Mapping genetic determinants for human immunodeficiency virus type 1 resistance to soluble CD4.
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Pathogenesis of human immunodeficiency virus infectionThe human immunodeficiency virus type 1 vpr gene arrests infected T cells in the G2 + M phase of the cell cycleSensitivity of human immunodeficiency virus type 1 to fusion inhibitors targeted to the gp41 first heptad repeat involves distinct regions of gp41 and is consistently modulated by gp120 interactions with the coreceptorAnti-human immunodeficiency virus type 1 activity of an oligocationic compound mediated via gp120 V3 interactionsHuman immunodeficiency virus type 1 envelope glycoprotein molecules containing membrane fusion-impairing mutations in the V3 region efficiently undergo soluble CD4-stimulated gp120 release.Primary virus envelope cross-reactivity of the broadening neutralizing antibody response during early chronic human immunodeficiency virus type 1 infection.Adoption of an "open" envelope conformation facilitating CD4 binding and structural remodeling precedes coreceptor switch in R5 SHIV-infected macaques.Adaptation of subtype a human immunodeficiency virus type 1 envelope to pig-tailed macaque cellsHIV type 1 Env precursor cleavage state affects recognition by both neutralizing and nonneutralizing gp41 antibodies.Virus receptors: implications for pathogenesis and the design of antiviral agents.Adaptation to persistent growth in the H9 cell line renders a primary isolate of human immunodeficiency virus type 1 sensitive to neutralization by vaccine seraCellular CD44S as a determinant of human immunodeficiency virus type 1 infection and cellular tropism.Human immunodeficiency virus 1 envelope proteins induce interleukin 1, tumor necrosis factor alpha, and nitric oxide in glial cultures derived from fetal, neonatal, and adult human brainIdentification of interdependent variables that influence coreceptor switch in R5 SHIV(SF162P3N)-infected macaques.Differential regulation of cellular tropism and sensitivity to soluble CD4 neutralization by the envelope gp120 of human immunodeficiency virus type 1.Cryptic nature of envelope V3 region epitopes protects primary monocytotropic human immunodeficiency virus type 1 from antibody neutralization.Two mechanisms of soluble CD4 (sCD4)-mediated inhibition of human immunodeficiency virus type 1 (HIV-1) infectivity and their relation to primary HIV-1 isolates with reduced sensitivity to sCD4.Distinct superinfection interference properties yet similar receptor utilization by cytopathic and noncytopathic feline leukemia viruses.Infection of macrophages with lymphotropic human immunodeficiency virus type 1 can be arrested after viral DNA synthesis.R5X4 viruses are evolutionary, functional, and antigenic intermediates in the pathway of a simian-human immunodeficiency virus coreceptor switchTransitions to and from the CD4-bound conformation are modulated by a single-residue change in the human immunodeficiency virus type 1 gp120 inner domainCoreceptor use in nonhuman primate models of HIV infection.Functional role of the V1/V2 region of human immunodeficiency virus type 1 envelope glycoprotein gp120 in infection of primary macrophages and soluble CD4 neutralization.Macrophage-tropic and T-cell line-adapted chimeric strains of human immunodeficiency virus type 1 differ in their susceptibilities to neutralization by soluble CD4 at different temperatures.Both neutralization resistance and high infectivity phenotypes are caused by mutations of interacting residues in the human immunodeficiency virus type 1 gp41 leucine zipper and the gp120 receptor- and coreceptor-binding domains.The N-terminal V3 loop glycan modulates the interaction of clade A and B human immunodeficiency virus type 1 envelopes with CD4 and chemokine receptors.Sensitivity of human immunodeficiency virus type 1 to the fusion inhibitor T-20 is modulated by coreceptor specificity defined by the V3 loop of gp120Primary isolates of human immunodeficiency virus type 1 are relatively resistant to neutralization by monoclonal antibodies to gp120, and their neutralization is not predicted by studies with monomeric gp120.Equal levels of gp120 retention and neutralization resistance of phenotypically distinct primary human immunodeficiency virus type 1 variants upon soluble CD4 treatment.Kinetics of human immunodeficiency virus type 1 reverse transcription in blood mononuclear phagocytes are slowed by limitations of nucleotide precursors.Direct antibody access to the HIV-1 membrane-proximal external region positively correlates with neutralization sensitivity.
P2860
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P2860
Mapping genetic determinants for human immunodeficiency virus type 1 resistance to soluble CD4.
description
1992 nî lūn-bûn
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1992年の論文
@ja
1992年論文
@yue
1992年論文
@zh-hant
1992年論文
@zh-hk
1992年論文
@zh-mo
1992年論文
@zh-tw
1992年论文
@wuu
1992年论文
@zh
1992年论文
@zh-cn
name
Mapping genetic determinants f ...... e 1 resistance to soluble CD4.
@ast
Mapping genetic determinants f ...... e 1 resistance to soluble CD4.
@en
type
label
Mapping genetic determinants f ...... e 1 resistance to soluble CD4.
@ast
Mapping genetic determinants f ...... e 1 resistance to soluble CD4.
@en
prefLabel
Mapping genetic determinants f ...... e 1 resistance to soluble CD4.
@ast
Mapping genetic determinants f ...... e 1 resistance to soluble CD4.
@en
P2093
P2860
P1433
P1476
Mapping genetic determinants f ...... e 1 resistance to soluble CD4.
@en
P2093
P2860
P304
P407
P577
1992-05-01T00:00:00Z