Database : MEDLINE
Search on : retroviridae and infections [Words]
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[PMID]: 28449719
[Au] Autor:Bongard N; Lapuente D; Windmann S; Dittmer U; Tenbusch M; Bayer W
[Ad] Address:Institute for Virology, University Hospital Essen, University Duisburg-Essen, Virchowstr. 179, 45147, Essen, Germany.
[Ti] Title:Interference of retroviral envelope with vaccine-induced CD8 T cell responses is relieved by co-administration of cytokine-encoding vectors.
[So] Source:Retrovirology;14(1):28, 2017 Apr 27.
[Is] ISSN:1742-4690
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Retroviral envelope (Env) proteins are known to exhibit immunosuppressive properties, which become apparent not only in retroviral infections, but also in gene-based immunizations using retroviral immunogens, where envelope interferes with the induction of CD8 T cell responses towards another, simultaneously or subsequently delivered, immunogen. RESULTS: In the Friend retrovirus mouse model, immunization with a plasmid encoding the Friend murine leukemia virus (F-MuLV) Leader-Gag protein resulted in induction of a strong GagL -specific CD8 T cell response, while the response was completely abrogated by co-immunization with an F-MuLV Env-encoding plasmid. In order to overcome this interference of retroviral envelope, we employed plasmids encoding the cytokines interleukin (IL) 1ß, IL2, IL12, IL15, IL21, IL28A or granulocyte-macrophage colony-stimulating factor (GM-CSF) as genetic adjuvants. Co-application of plasmids encoding IL2, IL12, IL21, IL28A and especially GM-CSF rescued the induction of GagL -specific CD8 T cells in mice vaccinated with FV Leader-Gag and Env. Mice that were immunized with plasmids encoding Leader-Gag and Env and the cytokines IL1ß, IL12, IL15, IL28A or GM-CSF, but not Leader-Gag and Env without any cytokine, showed significantly reduced viral loads upon a high-dose Friend virus challenge infection. CONCLUSIONS: Our data demonstrate the potency of cytokine-encoding vectors as adjuvants and immune modulators in composite vaccines for anti-retroviral immunization.
[Mh] MeSH terms primary: CD8-Positive T-Lymphocytes/immunology
Cytokines/genetics
Friend murine leukemia virus/immunology
Vaccines, DNA/immunology
Viral Envelope Proteins/immunology
Viral Vaccines/immunology
[Mh] MeSH terms secundary: Adjuvants, Immunologic
Animals
Cytokines/immunology
Female
Friend murine leukemia virus/genetics
Gene Products, gag/genetics
Gene Products, gag/immunology
Genetic Vectors
Immunization
Immunomodulation
Interleukin-15/genetics
Interleukin-15/immunology
Interleukin-2/genetics
Interleukin-2/immunology
Mice
Mice, Inbred BALB C
Plasmids
Retroviridae Infections/immunology
Vaccines, DNA/administration & dosage
Viral Envelope Proteins/genetics
Viral Envelope Proteins/metabolism
Viral Load
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Adjuvants, Immunologic); 0 (Cytokines); 0 (Gene Products, gag); 0 (Interleukin-15); 0 (Interleukin-2); 0 (Vaccines, DNA); 0 (Viral Envelope Proteins); 0 (Viral Vaccines)
[Em] Entry month:1802
[Cu] Class update date: 180226
[Lr] Last revision date:180226
[Js] Journal subset:IM
[Da] Date of entry for processing:170429
[St] Status:MEDLINE
[do] DOI:10.1186/s12977-017-0352-7

  2 / 5015 MEDLINE  
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[PMID]: 29224130
[Au] Autor:Wang M; Wang Y; Baloch AR; Pan Y; Xu F; Tian L; Zeng Q
[Ad] Address:College of Veterinary Medicine, Gansu Agricultural University, Lanzhou, China.
[Ti] Title:Molecular epidemiology and characterization of bovine leukemia virus in domestic yaks (Bos grunniens) on the Qinghai-Tibet Plateau, China.
