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[PMID]:28464889
[Au] Autor:de Azevedo SSD; Caetano DG; Côrtes FH; Teixeira SLM; Dos Santos Silva K; Hoagland B; Grinsztejn B; Veloso VG; Morgado MG; Bello G
[Ad] Endereço:Laboratório de AIDS & Imunologia Molecular, Instituto Oswaldo Cruz - FIOCRUZ, Av. Brasil 4365, Rio de Janeiro, RJ, 21045-900, Brazil.
[Ti] Título:Highly divergent patterns of genetic diversity and evolution in proviral quasispecies from HIV controllers.
[So] Source:Retrovirology;14(1):29, 2017 May 02.
[Is] ISSN:1742-4690
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Ongoing intra-host HIV-1 evolution has been shown in individuals that naturally suppress the viremia to low levels (HIV controllers) by the analysis of the RNA in plasma compartment. Detection of evolution at the DNA proviral compartment in HIV controllers, however, has been more challenging and the precise correlation between the systemic viral suppression level and rate of reservoir's reseeding in those individuals is not fully understood. In this sense, we examined the proviral DNA quasispecies by single genome amplification of the env gene in a cohort of 23 HIV controllers from Brazil, divided in three groups, according to the level of systemic viral suppression: (1) elite controllers with persistent undetectable viral load (PEC, n = 6); (2) elite controllers with occasional episodes of transient (51-400 copies/mL) viremia (EEC, n = 7); and (3) viremic controllers with persistent low-level (80-2000 copies/mL) viremia (VC, n = 10). RESULTS: The HIV-1 diversity of the PBMC-associated proviral quasispecies in EC was significantly (P < 0.01) lower than in VC, but not significantly different between PEC and EEC groups. We detected a considerable variation in the average pairwise nucleotide distance and proportion of unique sequences in the HIV-1 proviral quasispecies of PEC and EEC. Some PEC and EEC displayed highly homogenous proviral populations with large clusters of identical sequences, while others exhibited relatively diverse proviral populations with a high proportion of unique sequences comparable to VC subjects. The long-term (10-15 years) follow-up of the HIV-1 proviral populations revealed a complete evolutionary stasis in one PEC and measurable divergence rates in one EEC [3.1 (1.2-5.6) × 10 substitutions/site/year and one VC [2.9 (0.7-5.1) × 10 substitutions/site/year]. CONCLUSIONS: There is no simple relationship between systemic viral suppression and intra-host proviral diversity or rate of reservoir's reseeding in chronically infected HIV controllers. Our results demonstrate that very divergent patterns of intra-host viral diversity and divergence could be detected in the setting of natural suppression of HIV-1 replication and that ongoing evolution and reseeding of the PBMC proviral reservoir occurs in some elite controllers.
[Mh] Termos MeSH primário: Evolução Molecular
Variação Genética
Infecções por HIV/virologia
HIV-1/genética
Provírus/genética
Quase-Espécies
Carga Viral
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Brasil
Contagem de Linfócito CD4
Estudos de Coortes
Feminino
Genes env
Genoma Viral
Infecções por HIV/imunologia
HIV-1/fisiologia
Seres Humanos
Masculino
Meia-Idade
RNA Viral/sangue
Viremia
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Viral)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1186/s12977-017-0354-5


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[PMID]:29042218
[Au] Autor:Allavena C; Rodallec A; Leplat A; Hall N; Luco C; Le Guen L; Bernaud C; Bouchez S; André-Garnier E; Boutoille D; Ferré V; Raffi F
[Ad] Endereço:Infectious Diseases Department, CHU Hotel Dieu, University Hospital, Nantes, France; UIC 1413, INSERM, Nantes, France. Electronic address: clotilde.allavena@chu-nantes.fr.
[Ti] Título:Interest of proviral HIV-1 DNA genotypic resistance testing in virologically suppressed patients candidate for maintenance therapy.
[So] Source:J Virol Methods;251:106-110, 2018 Jan.
