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Related Concept Videos

T Cell Activation and Clonal Selection01:22

T Cell Activation and Clonal Selection

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T cells are integral to our adaptive immune system, recognizing and effectively responding to foreign antigens. T cell activation and clonal selection are pivotal in orchestrating this immune response. This article elucidates these mechanisms, detailing the roles of cluster of differentiation (CD) markers, major histocompatibility complex (MHC) molecules, costimulatory signals, and the process of clonal selection.
Naive T cells that have not yet encountered an antigen express two primary CD...
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B Cell Activation and Differentiation01:24

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The adaptive immune response, a sophisticated defense mechanism, relies on the activation and differentiation of B lymphocytes, or B cells. These processes enable our bodies to mount a tailored response against specific pathogens such as bacteria, free virus particles, toxins, and parasites.
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Cell-mediated Immune Responses01:40

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Related Experiment Video

Updated: Apr 26, 2026

A Restriction Enzyme Based Cloning Method to Assess the In vitro Replication Capacity of HIV-1 Subtype C Gag-MJ4 Chimeric Viruses
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A Restriction Enzyme Based Cloning Method to Assess the In vitro Replication Capacity of HIV-1 Subtype C Gag-MJ4 Chimeric Viruses

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B cell liaison confounds HIV-1 evolution.

Michael G McHeyzer-Williams1

  • 1Department of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA 92037, USA.

Cell
|August 2, 2014
PubMed
Summary

Researchers found that HIV-1 viral escape from one B cell lineage can unexpectedly drive another B cell lineage towards broad neutralization, revealing a new adaptive immunity mechanism.

Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • Potent and broadly neutralizing antibodies (bNAbs) against HIV-1 are crucial for viral control.
  • The emergence of bNAbs suggests adaptive immunity can overcome viral escape.
  • Understanding the B cell response dynamics during HIV-1 infection is key.

Purpose of the Study:

  • To investigate the intermediate stages of B cell responses during HIV-1 infection.
  • To elucidate how viral escape influences the development of broadly neutralizing antibody lineages.

Main Methods:

  • Analysis of B cell receptor sequences from HIV-1 infected individuals.
  • Viral sequence analysis to identify escape mutations.
  • Computational modeling of B cell lineage dynamics.

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Conformational Evaluation of HIV-1 Trimeric Envelope Glycoproteins Using a Cell-based ELISA Assay
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Conformational Evaluation of HIV-1 Trimeric Envelope Glycoproteins Using a Cell-based ELISA Assay

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Single-cell Quantitation of mRNA and Surface Protein Expression in Simian Immunodeficiency Virus-infected CD4+ T Cells Isolated from Rhesus macaques
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Single-cell Quantitation of mRNA and Surface Protein Expression in Simian Immunodeficiency Virus-infected CD4+ T Cells Isolated from Rhesus macaques

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Last Updated: Apr 26, 2026

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A Restriction Enzyme Based Cloning Method to Assess the In vitro Replication Capacity of HIV-1 Subtype C Gag-MJ4 Chimeric Viruses

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Conformational Evaluation of HIV-1 Trimeric Envelope Glycoproteins Using a Cell-based ELISA Assay
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Single-cell Quantitation of mRNA and Surface Protein Expression in Simian Immunodeficiency Virus-infected CD4+ T Cells Isolated from Rhesus macaques
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Single-cell Quantitation of mRNA and Surface Protein Expression in Simian Immunodeficiency Virus-infected CD4+ T Cells Isolated from Rhesus macaques

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Main Results:

  • HIV-1 escape from one B cell lineage was observed to select for viral variants.
  • These selected viral variants subsequently drove the expansion and diversification of a separate B cell lineage.
  • This process ultimately led to the development of broadly neutralizing antibodies.

Conclusions:

  • Viral escape can paradoxically facilitate the development of broadly neutralizing antibodies.
  • An intermediate stage exists where viral escape from one B cell lineage promotes a separate lineage's broad neutralization capacity.
  • This highlights a complex interplay between viral evolution and adaptive immune responses in HIV-1 infection.