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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...
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Viral replication and dissemination rely on efficient mechanisms for host cell entry, genome replication, assembly, and release. Influenza viruses, such as types A and B, are negative-sense single-stranded RNA viruses with a segmented genome, that depend on two critical surface glycoproteins to carry out these processes: hemagglutinin (HA) and neuraminidase (NA). HA initiates infection by binding to sialic acid residues on the surface of host epithelial cells, facilitating receptor-mediated...

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Related Experiment Video

Updated: Jun 25, 2026

A Simple Flow Cytometry Based Assay to Determine In Vitro Antibody Dependent Enhancement of Dengue Virus Using Zika Virus Convalescent Serum
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Characterization of Serotype-Specific Dengue Virus T-Cell Inhibition.

Jinhua Xiang1,2, James H McLinden1,2, Qing Chang1,2

  • 1Medical and Research Services, Iowa City VA HealthCare.

The Journal of Infectious Diseases
|May 8, 2025
PubMed
Summary

Dengue virus serotypes 1 and 4, unlike 2 and 3, inhibit T cell receptor signaling via envelope proteins. This difference in T cell activation may explain why DENV-2 and -3 cause more severe disease.

Keywords:
T-cell receptordengue virusflavivirusserotypesignaling

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Area of Science:

  • Immunology
  • Virology
  • Molecular Biology

Background:

  • Dengue virus (DENV) serotypes 2 and 3 infections are linked to more severe disease than serotypes 1 and 4.
  • The underlying biological mechanisms for this disparity remain unclear.

Purpose of the Study:

  • To investigate the differential effects of DENV serotypes on human T cell activation.
  • To identify the viral components responsible for modulating T cell responses.

Main Methods:

  • Assessed T cell receptor (TCR)-mediated IL-2 release upon stimulation in the presence of DENV serotypes.
  • Expressed DENV envelope (env) proteins in T cells to map inhibitory regions.
  • Utilized microscopy and immunoblotting to characterize TCR signaling pathway inhibition.
  • Employed reverse genetics to validate findings.

Main Results:

  • DENV-1 and -4 inhibited TCR signaling, while DENV-2 and -3 did not, independent of viral replication.
  • DENV envelope proteins interfered with proximal TCR signaling events.
  • Specific amino acids (aa 49-62, particularly 55 and 66) in DENV-1 env were critical for TCR inhibition.
  • Genetic manipulation confirmed the role of these specific amino acids in dictating TCR inhibition.

Conclusions:

  • DENV-1 and -4 viral particles and env proteins impair T cell responses by disrupting TCR signaling.
  • DENV-2 and -3 do not exhibit this inhibitory effect on T cell signaling.
  • These findings offer a potential explanation for the varying clinical severity observed across different DENV serotypes.