These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Cellular immune responses to Herpes simplex virus type 1 in recurrent herpes labialis: in vitro blastogenesis and cytotoxicity to infected cell line.
    Author: Steele RW, Vincent MM, Hensen SA, Fuccillo DA, Chapa IA, Canales L.
    Journal: J Infect Dis; 1975 May; 131(5):528-34. PubMed ID: 165245.
    Abstract:
    Cellular immunity to herpes simplex virus type 1 (HSV-1) in 12 volunteers with recurrent herpes labialis was evaluated by means of two microassays. In the blastogenesis assay, lymphocytes were incubated with tissue culture cells persistently infected with HSV-1. Uninfected cells were used as controls, and a blastogenic index was calculated. The mean blastogenic index (plus or minus SD) for subjects with recurrent herpes labialis was 26.9 (plus or minus 8.3); the mean blastogenic index (plus or minus SD) in control donors with antibody to HSV-1 was 13.4 (plus or minus 7.2). The difference between these values was statistically significant (t equals 4.154; P smaller than 0.001). In the cytotoxicity assay, cells of the same persistently infected line were used as target cells, and release of 51-Cr from these cells or from control cells served as the index of lymphocyte reactivity. Specific immune release attributable to HSV-1 averages 3.7% (plus or minus 1.8%) in subjects with recurrent herpes labialis, compared with 23.1% (plus or minus 9.8%) in controls (t equals 6.135; P smaller than 0.001). These data suggest a dissociation between mechanisms of cellular immunity, with enhanced lymphocyte blastogenesis but decreased cytotoxicity. Recurrent herpes labialis may thus result from subtle cellular immune deficiency involving at least one of the efferent mechanisms.
    [Abstract] [Full Text] [Related] [New Search]