[So] Source:Arch Virol;163(3):659-670, 2018 Mar.
[Is] ISSN:1432-8798
[Cp] Country of publication:Austria
[La] Language:eng
[Ab] Abstract:Bovine leukemia virus (BLV) is a member of the genus Deltaretrovirus of the family Retroviridae and cause a chronic lymphosarcoma, which is extensive in cattle. In yaks (Bos grunniens), the distribution, strains and genetic characteristics of BLV have rarely been studied. The aim of our study was to investigate BLV infections in domestic yaks and determine the genetic variability of BLV circulating in a region of the Qinghai Tibet Plateau, China. Blood samples were collected from 798 yaks, which were from different farms from Gansu, Qinghai and Sichuan provinces surrounding the Qinghai-Tibet Plateau. Nested PCR targeting BLV long terminal repeats was used to detect the BLV provirus. The highest prevalence of BLV infection was in Gansu province, where it was 18.93% (39/206) in white yaks from Tianzhu City and 19.14% (31/162) in black yaks from Gannan City. In Qinghai and Sichuan provinces, the prevalence of BLV in black yaks was 14.83% (35/236) and 14.94% (29/194), respectively. The prevalence of BLV was not significantly different in yaks up to one year old than in older animals. Phylogenetic analysis was performed using 16 different env-gp51 (497-bp) gene sequences from the three provinces and 71 known BLV strains, which revealed that in both Gansu and Qinghai provinces, genotypes 6 and 10 of the BLV strains were at high levels, whereas only genotype 10 was prevalent in Sichuan Province. Phylogenetic analysis and sequence comparisons revealed 95.7-99.8% sequence identity among the full-length env genes of 16 strains, nearly full-length genome sequences of six BLV strains, and those of the known genotypes 6 and 10 of BLV. This study provides comprehensive information is regarding the widespread infection of domestic yaks with BLV on the Qinghai-Tibet Plateau of China, and shows that at least two BLV genotypes (genotypes 6 and 10) are circulating in this population.
[Mh] MeSH terms primary: Enzootic Bovine Leukosis/epidemiology
Genes, env
Genotype
Leukemia Virus, Bovine/classification
Leukemia Virus, Bovine/genetics
Phylogeny
[Mh] MeSH terms secundary: Animals
Base Sequence
Cattle
Enzootic Bovine Leukosis/transmission
Enzootic Bovine Leukosis/virology
Gene Expression
Leukemia Virus, Bovine/isolation & purification
Molecular Epidemiology
Prevalence
Sequence Alignment
Sequence Homology, Nucleic Acid
Terminal Repeat Sequences
Tibet/epidemiology
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180220
[Lr] Last revision date:180220
[Js] Journal subset:IM
[Da] Date of entry for processing:171211
[St] Status:MEDLINE
[do] DOI:10.1007/s00705-017-3658-9

  3 / 5015 MEDLINE  
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Pissinatti, Alcides
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[PMID]: 28931021
[Au] Autor:Muniz CP; Cavalcante LTF; Jia H; Zheng H; Tang S; Augusto AM; Pissinatti A; Fedullo LP; Santos AF; Soares MA; Switzer WM
[Ad] Address:Departamento de Genética, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
[Ti] Title:Zoonotic infection of Brazilian primate workers with New World simian foamy virus.
