Increased sensitivity of human lymphoid lines to natural killer cells after induction of the Epstein-Barr viral cycle by superinfection or sodium butyrate
- PMID: 6244358
- PMCID: PMC2185807
- DOI: 10.1084/jem.151.3.614
Increased sensitivity of human lymphoid lines to natural killer cells after induction of the Epstein-Barr viral cycle by superinfection or sodium butyrate
Abstract
Superinfection of latently Epstein-Barr virus (EBV)-carrying Raji cells with the P3HR-1 substrain EBV, known to induce the entry of a substantial fraction of cells into an abortively lytic cycle, increased the susceptibility of the cells to natural killer (NK) effect of human blood lymphocytes. Reciprocal cold-target competition tests with known NK-cell sensitive and -resistant lymphoid cell ines showed that the increased susceptibility is a result of the appearance of an NK-sensitive target, rather than to a general increase in membrane fragility. Lymphocytes of EBV-seropositive and -negative donors were equally effective killers against P3HR-1 virus-superinfected targets. EBV-induced NK sensitivity increased with time. It was a result of some event associated with the intracellular viral cycle, and not to the adherence of viral particles to the cell surface. Induction of EBV-carrying P3HR-1 cells to entry into the viral cycle with n-butyrate also increased their NK sensitivity. A transforming, noncytopathic prototype strain of EBV, B95-8, failed to increase the susceptibility of theRaji cells to NK-lysis, although it had some effect on the Daudi line. Because NK cells can kill virus-producing cells at an early stage of the cycle, before the virus particles are assembled, they may restrict, in vivo, the spread of the virus from latently infected cells.
Similar articles
-
Induction of the EBV cycle in B-lymphocyte-derived lines is accompanied by increased natural killer (NK) sensitivity and the expression of EBV-related antigen(s) detected by the ADCC reaction.Int J Cancer. 1980 Sep 15;26(3):365-71. doi: 10.1002/ijc.2910260317. Int J Cancer. 1980. PMID: 6270007
-
Epstein-Barr virus (EBV)--lymphoid cell interactions. II. The influence of the EBV replication cycle on natural killing and antibody-dependent cellular cytotoxicity against EBV-infected cells.Clin Exp Immunol. 1982 Jun;48(3):589-601. Clin Exp Immunol. 1982. PMID: 6288292 Free PMC article.
-
[Suppressive effect of CDDP on induction of the Epstein-Barr virus antigen synthesis by n-butyrate].Nihon Jibiinkoka Gakkai Kaiho. 1989 Feb;92(2):189-93. doi: 10.3950/jibiinkoka.92.189. Nihon Jibiinkoka Gakkai Kaiho. 1989. PMID: 2545850 Japanese.
-
Two strains of Epstein-Barr virus (B95-8 and a P3HR-1 subclone) that lack defective genomes induce early antigen and cause abortive infection of Raji cells.J Virol. 1987 Jun;61(6):1985-91. doi: 10.1128/JVI.61.6.1985-1991.1987. J Virol. 1987. PMID: 3033325 Free PMC article.
-
Cellular responses to viral infection in humans: lessons from Epstein-Barr virus.Annu Rev Immunol. 2007;25:587-617. doi: 10.1146/annurev.immunol.25.022106.141553. Annu Rev Immunol. 2007. PMID: 17378764 Review.
Cited by
-
Primary immune responses by cord blood CD4(+) T cells and NK cells inhibit Epstein-Barr virus B-cell transformation in vitro.J Virol. 2002 May;76(10):5071-81. doi: 10.1128/jvi.76.10.5071-5081.2002. J Virol. 2002. PMID: 11967323 Free PMC article.
-
Immune regulation in Epstein-Barr virus-associated diseases.Microbiol Rev. 1995 Sep;59(3):387-405. doi: 10.1128/mr.59.3.387-405.1995. Microbiol Rev. 1995. PMID: 7565411 Free PMC article. Review.
-
Relationship between expression of herpes simplex virus glycoproteins and susceptibility of target cells to human natural killer activity.J Exp Med. 1983 May 1;157(5):1544-61. doi: 10.1084/jem.157.5.1544. J Exp Med. 1983. PMID: 6189940 Free PMC article.
-
Autologous lymphokine-activated killer cell therapy of lymphoproliferative disorders arising in organ transplant recipients.Transplant Proc. 1997 May;29(3):1905-6. doi: 10.1016/s0041-1345(96)00112-1. Transplant Proc. 1997. PMID: 9142315 Free PMC article. Clinical Trial.
-
Epstein-Barr serology in immunodeficiencies: an attempt to correlate with immune abnormalities in Wiskott-Aldrich and Chediak-Higashi syndromes and ataxia telangiectasia.Clin Exp Immunol. 1984 Feb;55(2):249-56. Clin Exp Immunol. 1984. PMID: 6321070 Free PMC article.