final goal of highlighting unshared event rate variations. Using a probabilistic approach based on success probability estimates and comparison (likelihood based), we can exploit an hypothesis testing procedure to identify clusters and relative clusters. Both the univariate and the novel multivariate extension of the scan statistic confirm previously published findings. CONCLUSION: The method described in the paper represents a challenging application of scan statistics framework to problem related to genomic data. From a biological perspective, these tools offer the possibility to clinicians and researcher to improve their knowledge on viral vectors integrations process, allowing to focus their attention to restricted over-targeted portion of the genome.
[Mh] MeSH terms primary: Algorithms
Genomics/methods
HIV/genetics
Leukemia Virus, Murine/genetics
Viral Proteins/genetics
[Mh] MeSH terms secundary: Cluster Analysis
Data Interpretation, Statistical
Hematopoietic Stem Cells/cytology
Hematopoietic Stem Cells/metabolism
Hematopoietic Stem Cells/virology
Humans
Likelihood Functions
Virus Integration
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Viral Proteins)
[Em] Entry month:1707
[Cu] Class update date: 170726
[Lr] Last revision date:170726
[Js] Journal subset:IM
[Da] Date of entry for processing:170211
[St] Status:MEDLINE
[do] DOI:10.1186/s12859-016-1173-8


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