[So] Source:PLoS One;12(9):e0184502, 2017.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Simian foamy viruses (SFVs) are retroviruses present in nearly all nonhuman primates (NHPs), including Old World primates (OWP) and New World primates (NWP). While all confirmed human infections with SFV are from zoonotic transmissions originating from OWP, little is known about the zoonotic transmission potential of NWP SFV. We conducted a longitudinal, prospective study of 56 workers occupationally exposed to NWP in Brazil. Plasma from these workers was tested using Western blot (WB) assays containing NWP SFV antigens. Genomic DNA from blood and buccal swabs was analyzed for the presence of proviral SFV sequences by three nested PCR tests and a new quantitative PCR assay. Exposure histories were obtained and analyzed for associations with possible SFV infection. Ten persons (18%) tested seropositive and two persons were seroindeterminate (3.6%) for NWP SFV. Six persons had seroreactivity over 2-3 years suggestive of persistent infection. All SFV NWP WB-positive workers reported at least one incident involving NWP, including six reporting NWP bites. NWP SFV viral DNA was not detected in the blood or buccal swabs from all 12 NWP SFV seroreactive workers. We also found evidence of SFV seroreversion in three workers suggestive of possible clearance of infection. Our findings suggest that NWP SFV can be transmitted to occupationally-exposed humans and can elicit specific humoral immune responses but infection remains well-controlled resulting in latent infection and may occasionally clear.
[Mh] MeSH terms primary: Retroviridae Infections/diagnosis
Simian foamy virus/genetics
Zoonoses/diagnosis
[Mh] MeSH terms secundary: Adult
Animals
Antigens, Viral/immunology
Antigens, Viral/metabolism
Brazil
DNA, Viral/blood
DNA, Viral/metabolism
Female
Humans
Leukocytes, Mononuclear/cytology
Leukocytes, Mononuclear/virology
Longitudinal Studies
Male
Middle Aged
Mouth Mucosa/virology
Polymerase Chain Reaction
Primates
Prospective Studies
Retroviridae Infections/transmission
Retroviridae Infections/virology
Risk
Simian foamy virus/isolation & purification
Zoonoses/virology
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Antigens, Viral); 0 (DNA, Viral)
[Em] Entry month:1710
[Cu] Class update date: 171020
[Lr] Last revision date:171020
[Js] Journal subset:IM
[Da] Date of entry for processing:170921
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184502

  4 / 5015 MEDLINE  
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[PMID]: 28904191
[Au] Autor:Littwitz-Salomon E; Schimmer S; Dittmer U
[Ad] Address:Institute for Virology of the University Hospital Essen, University of Duisburg-Essen, Essen, Germany Elisabeth.Littwitz@uni-due.de.
[Ti] Title:Dose of Retroviral Infection Determines Induction of Antiviral NK Cell Responses.
[So] Source:J Virol;91(22), 2017 Nov 15.
[Is] ISSN:1098-5514
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Natural killer (NK) cells are part of the innate immune system and recognize virus-infected cells as well as tumor cells. Conflicting data about the beneficial or even detrimental role of NK cells in different infectious diseases have been described previously. While the type of pathogen strongly influences NK cell functionality, less is known about how the infection dose influences the quality of a NK cell response against retroviruses. In this study, we used the well-established Friend retrovirus (FV) mouse model to investigate the impact of virus dose on the induction of antiviral NK cell functions. High-dose virus inoculation increased initial virus replication compared to that with medium- or low-dose viral challenge and significantly improved NK cell activation. Antiviral NK cell activity, including cytotoxicity toward infected target cells, was also enhanced by high-dose virus infection. NK cell activation following high-dose viral challenge was likely mediated by activated dendritic cells (DCs) and macrophages and the NK cell-stimulating cytokines interleukin 15 (IL-15) and IL-18. Neutralization of these cytokines decreased NK cell functions and increased viral loads, whereas IL-15 and IL-18 therapy improved NK cell activity. Here we demonstrate that virus dose positively correlates with antiviral NK cell activity and function, which are at least partly driven by IL-15 and IL-18. Our results suggest that NK cell activity may be therapeutically enhanced by administering IL-15 and IL-18 in virus infections that inadequately activate NK cells. In infections with retroviruses, like HIV and FV infection of mice, NK cells clearly mediate antiviral activities, but they are usually not sufficient to prevent severe pathology. Here we show that the initial infection dose impacts the induction of an antiviral NK cell response during an acute retroviral infection, which had not investigated before. High-dose infection resulted in a strong NK cell functionality, whereas no antiviral activities were detected after low- or medium-dose infection. Interestingly, DCs and macrophages were highly activated after high-dose FV challenge, which corresponded with increased levels of NK cell-stimulating cytokines IL-15 and IL-18. IL-15 and IL-18 neutralization decreased NK cell functions, whereas IL-15 and IL-18 therapy improved NK cell activity. Here we show the importance of cytokines for NK cell activation in retroviral infections; our findings suggest that immunotherapy combining the well-tolerated cytokines IL-15 and IL-18 might be an interesting approach for antiretroviral treatment.