[Is] ISSN:1879-0984
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Switch of antiretroviral therapy in virologically suppressed HIV-infected patients is frequent, to prevent toxicities, for simplification or convenience reasons. Pretherapeutic genotypic resistance testing on RNA can be lacking in some patients, which could enhance the risk of virologic failure, if resistance-associated mutations of the new regimen are not taken into account. Proviral DNA resistance testing in 69 virologically suppressed patients on antiretroviral treatment with no history of virological failure were pair-wised compared with pre-ART plasma RNA resistance testing. The median time between plasma (RNA testing) and whole blood (proviral DNA testing) was 47 months (IQR 29-63). A stop codon was evidenced in 23% (16/69) of proviral DNA sequences; these strains were considered as defective, non-replicative, and not taken into consideration. Within the non defective strains, concordance rate between plasma RNA and non-defective proviral DNA was high both on protease (194/220 concordant resistance-associated mutations=88%) and reverse transcriptase (28/37 concordant resistance-associated mutations=76%) genes. This study supports that proviral DNA testing might be an informative tool before switching antiretrovirals in virologically suppressed patients with no history of virological failure, but the interpretation should be restricted to non-defective viruses.
[Mh] Termos MeSH primário: DNA Viral/genética
Técnicas de Genotipagem/métodos
Infecções por HIV/virologia
HIV-1/genética
Testes de Sensibilidade Microbiana/métodos
Provírus/genética
[Mh] Termos MeSH secundário: Seres Humanos
RNA Viral/genética
[Pt] Tipo de publicação:COMPARATIVE STUDY; EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Viral); 0 (RNA, Viral)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180201
[Lr] Data última revisão:
180201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171019
[St] Status:MEDLINE


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[PMID]:29244184
[Au] Autor:Senigl F; Miklík D; Auxt M; Hejnar J
[Ad] Endereço:Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, Videnska 1083, CZ-14220 Prague 4, Czech Republic.
[Ti] Título:Accumulation of long-term transcriptionally active integrated retroviral vectors in active promoters and enhancers.
[So] Source:Nucleic Acids Res;45(22):12752-12765, 2017 Dec 15.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Most retroviruses preferentially integrate into certain genomic locations and, as a result, their genome-wide integration patterns are non-random. We investigate the epigenetic landscape of integrated retroviral vectors and correlate it with the long-term stability of proviral transcription. Retroviral vectors derived from the avian sarcoma/leukosis virus expressing the GFP reporter were used to transduce the human myeloid lymphoblastoma cell line K562. Because of efficient silencing of avian retrovirus in mammalian cells, only ∼3% of established clones displayed stable proviral expression. We analyzed the vector integration sites in non-selected cells and in clones selected for the GFP expression. This selection led to overrepresentation of proviruses integrated in active transcription units, with particular accumulation in promoter-proximal areas. In parallel, we investigated the integration of vectors equipped with an anti-silencing CpG island core sequence. Such modification increased the frequency of stably expressing proviruses by one order. The modified vectors are also overrepresented in active transcription units, but stably expressed in distal parts of transcriptional units further away from promoters with marked accumulation in enhancers. These results suggest that integrated retroviruses subject to gradual epigenetic silencing during long-term cultivation. Among most genomic compartments, however, active promoters and enhancers protect the adjacent retroviruses from transcriptional silencing.
[Mh] Termos MeSH primário: Alpharetrovirus/genética
Elementos Facilitadores Genéticos/genética
Regiões Promotoras Genéticas/genética
Transcrição Genética
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Ilhas de CpG/genética
Epigênese Genética
Inativação Gênica
Vetores Genéticos/genética
Seres Humanos
Células K562
Provírus/genética
Integração Viral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180115
[Lr] Data última revisão:
180115
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171216
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkx889


  4 / 3754 MEDLINE  
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[PMID]:28768863
[Au] Autor:Pecenka V; Pajer P; Karafiat V; Kasparova P; Dudlova J; Dvorak M
[Ad] Endereço:Institute of Molecular Genetics, Academy of Sciences CR, Prague, Czech Republic pecenkav@img.cas.cz.
[Ti] Título:, , , and Genes Are Recurrently Activated by Provirus Insertion in Liver Tumors Induced by the Retrovirus Myeloblastosis-Associated Virus 2.
