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Related Experiment Videos

Pathogenic Correlates of Simian Immunodeficiency Virus-Associated B Cell Dysfunction.

Egidio Brocca-Cofano1,2, David Kuhrt1,2, Basile Siewe3

  • 1Center for Vaccine Research, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.

Journal of Virology
|September 22, 2017
PubMed
Summary

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Longitudinal T-Cell Phenotypic Dynamics During Sustained Antiretroviral Therapy in People With HIV.

Open forum infectious diseases·2026

B cell loss is linked to pathogenic simian immunodeficiency virus (SIV) infection, while nonpathogenic SIV increases B cells in natural hosts. This B cell dysfunction impacts antibody production and disease progression, offering insights for HIV prevention strategies.

Area of Science:

  • Immunology
  • Virology
  • Primate Models

Background:

  • Simian immunodeficiency virus (SIV) infection in pig-tailed macaques (PTMs) is pathogenic, unlike in African green monkeys (AGMs).
  • B cell dysfunction is a hallmark of human immunodeficiency virus (HIV) and SIV infections, but its specific role in pathogenesis is unclear.

Purpose of the Study:

  • To compare B cell dynamics in pathogenic (PTM) versus nonpathogenic (AGM) SIV infections.
  • To assess the significance of B cell dysfunction in SIV/HIV pathogenesis and its impact on antibody responses.
  • To evaluate the utility of natural hosts as models for HIV immunization strategies.

Main Methods:

  • Comparative analysis of B cell populations (naive, memory, regulatory) in lymph nodes and blood of PTMs and AGMs during SIV infection.
Keywords:
B cellfollicular T helper cellshumoral immune responseimmune activationnonpathogenic infectionpathogenic infectionsimian immunodeficiency virus

Related Experiment Videos

  • Assessment of SIV-specific antibody production, neutralization titers, avidity, maturation, and conformational epitope recognition.
  • Correlation of B cell dynamics with disease progression and viral load.

    • Main Results:

    • Pathogenic SIV infection in PTMs is characterized by B cell loss, redistribution to the gut, increased regulatory B cells (Bregs), and expansion of exhausted memory B cells.
    • Nonpathogenic SIV infection in AGMs leads to a rapid increase in B cells in lymph nodes and the gut.
    • Despite B cell dysfunction, SIV-specific antibody production was higher in PTMs, but rapid progression correlated with a lack of anti-SIV antibodies. Conformational epitope recognition differed significantly, evolving in natural hosts.

    Conclusions:

    • B cell dysfunction, including loss of naive and memory B cells and increased Bregs, is specifically associated with pathogenic SIV infection.
    • Alterations in B cell populations do not correlate with neutralizing antibody levels but are linked to impaired SIV-specific antibody production in progressive disease.
    • Natural hosts of SIV exhibit humoral immune responses more similar to HIV-infected individuals, suggesting their value for modeling HIV immunization strategies.