[Mh] MeSH terms primary: Friend murine leukemia virus/immunology
Killer Cells, Natural/immunology
Lymphocyte Activation
Retroviridae Infections/immunology
[Mh] MeSH terms secundary: Animals
Dose-Response Relationship, Immunologic
Female
Interleukin-15/immunology
Interleukin-15/pharmacology
Interleukin-18/immunology
Interleukin-18/pharmacology
Mice
Retroviridae Infections/drug therapy
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Interleukin-15); 0 (Interleukin-18)
[Em] Entry month:1711
[Cu] Class update date: 171102
[Lr] Last revision date:171102
[Js] Journal subset:IM
[Da] Date of entry for processing:170915
[St] Status:MEDLINE

  5 / 5015 MEDLINE  
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Pissinatti, Alcides
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[PMID]: 28863180
[Au] Autor:Muniz CP; Zheng H; Jia H; Cavalcante LTF; Augusto AM; Fedullo LP; Pissinatti A; Soares MA; Switzer WM; Santos AF
[Ad] Address:Departamento de Genética, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
[Ti] Title:A non-invasive specimen collection method and a novel simian foamy virus (SFV) DNA quantification assay in New World primates reveal aspects of tissue tropism and improved SFV detection.
[So] Source:PLoS One;12(9):e0184251, 2017.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Simian foamy viruses (SFVs) co-evolved with a wide range of Old World and New World primates (OWPs and NWPs, respectively) and occasionally transmit to humans. Previous studies of OWPs showed that the predominant site of SFV replication is the oral mucosa. However, very little is known about SFV viral loads (VLs) in the oral mucosa or blood of NWPs. NWPs have smaller body sizes, limiting collection of sufficient whole blood volumes to molecularly detect and quantify SFV. Our study evaluated the use of noninvasively collected buccal swabs to detect NWP SFV compared with detection in blood using a new NWP SFV quantitative PCR (qPCR) assay. Buccal and blood samples were collected from 107 captive NWPs in Brazil comprising eleven distinct genera at the Primate Center of Rio de Janeiro (n = 58) and at Fundação Jardim Zoológico da Cidade do Rio Janeiro (n = 49). NWP SFV western blot (WB) testing was performed on a subset of animals for comparison with PCR results. The qPCR assay was validated using distinct SFV polymerase sequences from seven NWP genera (Callithrix, Sapajus, Saimiri, Ateles, Alouatta, Cacajao and Pithecia). Assay sensitivity was 20 copies/106 cells, detectable in 90% of replicates. SFV DNA VLs were higher in buccal swabs (5 log copies/106 cells) compared to peripheral blood mononuclear cells (PBMCs) (3 log copies/106 cells). The qPCR assay was also more sensitive than nested PCR for detection of NWP SFV infection and identified an additional 27 SFV-infected monkeys of which 18 (90%) were WB-positive and three that were WB-negative. We show the utility of using both blood and buccal swabs and our new qPCR assay for detection and quantification of diverse NWP SFV, which will assist a better understanding of the epidemiology of SFV in NWPs and any potential zoonotic infection risk for humans exposed to NWPs.