[So] Source:J Virol;91(20), 2017 Oct 15.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Myeloblastosis-associated virus 2 (MAV-2) is a highly tumorigenic simple avian retrovirus. Chickens infected with MAV-2 develop tumors in the kidneys, lungs, and liver with a short latency, less than 8 weeks. Here we report the results of molecular analyses of MAV-2-induced liver tumors that fall into three classes: hepatic hemangiosarcomas (HHSs), intrahepatic cholangiocarcinomas (ICCs), and hepatocellular carcinomas (HCCs). Comprehensive inverse PCR-based screening of 92 chicken liver tumors revealed that in ca. 86% of these tumors, MAV-2 provirus had integrated into one of four gene loci: , , , and Insertionally mutated genes correlated with tumor type: was hit in HHSs, in ICCs, mostly in ICCs, and mostly in HCCs. The provirus insertions led to the overexpression of the affected genes and, in the case of and , also to the truncation of exons encoding the extracellular ligand-binding domains of these transmembrane receptors. The structures of truncated and closely mimic the structures of oncogenic variants of these genes frequently found in human tumors ( and ). These data describe the mechanisms of oncogenesis induced in chickens by the MAV-2 retrovirus. They also show that molecular processes converting cellular regulatory genes to cancer genes may be remarkably similar in chickens and humans. We suggest that the MAV-2 retrovirus-based model can complement experiments performed using mouse models and provide data that could translate to human medicine.
[Mh] Termos MeSH primário: Vírus da Mieloblastose Aviária/fisiologia
Carcinogênese
Genes erbB-1
Neoplasias Hepáticas/virologia
Mutagênese Insercional
Proteínas Proto-Oncogênicas c-met/genética
Receptores Proteína Tirosina Quinases/genética
[Mh] Termos MeSH secundário: Animais
Vírus da Mieloblastose Aviária/genética
Proteínas Aviárias/genética
Carcinoma Hepatocelular/genética
Carcinoma Hepatocelular/virologia
Galinhas/genética
Colangiocarcinoma/genética
Colangiocarcinoma/virologia
Hemangiossarcoma/genética
Hemangiossarcoma/virologia
Seres Humanos
Neoplasias Hepáticas/genética
Oncogenes
Provírus/genética
Provírus/fisiologia
Integração Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Avian Proteins); EC 2.7.10.1 (Proto-Oncogene Proteins c-met); EC 2.7.10.1 (RON protein); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE


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[PMID]:28768854
[Au] Autor:Kawasaki J; Kawamura M; Ohsato Y; Ito J; Nishigaki K
[Ad] Endereço:Laboratory of Molecular Immunology and Infectious Disease, Joint Faculty of Veterinary Medicine, Yamaguchi University, Yamaguchi, Japan.
[Ti] Título:Presence of a Shared 5'-Leader Sequence in Ancestral Human and Mammalian Retroviruses and Its Transduction into Feline Leukemia Virus.
[So] Source:J Virol;91(20), 2017 Oct 15.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recombination events induce significant genetic changes, and this process can result in virus genetic diversity or in the generation of novel pathogenicity. We discovered a new recombinant feline leukemia virus (FeLV) gene harboring an unrelated insertion, termed the X region, which was derived from endogenous gammaretrovirus 4 (FcERV-gamma4). The identified FcERV-gamma4 proviruses have lost their coding capabilities, but some can express their viral RNA in feline tissues. Although the X-region-carrying recombinant FeLVs appeared to be replication-defective viruses, they were detected in 6.4% of tested FeLV-infected cats. All isolated recombinant FeLV clones commonly incorporated a middle part of the FcERV-gamma4 5'-leader region as an X region. Surprisingly, a sequence corresponding to the portion contained in all X regions is also present in at least 13 endogenous retroviruses (ERVs) observed in the cat, human, primate, and pig genomes. We termed this shared genetic feature the commonly shared (CS) sequence. Despite our phylogenetic analysis indicating that all CS-sequence-carrying ERVs are classified as gammaretroviruses, no obvious closeness was revealed among these ERVs. However, the Shannon entropy in the CS sequence was lower than that in other parts of the provirus genome. Notably, the CS sequence of human endogenous retrovirus T had 73.8% similarity with that of FcERV-gamma4, and specific signals were detected in the human genome by Southern blot analysis using a probe for the FcERV-gamma4 CS sequence. Our results provide an interesting evolutionary history for CS-sequence circulation among several distinct ancestral viruses and a novel recombined virus over a prolonged period. Recombination among ERVs or modern viral genomes causes a rapid evolution of retroviruses, and this phenomenon can result in the serious situation of viral disease reemergence. We identified a novel recombinant FeLV gene that contains an unrelated sequence, termed the X region. This region originated from the 5' leader of FcERV-gamma4, a replication-incompetent feline ERV. Surprisingly, a sequence corresponding to the X region is also present in the 5' portion of other ERVs, including human endogenous retroviruses. Scattered copies of the ERVs carrying the unique genetic feature, here named the commonly shared (CS) sequence, were found in each host genome, suggesting that ancestral viruses may have captured and maintained the CS sequence. More recently, a novel recombinant FeLV hijacked the CS sequence from inactivated FcERV-gamma4 as the X region. Therefore, tracing the CS sequences can provide unique models for not only the modern reservoir of new recombinant viruses but also the genetic features shared among ancient retroviruses.
