Role of mucosal immunity in herpes simplex virus infection

J Immunol. 1998 Jun 15;160(12):5998-6003.

Abstract

This study evaluates whether the vaginal mucosal surface of immunized mice can prevent invasion by herpes simplex virus (HSV) and aims to identify immune components that affect immunity after challenge at the vaginal mucosa. Despite the induction of both IgA and IgG vaginal Ab following immunization with recombinant vaccinia virus vectors expressing either glycoproteins B or D, viral infection occurred in most animals even after minimal viral dose challenge. Challenged immune animals, including those genetically unable to generate anti-HSV Ab, survived and showed few if any clinical signs of infection. Experiments with T cell subtype knockout animals and depletion with T cell subset-specific MAb indicated that immunity following vaginal challenge was principally dependent on the function of CD4+ T cells. Our results indicate that anti-HSV vaccines may not provide barrier immunity at the vaginal mucosal site but may be adequate to minimize clinical expression of disease.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Administration, Intranasal
  • Animals
  • Antibodies, Viral / biosynthesis
  • B-Lymphocytes / immunology
  • CD4-Positive T-Lymphocytes / immunology
  • Female
  • Herpes Simplex / immunology*
  • Immunity, Mucosal
  • Immunoglobulin A / biosynthesis
  • Immunoglobulin G / biosynthesis
  • Mice
  • Mice, Inbred BALB C
  • Recombinant Proteins / immunology
  • Vaccinia virus
  • Vaginitis / immunology
  • Vaginitis / virology
  • Viral Envelope Proteins / immunology
  • Viral Vaccines / administration & dosage
  • Viral Vaccines / immunology

Substances

  • Antibodies, Viral
  • Immunoglobulin A
  • Immunoglobulin G
  • Recombinant Proteins
  • Viral Envelope Proteins
  • Viral Vaccines
  • glycoprotein B, Simplexvirus
  • glycoprotein D, Human herpesvirus 1