[Mh] MeSH terms primary: Leukocytes, Mononuclear/virology
Primates/virology
Retroviridae Infections/diagnosis
Simian foamy virus/genetics
Specimen Handling/methods
[Mh] MeSH terms secundary: Animals
Brazil
DNA, Viral/genetics
Humans
Monkey Diseases/diagnosis
Monkey Diseases/virology
Mouth Mucosa/virology
Phylogeny
Plasmids/metabolism
Polymerase Chain Reaction
Real-Time Polymerase Chain Reaction
Retroviridae Infections/veterinary
Sensitivity and Specificity
Species Specificity
Viral Tropism
Zoonoses/virology
[Pt] Publication type:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Name of substance:0 (DNA, Viral)
[Em] Entry month:1710
[Cu] Class update date: 171023
[Lr] Last revision date:171023
[Js] Journal subset:IM
[Da] Date of entry for processing:170902
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184251

  6 / 5015 MEDLINE  
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[PMID]: 28813660
[Au] Autor:Denzin LK; Khan AA; Virdis F; Wilks J; Kane M; Beilinson HA; Dikiy S; Case LK; Roopenian D; Witkowski M; Chervonsky AV; Golovkina TV
[Ad] Address:Child Health Institute of NJ, Department of Pediatrics, Rutgers Robert Wood Johnson Medical School, Rutgers, The State University of NJ, New Brunswick, NJ 08901, USA.
[Ti] Title:Neutralizing Antibody Responses to Viral Infections Are Linked to the Non-classical MHC Class II Gene H2-Ob.
[So] Source:Immunity;47(2):310-322.e7, 2017 Aug 15.
[Is] ISSN:1097-4180
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Select humans and animals control persistent viral infections via adaptive immune responses that include production of neutralizing antibodies. The precise genetic basis for the control remains enigmatic. Here, we report positional cloning of the gene responsible for production of retrovirus-neutralizing antibodies in mice of the I/LnJ strain. It encodes the beta subunit of the non-classical major histocompatibility complex class II (MHC-II)-like molecule H2-O, a negative regulator of antigen presentation. The recessive and functionally null I/LnJ H2-Ob allele supported the production of virus-neutralizing antibodies independently of the classical MHC haplotype. Subsequent bioinformatics and functional analyses of the human H2-Ob homolog, HLA-DOB, revealed both loss- and gain-of-function alleles, which could affect the ability of their carriers to control infections with human hepatitis B (HBV) and C (HCV) viruses. Thus, understanding of the previously unappreciated role of H2-O (HLA-DO) in immunity to infections may suggest new approaches in achieving neutralizing immunity to viruses.
[Mh] MeSH terms primary: Antibodies, Neutralizing
HLA-D Antigens/metabolism
Histocompatibility Antigens Class II/metabolism
Immunity, Humoral
Mammary Tumor Virus, Mouse/immunology
Rauscher Virus/immunology
Retroviridae Infections/immunology
[Mh] MeSH terms secundary: Animals
Antibodies, Neutralizing/metabolism
Antibodies, Viral/metabolism
Antigen Presentation/genetics
Computational Biology
Female
Genetic Predisposition to Disease
HLA-D Antigens/genetics
HeLa Cells
Hepatitis B/immunology
Hepatitis B/transmission
Hepatitis C/immunology
Hepatitis C/transmission
Histocompatibility Antigens Class II/genetics
Humans
Immunity, Humoral/genetics
Male
Mice
Mice, Inbred Strains
Mice, Knockout
Mutation/genetics
Polymorphism, Genetic
Retroviridae Infections/transmission
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Antibodies, Neutralizing); 0 (Antibodies, Viral); 0 (H-2O antigen); 0 (HLA-D Antigens); 0 (HLA-DO antigens); 0 (Histocompatibility Antigens Class II)
[Em] Entry month:1709
[Cu] Class update date: 170928
[Lr] Last revision date:170928
[Js] Journal subset:IM
[Da] Date of entry for processing:170817
[St] Status:MEDLINE

  7 / 5015 MEDLINE  
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[PMID]: 28809145
[Au] Autor:Konstantoulas CJ; Hagen B; Indik S
[Ad] Address:Institute of Virology, University of Veterinary Medicine, Veterinaerplatz 1, 1210 Vienna, Austria.
[Ti] Title:Moderate sensitivity of mouse mammary tumour virus to inhibition by human APOBEC3G.
