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Related Experiment Video

Updated: Dec 16, 2025

Assessing the Innate Sensing of HIV-1 Infected CD4+ T Cells by Plasmacytoid Dendritic Cells Using an Ex vivo Co-culture System.
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HIV-1 subtype C transmitted founders modulate dendritic cell inflammatory responses.

Evelyn Ngwa Lumngwena1,2,3, Simon Metenou4, Lindi Masson5

  • 1Division of Cardiology, Department of Medicine, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa. lumngwena@yahoo.co.uk.

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Summary

Transmitted founder HIV Envelope proteins trigger greater inflammation in dendritic cells than chronic infection variants, potentially aiding initial viral spread. This suggests viral genetics influence early HIV infection dynamics.

Keywords:
HIV-subtype C EnvImmunosuppressionInflammatory responsesTransmissionTransmitter/Founder EnvelopesVirus survival

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Area of Science:

  • Immunology
  • Virology
  • Infectious Diseases

Background:

  • Heterosexual transmission is the primary HIV-1 transmission route.
  • Female genital tract (FGT) inflammation heightens HIV-1 infection risk.
  • Mechanisms linking inflammation to increased HIV-1 susceptibility are not fully understood.

Purpose of the Study:

  • To investigate the mechanisms of dendritic cell (DC)-mediated HIV infection.
  • To compare chemokine and pro-inflammatory cytokine production in response to transmitted founder (TF) and chronic infection (CI) HIV Envelope (Env) pseudotyped viruses (PSV).

Main Methods:

  • Monocyte-derived DCs (MDDCs) were stimulated with TF and CI Env PSV and recombinant gp140.
  • Cytokine secretion was measured using multiplex immunoassay.
  • Signaling pathways (ERK, JNK) and DC-SIGN involvement were assessed.

Main Results:

  • Three of nine TF Env clones induced robust MDDC inflammatory responses, more than CI Env.
  • TF Env induced higher inflammatory cytokine and chemokine secretion from MDDCs compared to CI Env.
  • Env-DC-SIGN binding partially mediated MDDC stimulation and cytokine release.

Conclusions:

  • Transmitted founder HIV Env proteins are more potent inducers of MDDC inflammatory responses than chronic infection variants.
  • Viral genetics may influence inflammatory responses during early HIV infection.
  • Enhanced inflammation by TF Env could facilitate initial viral spread by increasing target cell influx and potentially suppressing immune responses.