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Related Concept Videos

Immune Response Against Viral Pathogens01:29

Immune Response Against Viral Pathogens

The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
NK Cells
NK cells are a crucial part of our innate immune system, acting as the first line of defense against viral infections. These cells can recognize and kill infected cells without prior exposure to the virus, effectively slowing down the spread of infection. Additionally, NK cells produce proinflammatory...
Cell-mediated Immune Responses01:40

Cell-mediated Immune Responses

Overview
Sexually Transmitted Infections01:26

Sexually Transmitted Infections

Sexually transmitted infections (STIs) are diseases transmitted primarily through unsafe sexual interactions. Bacteria, viruses, or parasites cause them and can result in severe health complications if untreated.ChlamydiaThe bacterium Chlamydia trachomatis is responsible for the disease Chlamydia, the most common STI in the United States. This peculiar pathogen requires human cells to reproduce, residing intracellularly. The initial infection often goes unnoticed because it typically does not...
Inhibitors of Virion Maturation and Assembly01:19

Inhibitors of Virion Maturation and Assembly

As part of their replication cycle, certain viruses synthesize long precursor proteins called polyproteins within infected host cells. In human immunodeficiency virus (HIV), two major polyproteins are produced: Gag and Gag-Pol. The Gag polyprotein supplies the structural components of the virus, while Gag-Pol includes essential viral enzymes such as reverse transcriptase, integrase, and protease. After synthesis, these polyproteins move to the host cell membrane, where they assemble into an...
Antigens Involved in Adaptive Immunity01:26

Antigens Involved in Adaptive Immunity

An antigen is any substance the immune system identifies as foreign and potentially harmful to the body, prompting an immune response. Antigens have two functional properties: immunogenicity and reactivity. Immunogenicity is the ability of an antigen to stimulate a specific immune response. At the same time, reactivity describes the antigen's ability to react with the cells and antibodies produced in response to it.
Complete Antigens
Complete antigens possess both immunogenicity and reactivity.
Humoral Immune Responses01:36

Humoral Immune Responses

Overview

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Related Experiment Video

Updated: May 29, 2026

Isolation of Exosomes from the Plasma of HIV-1 Positive Individuals
06:46

Isolation of Exosomes from the Plasma of HIV-1 Positive Individuals

Published on: January 5, 2016

Host immune responses that promote initial HIV spread.

K Wendelsdorf1, G Dean, Shuhua Hu

  • 1Virginia Bioinformatics Institute, Virginia Polytechnic Institute and University, Washington Street, MC 0477, Blacksburg, VA 24061, USA.

Journal of Theoretical Biology
|August 30, 2011
PubMed
Summary

Activating natural regulatory T-cells (nTreg) can paradoxically accelerate HIV spread by increasing viral production. Targeting dendritic cell (DC) deactivation by nTreg is key to inhibiting viral proliferation while preserving antiviral activity.

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Peptide-based Identification of Functional Motifs and their Binding Partners
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Last Updated: May 29, 2026

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06:46

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Published on: January 5, 2016

Peptide-based Identification of Functional Motifs and their Binding Partners
14:28

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Assessing the Innate Sensing of HIV-1 Infected CD4+ T Cells by Plasmacytoid Dendritic Cells Using an Ex vivo Co-culture System.
08:11

Assessing the Innate Sensing of HIV-1 Infected CD4+ T Cells by Plasmacytoid Dendritic Cells Using an Ex vivo Co-culture System.

Published on: September 1, 2015

Area of Science:

  • Immunology
  • Virology
  • Computational Biology

Background:

  • The host inflammatory response is crucial for controlling HIV, but it relies on CD4+ T-helper 1 (Th1) cells, which are also susceptible to HIV.
  • This reliance creates a paradox where enhancing the inflammatory response can inadvertently promote viral spread.
  • Natural regulatory T-cells (nTreg) at mucosal sites can dampen inflammatory responses, offering a potential regulatory mechanism.

Purpose of the Study:

  • To model the inflammatory response to viral invasion and nTreg-mediated regulation.
  • To investigate the net effect of nTreg activation on viral proliferation.
  • To identify optimal targets within the inflammatory response for inhibiting viral spread without compromising initial antiviral activity.

Main Methods:

  • Development of a mathematical model simulating the inflammatory response to viral infection and nTreg regulation.
  • Utilizing computational simulations to analyze the impact of nTreg activation and inflammatory pathways.
  • Evaluating the roles of Natural Killer (NK) cells, dendritic cells (DCs), and Th1 cells in viral proliferation.

Main Results:

  • Induction of nTreg accelerates viral proliferation due to direct viral production by nTreg, not reduced NK cell activity.
  • Both DC and Th1 activation expedite viral proliferation.
  • NK cell response effectively controls viral proliferation, while DC-mediated T-cell stimulation drives it.
  • nTreg-mediated DC deactivation significantly slows viral proliferation by inhibiting T-cell stimulation, aiding the antiviral response.

Conclusions:

  • Activating nTreg can paradoxically enhance HIV proliferation.
  • Targeting DC deactivation by nTreg is a promising strategy to inhibit viral spread.
  • The interplay between nTreg, DCs, and Th1 cells is critical in managing HIV infection and warrants further investigation for therapeutic interventions.