[So] Source:J Gen Virol;98(9):2362-2367, 2017 Sep.
[Is] ISSN:1465-2099
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Infectivity of the mouse mammary tumour virus (MMTV) is inhibited by mouse APOBEC3 (mA3) which is efficiently packaged into virions. As the inhibition is only partial, the virus can replicate in tissues expressing mA3 and complete its replication cycle. Here, we have examined the sensitivity of MMTV to inhibition by a human orthologue of mA3, A3G. We report that the virus containing A3G is only moderately susceptible to inhibition by the human factor. Whereas the vif-deficient HIV-1 vector produced in human epithelial cells expressing endogenous levels of A3G was efficiently inhibited, an MMTV vector remained fully infectious. Greater A3G expression levels were necessary to restrict infectivity of MMTV, but only when the factor retained its deaminase activity. Furthermore, the spreading kinetic of a replication competent MMTV was only moderately accelerated in cells with downmodulated A3G expression. These data suggest that MMTV has evolved a mechanism to neutralize antiviral activity of APOBEC3 proteins.
[Mh] MeSH terms primary: APOBEC-3G Deaminase/metabolism
Mammary Tumor Virus, Mouse/physiology
Retroviridae Infections/veterinary
Rodent Diseases/enzymology
[Mh] MeSH terms secundary: APOBEC-3G Deaminase/genetics
Animals
Humans
Mammary Tumor Virus, Mouse/genetics
Mice
Retroviridae Infections/enzymology
Retroviridae Infections/genetics
Retroviridae Infections/virology
Rodent Diseases/genetics
Rodent Diseases/virology
Virus Assembly
Virus Replication
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:EC 3.5.4.5 (APOBEC-3G Deaminase); EC 3.5.4.5 (APOBEC3G protein, human); EC 3.5.4.5 (APOBEC3G protein, mouse)
[Em] Entry month:1709
[Cu] Class update date: 170919
[Lr] Last revision date:170919
[Js] Journal subset:IM
[Da] Date of entry for processing:170816
[St] Status:MEDLINE
[do] DOI:10.1099/jgv.0.000897

  8 / 5015 MEDLINE  
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[PMID]: 28794032
[Au] Autor:Bamunusinghe D; Liu Q; Plishka R; Dolan MA; Skorski M; Oler AJ; Yedavalli VRK; Buckler-White A; Hartley JW; Kozak CA
[Ad] Address:Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland, USA.
[Ti] Title:Recombinant Origins of Pathogenic and Nonpathogenic Mouse Gammaretroviruses with Polytropic Host Range.
[So] Source:J Virol;91(21), 2017 Nov 01.
[Is] ISSN:1098-5514
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Ecotropic, xenotropic, and polytropic mouse leukemia viruses (E-, X-, and P-MLVs) exist in mice as infectious viruses and endogenous retroviruses (ERVs) inserted into mouse chromosomes. All three MLV subgroups are linked to leukemogenesis, which involves generation of recombinants with polytropic host range. Although P-MLVs are deemed to be the proximal agents of disease induction, few biologically characterized infectious P-MLVs have been sequenced for comparative analysis. We analyzed the complete genomes of 16 naturally occurring infectious P-MLVs, 12 of which were typed for pathogenic potential. We sought to identify ERV progenitors, recombinational hot spots, and segments that are always replaced, never replaced, or linked to pathogenesis or host range. Each P-MLV has an E-MLV backbone with P- or X-ERV replacements that together cover 100% of the recombinant genomes, with different substitution patterns for X- and P-ERVs. Two segments are always replaced, both coding for envelope (Env) protein segments: the N terminus of the surface subunit and the cytoplasmic tail R peptide. Viral gene replacements are influenced by host restriction genes and Pathogenic potential maps to the transmembrane subunit segment encoding the N-heptad repeat (HR1). Molecular dynamics simulations identified three novel interdomain salt bridges in the lymphomagenic virus HR1 that could affect structural stability, entry or sensitivity to host