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Your search keyword '"hiv-1 tropism"' showing total 4 results
Start Over Descriptor "hiv-1 tropism" Journal virology
4 results on '"hiv-1 tropism"'

1. Evolution and recombination of genes encoding HIV-1 drug resistance and tropism during antiretroviral therapy

Author

Shi, Binshan, Kitchen, Christina, Weiser, Barbara, Mayers, Douglas, Foley, Brian, Kemal, Kimdar, Anastos, Kathryn, Suchard, Marc, Parker, Monica, Brunner, Cheryl, and Burger, Harold

Subjects
*DRUG resistance, *ANTIRETROVIRAL agents, *HIV, *VIREMIA, *VIRAL genomes, *GENETIC recombination, *VIRAL genetics, *VIRAL evolution
Abstract

Abstract: Characterization of residual plasma virus during antiretroviral therapy (ART) is a high priority to improve understanding of HIV-1 pathogenesis and therapy. To understand the evolution of HIV-1 pol and env genes in viremic patients under selective pressure of ART, we performed longitudinal analyses of plasma-derived pol and env sequences from single HIV-1 genomes. We tested the hypotheses that drug resistance in pol was unrelated to changes in coreceptor usage (tropism), and that recombination played a role in evolution of viral strains. Recombinants were identified by using Bayesian and other computational methods. High-level genotypic resistance was seen in ∼70% of X4 and R5 strains during ART. There was no significant association between resistance and tropism. Each patient displayed at least one recombinant encompassing env and representing a change in predicted tropism. These data suggest that, in addition to mutation, recombination can play a significant role in shaping HIV-1 evolution. [Copyright &y& Elsevier]

Published
2010
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2. Constrained use of CCR5 on CD4+ lymphocytes by R5X4 HIV-1: Efficiency of Env–CCR5 interactions and low CCR5 expression determine a range of restricted CCR5-mediated entry

Author

Loftin, Lamorris M., Kienzle, Martha F., Yi, Yanjie, Lee, Benhur, Lee, Fang-Hua, Gray, Lachlan, Gorry, Paul R., and Collman, Ronald G.

Subjects
*LYMPHOCYTES, *HIV, *GENE expression, *VIRAL genetics, *NUCLEOTIDE sequence, *TROPISMS, *PLANT viruses
Abstract

Abstract: R5X4 HIV-1 has impaired utilization of CCR5 on primary CD4+ lymphocytes but the mechanisms responsible are not well defined. Using a panel of diverse R5X4 Envs we identified a spectrum of CCR5 use on CD4+ lymphocytes. Greater lymphocyte CCR5 use correlated with relative resistance to CCR5 mAbs and small molecule antagonists. Increasing CCR5 expression on lymphocytes increased the proportion of entry mediated by CCR5 for all R5X4 isolates except 89.6. In cell lines with regulated CCR5 expression, strains with greater lymphocyte CCR5 use better exploited limiting levels of CCR5. Introduction of an R306S mutation in the 89.6 V3 domain enhanced its utilization of CCR5 at low levels and switched its preference to CCR5 for lymphocyte entry. Thus, the degree to which R5X4 HIV-1 use primary lymphocyte CCR5 is determined by low CCR5 expression coupled with variations in the efficiency of Env–CCR5 interactions, which is in part governed by V3 sequences. [Copyright &y& Elsevier]

Published
2010
Full Text
View/download PDF

3. Evolution and recombination of genes encoding HIV-1 drug resistance and tropism during antiretroviral therapy

Author

Harold Burger, Christina M. R. Kitchen, Binshan Shi, Kimdar Sherefa Kemal, Barbara Weiser, Cheryl Brunner, Kathryn Anastos, Marc A. Suchard, Brian T. Foley, Monica M. Parker, and Douglas L. Mayers

