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Xiping Wei

Researcher at University of Alabama at Birmingham

Publications -  14
Citations -  12525

Xiping Wei is an academic researcher from University of Alabama at Birmingham. The author has contributed to research in topics: Virus & Viral replication. The author has an hindex of 12, co-authored 13 publications receiving 12087 citations. Previous affiliations of Xiping Wei include Howard Hughes Medical Institute.

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Journal ArticleDOI

Viral dynamics in human immunodeficiency virus type 1 infection

TL;DR: Almost complete replacement of wild-type virus in plasma by drug-resistant variants occurs after fourteen days, indicating that HIV-1 viraemia is sustained primarily by a dynamic process involving continuous rounds of de novo virus infection and replication and rapid cell turnover.
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Antibody neutralization and escape by HIV-1

TL;DR: The detection of autologous Nab as early as 52 days after detection of HIV-specific antibodies is reported, indicating a new mechanism contributing to HIV-1 persistence in the face of an evolving antibody repertoire.
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Identification and characterization of transmitted and early founder virus envelopes in primary HIV-1 infection

TL;DR: A mathematical model of random viral evolution and phylogenetic tree construction is developed and used to analyze 3,449 complete env sequences derived by single genome amplification from 102 subjects with acute HIV-1 (clade B) infection, suggesting a finite window of potential vulnerability of HIV- 1 to vaccine-elicited immune responses, although phenotypic properties of transmitted Envs pose a formidable defense.
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Emergence of Resistant Human Immunodeficiency Virus Type 1 in Patients Receiving Fusion Inhibitor (T-20) Monotherapy

TL;DR: These findings provide the first evidence for the rapid emergence of clinical resistance to a novel class of HIV-1 entry inhibitors and may be relevant to future treatment strategies involving these agents.
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Antiviral pressure exerted by HIV-1-specific cytotoxic T lymphocytes (CTLs) during primary infection demonstrated by rapid selection of CTL escape virus.

TL;DR: It is shown that in a patient whose early CTL response was focused on a highly immunodominant epitope in gp160, there was rapid elimination of the transmitted virus strain and selection for a virus population bearing amino acid changes at a single residue within this epitope, which conferred escape from recognition by epitope-specific CTL.