immune responses. The long terminal repeats of lymphomagenic P-MLVs are differentially altered by recombinations, duplications, or mutations. This analysis of the naturally occurring, sometimes pathogenic P-MLV recombinants defines the limits and extent of intersubgroup recombination and identifies specific sequence changes linked to pathogenesis and host interactions. During virus-induced leukemogenesis, ecotropic mouse leukemia viruses (MLVs) recombine with nonecotropic endogenous retroviruses (ERVs) to produce polytropic MLVs (P-MLVs). Analysis of 16 P-MLV genomes identified two segments consistently replaced: one at the envelope N terminus that alters receptor choice and one in the R peptide at the envelope C terminus, which is removed during virus assembly. Genome-wide analysis shows that nonecotropic replacements in the progenitor ecotropic MLV genome are more extensive than previously appreciated, covering 100% of the genome; contributions from xenotropic and polytropic ERVs differentially alter the regions responsible for receptor determination or subject to APOBEC3 and Fv1 restriction. All pathogenic viruses had modifications in the regulatory elements in their long terminal repeats and differed in a helical segment of envelope involved in entry and targeted by the host immune system. Virus-induced leukemogenesis thus involves generation of complex recombinants, and specific replacements are linked to pathogenesis and host restrictions.
[Mh] MeSH terms primary: Host Specificity/genetics
Leukemia Virus, Murine/classification
Leukemia Virus, Murine/pathogenicity
Leukemia, Experimental/virology
Retroviridae Infections/virology
Tumor Virus Infections/virology
Viral Proteins/genetics
[Mh] MeSH terms secundary: Amino Acid Sequence
Animals
Base Sequence
Evolution, Molecular
Genome, Viral
Leukemia Virus, Murine/genetics
Mice
Molecular Dynamics Simulation
Protein Conformation
Receptors, Virus/genetics
Receptors, Virus/metabolism
Sequence Homology
Terminal Repeat Sequences
Viral Proteins/chemistry
Viral Proteins/metabolism
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Receptors, Virus); 0 (Viral Proteins)
[Em] Entry month:1711
[Cu] Class update date: 171109
[Lr] Last revision date:171109
[Js] Journal subset:IM
[Da] Date of entry for processing:170811
[St] Status:MEDLINE

  9 / 5015 MEDLINE  
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[PMID]: 28437635
[Au] Autor:Colon-Moran W; Argaw T; Wilson CA
[Ad] Address:Center for Biologics Evaluation and Research, US Food and Drug Administration, Silver Spring, MD, USA.
[Ti] Title:Three cysteine residues of SLC52A1, a receptor for the porcine endogenous retrovirus-A (PERV-A), play a critical role in cell surface expression and infectivity.
[So] Source:Virology;507:140-150, 2017 Jul.
[Is] ISSN:1096-0341
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Porcine endogenous retrovirus-A (PERV-A), a gammaretrovirus, infects human cells in vitro, thus raising the potential risk of cross-species transmission in xenotransplantation. Two members of the solute carrier family 52 (SLC52A1 and SLC52A2) are PERV-A receptors. Site-directed mutagenesis of the cDNA encoding SLC52A1 identified that only one of two putative glycosylation signals is occupied by glycans. In addition, we showed that glycosylation of SLC52A1 is not necessary for PERV-A receptor function. We also identified that at a minimum, three cysteine residues are sufficient for SLC52A1 cell surface expression. Mutation of cysteine at position 365 and either of the two cysteine residues in the C-terminal tail at positions 442 or 446 reduced SLC52A1 surface expression and PERV-A infection suggesting that these residues may contribute to overall structural stability and receptor function. Understanding interactions between PERV-A and its cellular receptor may provide novel strategies to prevent zoonotic infection in the setting of xenotransplantation.