Subjects
Anti-HIV Agents, viruses, Molecular Sequence Data, Sequence Homology, HIV Infections, Drug resistance, Biology, medicine.disease_cause, Genome, Article, Virus, Evolution, Molecular, Viral Proteins, Antiretroviral Therapy, Highly Active, Virology, Drug Resistance, Viral, Genotype, medicine, Cluster Analysis, Humans, Selection, Genetic, HIV-1 recombination, Gene, Phylogeny, Tropism, Recombination, Genetic, Genetics, Mutation, env Gene Products, Human Immunodeficiency Virus, virus diseases, Sequence Analysis, DNA, Viral Tropism, pol Gene Products, Human Immunodeficiency Virus, HIV-1, Tissue tropism, Female, HIV-1 tropism, HIV-1 drug resistance
Abstract

Characterization of residual plasma virus during antiretroviral therapy (ART) is a high priority to improve understanding of HIV-1 pathogenesis and therapy. To understand the evolution of HIV-1 pol and env genes in viremic patients under selective pressure of ART, we performed longitudinal analyses of plasma-derived pol and env sequences from single HIV-1 genomes. We tested the hypotheses that drug resistance in pol was unrelated to changes in coreceptor usage (tropism), and that recombination played a role in evolution of viral strains. Recombinants were identified by using Bayesian and other computational methods. High-level genotypic resistance was seen in approximately 70% of X4 and R5 strains during ART. There was no significant association between resistance and tropism. Each patient displayed at least one recombinant encompassing env and representing a change in predicted tropism. These data suggest that, in addition to mutation, recombination can play a significant role in shaping HIV-1 evolution.

Published
2010

4. Constrained use of CCR5 on CD4+ lymphocytes by R5X4 HIV-1: efficiency of Env-CCR5 interactions and low CCR5 expression determine a range of restricted CCR5-mediated entry

Author

Lamorris M Loftin, Paul R Gorry, Yanjie Yi, Martha Kienzle, Benhur Lee, Lachlan Robert Gray, Fang-Hua Lee, and Ronald G. Collman

Subjects
CD4-Positive T-Lymphocytes, Receptors, CCR5, medicine.drug_class, Lymphocyte, viruses, Molecular Sequence Data, Mutation, Missense, Gene Expression, Plasma protein binding, Biology, medicine.disease_cause, Monoclonal antibody, R5X4 HIV-1, Article, 03 medical and health sciences, Receptors, HIV, CD4+ lymphocytes, Viral entry, Virology, Gene expression, medicine, Humans, Amino Acid Sequence, Gene, Cells, Cultured, 030304 developmental biology, 0303 health sciences, Mutation, 030306 microbiology, env Gene Products, Human Immunodeficiency Virus, virus diseases, Virus Internalization, Small molecule, 3. Good health, Cell biology, medicine.anatomical_structure, Amino Acid Substitution, Immunology, HIV-1, Coreceptor use, HIV-1 tropism, CCR5, Protein Binding
Abstract

R5X4 HIV-1 has impaired utilization of CCR5 on primary CD4+ lymphocytes but the mechanisms responsible are not well defined. Using a panel of diverse R5X4 Envs we identified a spectrum of CCR5 use on CD4+ lymphocytes. Greater lymphocyte CCR5 use correlated with relative resistance to CCR5 mAbs and small molecule antagonists. Increasing CCR5 expression on lymphocytes increased the proportion of entry mediated by CCR5 for all R5X4 isolates except 89.6. In cell lines with regulated CCR5 expression, strains with greater lymphocyte CCR5 use better exploited limiting levels of CCR5. Introduction of an R306S mutation in the 89.6 V3 domain enhanced its utilization of CCR5 at low levels and switched its preference to CCR5 for lymphocyte entry. Thus, the degree to which R5X4 HIV-1 use primary lymphocyte CCR5 is determined by low CCR5 expression coupled with variations in the efficiency of Env–CCR5 interactions, which is in part governed by V3 sequences.

Published
2010

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