February 1985
Volume 26, Issue 2
Free
Articles  |   February 1985
Lysis of herpes simplex virus (HSV) infected targets. IV. HSV-induced change in the effector population.
Investigative Ophthalmology & Visual Science February 1985, Vol.26, 208-213. doi:
  • Views
  • PDF
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      R L Hendricks, J Sugar; Lysis of herpes simplex virus (HSV) infected targets. IV. HSV-induced change in the effector population.. Invest. Ophthalmol. Vis. Sci. 1985;26(2):208-213.

      Download citation file:


      © ARVO (1962-2015); The Authors (2016-present)

      ×
  • Supplements
Abstract

Herpes simplex virus type 1 (HSV-1) stimulation of peripheral blood lymphocytes from patients (PBL-P) with both recurrent corneal and oral-facial HSV-1 lesions results in altered natural killer (NK) activity. Freshly isolated PBL-P exhibit high lysis of HSV-1 infected allogeneic fibroblasts but low lysis of uninfected fibroblasts. After stimulation with HSV-1, PBL-P exhibit markedly increased lysis of uninfected fibroblasts such that the HSV-1 infected and uninfected fibroblasts are lysed with equal efficiency. The NK activity in freshly isolated PBL-P is mediated by effector cells that are phenotypically distinct from those responsible for the NK activity in HSV-1 stimulated PBL-P. In freshly isolated PBL-P most of the lysis of HSV-1 infected fibroblasts is mediated by lymphocytes expressing the phenotype OKM1+, OKT3+, and Leu-7+. After incubation with HSV-1, most of the lysis of HSV-1 infected and uninfected fibroblasts is mediated by lymphocytes that express the OKM1 antigen but lack detectable OKT3 or Leu-7 antigens. The change in function and phenotype appears to reflect in part the activation of Leu-7-, OKM1+, and OKT3- precursors of cytotoxic lymphocytes that are inactive in freshly isolated PBL-P.

×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×