[Mh] Termos MeSH primário: Regiões 5´ não Traduzidas/genética
Retrovirus Endógenos/genética
Genes gag
Genoma Viral
Vírus da Leucemia Felina/genética
Recombinação Genética
[Mh] Termos MeSH secundário: Animais
Gatos/virologia
Evolução Molecular
Gammaretrovirus/genética
Seres Humanos/virologia
Leucemia Felina/virologia
Mamíferos/genética
Mamíferos/virologia
Filogenia
Provírus/genética
Provírus/fisiologia
RNA Viral/genética
Suínos/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (5' Untranslated Regions); 0 (RNA, Viral)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE


  6 / 3754 MEDLINE  
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[PMID]:28715973
[Au] Autor:Mbonye U; Karn J
[Ad] Endereço:Department of Molecular Biology and Microbiology, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106; email: jonathan.karn@case.edu.
[Ti] Título:The Molecular Basis for Human Immunodeficiency Virus Latency.
[So] Source:Annu Rev Virol;4(1):261-285, 2017 Sep 29.
[Is] ISSN:2327-0578
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Although potent combination antiretroviral therapy can effectively block viral replication in the host, human immunodeficiency virus (HIV) persists due to the existence of latent but replication-competent proviruses residing primarily in a very small population of resting memory CD4 T cells. Viral latency is established when the expression of the autoregulatory viral trans-activating factor Tat is reduced to subthreshold levels. The absence of Tat reduces HIV transcription and protein production to levels that make the host cell invisible to the immune system and refractory to antiretroviral treatment. Key host cell mechanisms that drive HIV into latency are sequestration of transcription initiation factors, establishment of epigenetic barriers inactivating the proviral promoter, and blockage of the assembly of the host elongation factor P-TEFb. This comprehensive understanding of the molecular control of HIV transcription is leading to the development of optimized combinatorial reactivation and immune surveillance strategies designed to purge the latent viral reservoir.
[Mh] Termos MeSH primário: Regulação Viral da Expressão Gênica
HIV-1/genética
HIV-1/fisiologia
Transcrição Genética
Latência Viral/genética
[Mh] Termos MeSH secundário: Linfócitos T CD4-Positivos/virologia
Interações Hospedeiro-Patógeno
Seres Humanos
Fator B de Elongação Transcricional Positiva/genética
Regiões Promotoras Genéticas
Provírus/genética
Provírus/fisiologia
Replicação Viral
Produtos do Gene tat do Vírus da Imunodeficiência Humana/genética
Produtos do Gene tat do Vírus da Imunodeficiência Humana/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (tat Gene Products, Human Immunodeficiency Virus); EC 2.7.11.- (Positive Transcriptional Elongation Factor B)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170719
[St] Status:MEDLINE
[do] DOI:10.1146/annurev-virology-101416-041646


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[PMID]:28628041
[Au] Autor:Kwon KJ; Siliciano RF
[Ad] Endereço:Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
[Ti] Título:HIV persistence: clonal expansion of cells in the latent reservoir.
