Correlation between low natural killing of fibroblasts infected with herpes simplex virus type 1 and susceptibility to herpesvirus infections. NLM AIDSLINE Important note: Information in this article was accurate in 1983. The state of the art may have changed since the publication date.

Click here to return to AIDSLINE main menu
DonateNow
Print this Article


Correlation between low natural killing of fibroblasts infected with herpes simplex virus type 1 and susceptibility to herpesvirus infections.

J Infect Dis. 1983 Jun;147(6):1030-5. Unique Identifier : AIDSLINE MED/83214784
Lopez C; Kirkpatrick D; Read SE; Fitzgerald PA; Pitt J; Pahwa S; Ching CY; Smithwick EM


Abstract: Natural killer cells capable of lysing herpes simplex virus type 1 (HSV-1)-infected fibroblasts were studied in three groups of patients unusually susceptible to severe herpes-virus infections. Cord blood was evaluated because of the known susceptibility of neonates to disseminated infections due to herpes simplex virus type 2 at birth. Only 30% of the cord blood specimens tested demonstrated normal lysis of HSV-1-infected fibroblasts and a normal increment in the lysis of infected over uninfected cells. Five out of six patients with Wiskott-Aldrich Syndrome (WAS) also were found to have abnormally low responses by these criteria. The one WAS patient with normal responses had had little difficulty with infections and had survived much longer than usual. Five patients with severe herpesvirus infections and no known primary cellular immunodeficiency had natural killer cell function significantly below normal (P less than 0.001). These data suggest that natural killer cells probably play an important role in human resistance to herpesvirus infection and that deficiencies of this system may result in unusual susceptibility to herpesvirus infections.
Keywords: Adolescence Adult Child Child, Preschool Cytotoxicity, Immunologic Disease Susceptibility Fibroblasts/MICROBIOLOGY Herpes Simplex/*IMMUNOLOGY Herpesviridae Infections/*IMMUNOLOGY Human Infant Infant, Newborn Killer Cells, Natural/IMMUNOLOGY/*PHYSIOLOGY Middle Age Simplexvirus/IMMUNOLOGY Support, Non-U.S. Gov't Support, U.S. Gov't, P.H.S. Wiskott-Aldrich Syndrome/IMMUNOLOGY JOURNAL ARTICLE

KWDadolescenceadultchildchild,preschoolcytotoxicity,immunologicdiseasesusceptibilityfibroblasts/microbiologyherpessimplex/KWDimmunologyherpesviridaeinfections/KWDimmunologyhumaninfantinfant,newbornkillercells,natural/immunology/KWDphysiologymiddleagesimplexvirus/immunologysupport,non-uKWDsKWDgov'tsupport,uKWDsKWDgov't,pKWDhKWDsKWDwiskott-aldrichsyndrome/immunologyjournalarticle
830930
M8390014


Copyright © 1983 - National Library of Medicine. Reproduced under license with the National Library of Medicine, Bethesda, MD.

AEGiS is a 501(c)3, not-for-profit, tax-exempt, educational corporation. AEGiS is made possible through unrestricted funding from Boehringer Ingelheim, Bridgestone/Firestone Charitable Trust, Bristol-Myers Squibb Company, Elton John AIDS Foundation, Gill Foundation, the National Library of Medicine, Quest Diagnostics, Roche and Trimeris, and donations from users like you. Always watch for outdated information. This article first appeared in 1983. This material is designed to support, not replace, the relationship that exists between you and your doctor.

AEGiS presents published material, reprinted with permission and neither endorses nor opposes any material. All information contained on this website, including information relating to health conditions, products, and treatments, is for informational purposes only. It is often presented in summary or aggregate form. It is not meant to be a substitute for the advice provided by your own physician or other medical professionals. Always discuss treatment options with a doctor who specializes in treating HIV.

Copyright ©1980, 1983. AEGiS. All materials appearing on AEGiS are protected by copyright as a collective work or compilation under U.S. copyright and other laws and are the property of AEGiS, or the party credited as the provider of the content. .