Human immunodeficiency virus type 1 DNA sequences genetically damaged by hypermutation are often abundant in patient peripheral blood mononuclear cells and may be generated during near-simultaneous infection and activation of CD4(+) T cells.
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Natural polymorphisms in human APOBEC3H and HIV-1 Vif combine in primary T lymphocytes to affect viral G-to-A mutation levels and infectivityThe cytidine deaminase CEM15 induces hypermutation in newly synthesized HIV-1 DNAAPOBEC3A, APOBEC3B, and APOBEC3H haplotype 2 restrict human T-lymphotropic virus type 1Human and rhesus APOBEC3D, APOBEC3F, APOBEC3G, and APOBEC3H demonstrate a conserved capacity to restrict Vif-deficient HIV-1Mutational comparison of the single-domained APOBEC3C and double-domained APOBEC3F/G anti-retroviral cytidine deaminases provides insight into their DNA target site specificitiesRole and mechanism of action of the APOBEC3 family of antiretroviral resistance factorsThe restriction factors of human immunodeficiency virusDifferential anti-APOBEC3G activity of HIV-1 Vif proteins derived from different subtypesAPOBEC3G contributes to HIV-1 variation through sublethal mutagenesisRestriction of retroviral replication by APOBEC3G/F and TRIM5alphaCytidine deamination induced HIV-1 drug resistanceNatural variation in Vif: differential impact on APOBEC3G/3F and a potential role in HIV-1 diversificationMultiple APOBEC3 restriction factors for HIV-1 and one Vif to rule them allThe APOBEC3 family of retroelement restriction factorsDNA deamination: not just a trigger for antibody diversification but also a mechanism for defense against retrovirusesTarget cell APOBEC3C can induce limited G-to-A mutation in HIV-1Endogenous origins of HIV-1 G-to-A hypermutation and restriction in the nonpermissive T cell line CEM2nAPOBEC3G: an intracellular centurionHypermutation of an ancient human retrovirus by APOBEC3GA classification approach for genotyping viral sequences based on multidimensional scaling and linear discriminant analysis.T cells contain an RNase-insensitive inhibitor of APOBEC3G deaminase activity.APOBEC3G inhibits elongation of HIV-1 reverse transcripts.Genetic editing of HBV DNA by monodomain human APOBEC3 cytidine deaminases and the recombinant nature of APOBEC3G.Massive APOBEC3 editing of hepatitis B viral DNA in cirrhosis.Quantification of deaminase activity-dependent and -independent restriction of HIV-1 replication mediated by APOBEC3F and APOBEC3G through experimental-mathematical investigation.Quasispecies theory and the behavior of RNA viruses.Leveraging APOBEC3 proteins to alter the HIV mutation rate and combat AIDS.G-->A hypermutation in protease and reverse transcriptase regions of human immunodeficiency virus type 1 residing in resting CD4+ T cells in vivoInteractions of host APOBEC3 restriction factors with HIV-1 in vivo: implications for therapeutics.Extensive editing of both hepatitis B virus DNA strands by APOBEC3 cytidine deaminases in vitro and in vivo.APOBEC3G hypermutates genomic DNA and inhibits Ty1 retrotransposition in yeast.Human APOBEC3 induced mutation of human immunodeficiency virus type-1 contributes to adaptation and evolution in natural infection.Expression of APOBEC3G/3F and G-to-A hypermutation levels in HIV-1-infected children with different profiles of disease progression.Innate immune signaling induces high levels of TC-specific deaminase activity in primary monocyte-derived cells through expression of APOBEC3A isoformsIn vivo HIV-1 hypermutation and viral loads among antiretroviral-naive Brazilian patients.Remarkable lethal G-to-A mutations in vif-proficient HIV-1 provirus by individual APOBEC3 proteins in humanized miceHuman immunodeficiency virus type 1 can establish latent infection in resting CD4+ T cells in the absence of activating stimuli.Stably expressed APOBEC3F has negligible antiviral activity.APOBEC3G-induced hypermutation of human immunodeficiency virus type-1 is typically a discrete "all or nothing" phenomenon.Retroviral vectors for analysis of viral mutagenesis and recombination.
P2860
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P2860
Human immunodeficiency virus type 1 DNA sequences genetically damaged by hypermutation are often abundant in patient peripheral blood mononuclear cells and may be generated during near-simultaneous infection and activation of CD4(+) T cells.
description
2001 nî lūn-bûn
@nan
2001 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած
@hyw
2001 թվականի սեպտեմբերին հրատարակված գիտական հոդված
@hy
2001年の論文
@ja
2001年学术文章
@wuu
2001年学术文章
@zh-cn
2001年学术文章
@zh-hans
2001年学术文章
@zh-my
2001年学术文章
@zh-sg
2001年學術文章
@yue
name
Human immunodeficiency virus t ...... activation of CD4(+) T cells.
@ast
Human immunodeficiency virus t ...... activation of CD4(+) T cells.
@en
type
label
Human immunodeficiency virus t ...... activation of CD4(+) T cells.
@ast
Human immunodeficiency virus t ...... activation of CD4(+) T cells.
@en
prefLabel
Human immunodeficiency virus t ...... activation of CD4(+) T cells.
@ast
Human immunodeficiency virus t ...... activation of CD4(+) T cells.
@en
P2093
P2860
P1433
P1476
Human immunodeficiency virus t ...... activation of CD4(+) T cells.
@en
P2093
P2860
P304
P356
10.1128/JVI.75.17.7973-7986.2001
P577
2001-09-01T00:00:00Z