[So] Source:J Clin Invest;127(7):2536-2538, 2017 Jun 30.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:While antiretroviral therapy (ART) can reduce HIV-1 to undetectable levels, the virus generally reappears if treatment is stopped. Resurgence of the virus is due to the reactivation of T cells harboring latent integrated provirus, and recent studies indicate that proliferation of these latently infected cells helps maintain the HIV-1 reservoir. In this issue of the JCI, Lee et al. evaluated CD4+ T cell subsets to determine whether certain populations are more likely to harbor full-length, replication-competent provirus. The authors identified an enrichment of clonally expanded Th1 cells containing intact HIV-1 proviruses, suggesting that this polarized subset contributes to the persistence of the reservoir. Strategies to target these provirus-harboring cells need to be considered for future therapies aimed toward HIV-1 cure.
[Mh] Termos MeSH primário: Infecções por HIV/imunologia
HIV-1/imunologia
Provírus/imunologia
Células Th1/imunologia
[Mh] Termos MeSH secundário: Animais
Infecções por HIV/patologia
Seres Humanos
Células Th1/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170914
[Lr] Data última revisão:
170914
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170620
[St] Status:MEDLINE


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[PMID]:28615198
[Au] Autor:Meissner ME; Mendonça LM; Zhang W; Mansky LM
[Ad] Endereço:Institute for Molecular Virology, University of Minnesota, Minneapolis, Minnesota, USA.
[Ti] Título:Polymorphic Nature of Human T-Cell Leukemia Virus Type 1 Particle Cores as Revealed through Characterization of a Chronically Infected Cell Line.
[So] Source:J Virol;91(16), 2017 Aug 15.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human T-cell leukemia virus type 1 (HTLV-1) is the etiological agent of adult T-cell leukemia (ATL) and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). HTLV-1 cell-to-cell transmission is dependent on the release of infectious virus particles into the virological synapse. The HTLV-1 particle structure is still poorly understood, and previous studies analyzed viruses produced by transformed lymphocytic cell lines chronically infected with HTLV-1, particularly the MT-2 cell line, which harbors truncated proviruses and expresses aberrant forms of the Gag protein. In this study, we demonstrate that the chronically infected SP cell line harbors a relatively low number of proviruses, making it a more promising experimental system for the study of the HTLV-1 particle structure. We first identified the genomic sites of integration and characterized the genetic structure of the region in each provirus. We also determined that despite encoding a truncated Gag protein, only the full-length Gag protein was incorporated into virus particles. Cryo-transmission electron microscopy analyses of the purified virus particles revealed three classes of particles based upon capsid core morphology: complete cores, incomplete cores, and particles without distinct electron densities that would correlate with the capsid region of a core structure. Observed cores were generally polygonal, and virus particles were on average 115 nm in diameter. These data corroborate particle morphologies previously observed for MT-2 cells and provide evidence that the known poor infectivity of HTLV-1 particles may correlate with HTLV-1 particle populations containing few virus particles possessing a complete capsid core structure. Studies of retroviral particle core morphology have demonstrated a correlation between capsid core stability and the relative infectivity of the virus. In this study, we used cryo-transmission electron microscopy to demonstrate that HTLV-1 particles produced from a distinct chronically infected cell line are polymorphic in nature, with many particles lacking organized electron densities that would correlate with a complete core structure. These findings have important implications for infectious HTLV-1 spread, particularly in the context of cell-to-cell transmission, a critical step in HTLV-1 transmission and pathogenesis.
[Mh] Termos MeSH primário: Deltaretrovirus/fisiologia
Deltaretrovirus/ultraestrutura
Provírus/genética
Vírion/ultraestrutura
Integração Viral
[Mh] Termos MeSH secundário: Linhagem Celular
Microscopia Crioeletrônica
Deltaretrovirus/genética
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170810
[Lr] Data última revisão:
170810
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170616
[St] Status:MEDLINE


  9 / 3754 MEDLINE  
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[PMID]:28577855
[Au] Autor:Kim J; Jobe O; Peachman KK; Michael NL; Robb ML; Rao M; Rao VB
[Ad] Endereço:US Military HIV Research Program, Henry M. Jackson Foundation for the Advancement of Military Medicine, 6720A Rockledge Drive, Bethesda, MD 20817, USA; Laboratory of Adjuvant and Antigen Research, US Military HIV Research Program, Walter Reed Army Institute of Research, Silver Spring 20910, MD, USA.