[Mh] MeSH terms primary: Cysteine/metabolism
Endogenous Retroviruses/pathogenicity
Gammaretrovirus/metabolism
Receptors, G-Protein-Coupled/chemistry
Receptors, Virus/chemistry
Receptors, Virus/metabolism
Retroviridae Infections/veterinary
Swine Diseases/metabolism
[Mh] MeSH terms secundary: Animals
Cysteine/chemistry
Cysteine/genetics
Endogenous Retroviruses/genetics
Endogenous Retroviruses/physiology
Gammaretrovirus/classification
Gammaretrovirus/genetics
Glycosylation
Receptors, G-Protein-Coupled/genetics
Receptors, G-Protein-Coupled/metabolism
Receptors, Virus/genetics
Retroviridae Infections/genetics
Retroviridae Infections/metabolism
Retroviridae Infections/virology
Swine
Swine Diseases/genetics
Swine Diseases/virology
Virulence
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Receptors, G-Protein-Coupled); 0 (Receptors, Virus); K848JZ4886 (Cysteine)
[Em] Entry month:1707
[Cu] Class update date: 170717
[Lr] Last revision date:170717
[Js] Journal subset:IM
[Da] Date of entry for processing:170425
[St] Status:MEDLINE

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[PMID]: 28387759
[Au] Autor:Liao J; Wei Q; Fan J; Zou Y; Song D; Liu J; Liu F; Ma C; Hu X; Li L; Yu Y; Qu X; Chen L; Yu X; Zhang Z; Zhao C; Zeng Z; Zhang R; Yan S; Wu T; Wu X; Shu Y; Lei J; Li Y; Zhang W; Wang J; Reid RR; Lee MJ; Huang W; Wolf JM; He TC; Wang J
[Ad] Address:Department of Orthopaedic Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
[Ti] Title:Characterization of retroviral infectivity and superinfection resistance during retrovirus-mediated transduction of mammalian cells.
[So] Source:Gene Ther;24(6):333-341, 2017 Jun.
[Is] ISSN:1476-5462
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Retroviral vectors including lentiviral vectors are commonly used tools to stably express transgenes or RNA molecules in mammalian cells. Their utilities are roughly divided into two categories, stable overexpression of transgenes and RNA molecules, which requires maximal transduction efficiency, or functional selection with retrovirus (RV)-based libraries, which takes advantage of retroviral superinfection resistance. However, the dynamic features of RV-mediated transduction are not well characterized. Here, we engineered two murine stem cell virus-based retroviral vectors expressing dual fluorescence proteins and antibiotic markers, and analyzed virion production efficiency and virion stability, dynamic infectivity and superinfection resistance in different cell types, and strategies to improve transduction efficiency. We found that the highest virion production occurred between 60 and 72 h after transfection. The stability of the collected virion supernatant decreased by >60% after 3 days in storage. We found that RV infectivity varied drastically in the tested human cancer lines, while low transduction efficiency was partially overcome with increased virus titer, prolonged infection duration and/or repeated infections. Furthermore, we demonstrated that RV receptors PIT1 and PIT2 were lowly expressed in the analyzed cells, and that PIT1 and/or PIT2 overexpression significantly improved transduction efficiency in certain cell lines. Thus, our findings provide resourceful information for the optimal conditions of retroviral-mediated gene delivery.
[Mh] MeSH terms primary: Retroviridae/genetics
Transfection/methods
[Mh] MeSH terms secundary: Animals
Cell Line, Tumor
Genes, Reporter
Green Fluorescent Proteins/genetics
Green Fluorescent Proteins/metabolism
Humans
Mice
Receptors, Virus/genetics
Receptors, Virus/metabolism
Retroviridae/metabolism
Retroviridae/pathogenicity
Transfection/standards
Virion/genetics
Virion/metabolism
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Receptors, Virus); 147336-22-9 (Green Fluorescent Proteins)
[Em] Entry month:1710
[Cu] Class update date: 171003
[Lr] Last revision date:171003
[Js] Journal subset:IM
[Da] Date of entry for processing:170408
[St] Status:MEDLINE
[do] DOI:10.1038/gt.2017.24


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