Activation of a varicella-zoster virus-specific IgA response during acute Epstein-Barr virus infection.
The influence of an acute Epstein-Barr virus (EBV) infection on the serological parameters of persistent varicella-zoster virus (VZV) and herpes simplex virus (HSV) was studied. Sera from 161 patients with infectious mononucleosis caused by EBV and 178 age-matched controls were tested for HSV- and VZV-specific IgA. 98.7 percent of VZV-IgG-positive controls were negative for VZV-IgA, pointing to the stringent control of latent VZV in healthy individuals. During acute EBV infection, 33.8% of VZV-IgG-positive infectious mononucleosis patients produced VZV-specific IgA. This result may be explained either by reactivation of VZV due to transient suppression of cellular immune functions during acute EBV infection or by polyclonal stimulation caused by EBV. Due to the high incidence of HSV-IgA in healthy HSV-IgG-positive individuals, only a marginal effect of acute EBV infection on the appearance of HSV-specific IgA was found.
Karner
W
W
Abteilung Virologie, Universität Freiburg, Germany.
Bauer
G
G
D000293:Adolescent; D000328:Adult; D000914:Antibodies, Viral / Q000097:blood*; D000917:Antibody Formation; D002648:Child; D002675:Child, Preschool; D006561:Herpes Simplex / Q000209:etiology / Q000276:immunology; D006562:Herpes Zoster / Q000209:etiology / Q000276:immunology*; D006801:Humans; D007070:Immunoglobulin A / Q000097:blood*; D007074:Immunoglobulin G / Q000097:blood; D007223:Infant; D007244:Infectious Mononucleosis / Q000150:complications*; D014775:Virus Activation; D017735:Virus Latency
D000914:Antibodies, Viral; D007070:Immunoglobulin A; D007074:Immunoglobulin G