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Replication-defective viruses modulate immune responses.

M J Browning1, B S Huneycutt, A S Huang

  • 1Division of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA.

Journal of Immunology (Baltimore, Md. : 1950)
|October 15, 1991
PubMed
Summary
This summary is machine-generated.

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Defective virus particles, like vesicular stomatitis virus (VSV) defective interfering particles, impair T lymphocyte responses and viral antigen presentation. This impacts cellular immunity, with CD8+ cytotoxic T lymphocytes (CTL) showing reduced function against infected cells.

Area of Science:

  • Immunology
  • Virology
  • Cellular Immunity

Background:

  • Cellular immunity relies on T lymphocytes to recognize and eliminate virus-infected cells.
  • Virus replication can be modulated by defective interfering particles (DI particles).

Purpose of the Study:

  • To investigate the differential effects of replication-competent and defective virus particles on the cellular immune system.
  • To elucidate the impact of vesicular stomatitis virus (VSV) defective interfering particles (DI 0.33) on T lymphocyte responses and antigen presentation.

Main Methods:

  • Immunization of inbred mice (BALB/c) with purified replication-competent virus, defective virus particles, or a mixture.
  • Assessment of Ag-specific T lymphocyte proliferation, IL-2 secretion, and cytolytic activity.
  • Analysis of target cell recognition and lysis by CD8+ cytotoxic T lymphocytes (CTL) and CD4+ T lymphocyte clones.

Related Experiment Videos

  • Metabolic labeling studies to evaluate viral protein synthesis.

    • Main Results:

    • Defective VSV particles induced lower levels of proliferating, IL-2 secreting, and cytolytic Ag-specific T lymphocytes compared to standard virus.
    • Mice primed with a mixture of wild-type (wt) and DI virus showed reduced T lymphocyte proliferation.
    • DI particles impaired the recognition and lysis of infected target cells by CD8+ CTL, dependent on DI particle concentration.
    • DI particles suppressed viral protein synthesis in dually infected cells.
    • CD4+ T lymphocyte clones efficiently lysed cells infected with DI particles alone or with both wt and DI virus.

    Conclusions:

    • Defective virus particles lead to reduced efficiency in priming Ag-specific T lymphocytes.
    • DI particles interfere with the presentation of viral antigens to CD8+ CTL, potentially by suppressing viral protein synthesis.
    • While CD8+ CTL responses are impaired, CD4+ T lymphocyte recognition and lysis of infected cells remain effective.