[Ti] Título:Quantitative analyses reveal distinct sensitivities of the capture of HIV-1 primary viruses and pseudoviruses to broadly neutralizing antibodies.
[So] Source:Virology;508:188-198, 2017 Aug.
[Is] ISSN:1096-0341
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Development of vaccines capable of eliciting broadly neutralizing antibodies (bNAbs) is a key goal to controlling the global AIDS epidemic. To be effective, bNAbs must block the capture of HIV-1 to prevent viral acquisition and establishment of reservoirs. However, the role of bNAbs, particularly during initial exposure of primary viruses to host cells, has not been fully examined. Using a sensitive, quantitative, and high-throughput qRT-PCR assay, we found that primary viruses were captured by host cells and converted into a trypsin-resistant form in less than five minutes. We discovered, unexpectedly, that bNAbs did not block primary virus capture, although they inhibited the capture of pseudoviruses/IMCs and production of progeny viruses at 48h. Further, viruses escaped bNAb inhibition unless the bNAbs were present in the initial minutes of exposure of virus to host cells. These findings will have important implications for HIV-1 vaccine design and determination of vaccine efficacy.
[Mh] Termos MeSH primário: Anticorpos Neutralizantes/imunologia
Anticorpos Anti-HIV/imunologia
Infecções por HIV/imunologia
HIV-1/imunologia
Provírus/imunologia
[Mh] Termos MeSH secundário: Feminino
Infecções por HIV/virologia
HIV-1/genética
Seres Humanos
Masculino
Provírus/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Neutralizing); 0 (HIV Antibodies)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170818
[Lr] Data última revisão:
170818
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170605
[St] Status:MEDLINE


  10 / 3754 MEDLINE  
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[PMID]:28520964
[Au] Autor:Margolis DM; Archin NM
[Ad] Endereço:UNC HIV Cure Center.
[Ti] Título:Proviral Latency, Persistent Human Immunodeficiency Virus Infection, and the Development of Latency Reversing Agents.
[So] Source:J Infect Dis;215(suppl_3):S111-S118, 2017 Mar 15.
[Is] ISSN:1537-6613
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Quiescent proviral genomes that persist during human immunodeficiency virus type 1 (HIV-1) infection despite effective antiretroviral therapy (ART) can fuel rebound viremia after ART interruption and is a central obstacle to the cure of HIV infection. The induction of quiescent provirus is the goal of a new class of potential therapeutics, latency reversing agents (LRAs). The discovery, development, and testing of HIV LRAs is a key part of current efforts to develop latency reversal and viral clearance strategies to eradicate established HIV infection. The development of LRAs is burdened by many uncertainties that make drug discovery difficult. The biology of HIV latency is complex and incompletely understood. Potential targets for LRAs are host factors, and the potential toxicities of host-directed therapies in individuals that are otherwise clinically stable may be unacceptable. Assays to measure latency reversal and assess the effectiveness of potential therapeutics are complex and incompletely validated. Despite these obstacles, novel LRAs are under development and beginning to enter combination testing with viral clearance strategies. It is hoped that the steady advances in the development of LRAs now being paired with emerging immunotherapeutics to clear persistently infected cells will soon allow measurable clinical advances toward an HIV cure.
[Mh] Termos MeSH primário: Fármacos Anti-HIV/isolamento & purificação
Infecções por HIV/virologia
HIV/efeitos dos fármacos
HIV/fisiologia
Provírus/efeitos dos fármacos
Ativação Viral
Latência Viral/efeitos dos fármacos
[Mh] Termos MeSH secundário: Fármacos Anti-HIV/farmacologia
Infecções por HIV/tratamento farmacológico
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-HIV Agents)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170703
[Lr] Data última revisão:
170703
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170519
[St] Status:MEDLINE
[do] DOI:10.1093/infdis/jiw618



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