Specific lysis of varicella zoster virus-infected B lymphoblasts by human T cells

Hayward, Anthony R.; Pontesilli, O.; Herberger, Mark; László, M; Levin, Myron J.

doi:10.1128/jvi.58.1.179-184.1986

Cited by 51 publications

(13 citation statements)

References 16 publications

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“…Cytotoxic T lymphocytes recognize viral peptides complexed with class I or II MHC antigens. CD8 ϩ T lymphocytes were first recognized as having cytotoxic function against infected cells that express class I MHC markers; in the case of VZV and other herpesviruses, cytotoxic T-lymphocyte function is also mediated by CD4 ϩ T lymphocytes that recognize viral peptides associated with class II MHC proteins (13,125,128). Primary VZV infection elicits cytotoxic T lymphocytes that recognize VZV glycoproteins and the IE62 protein (13).…”

Section: Cell-mediated Immunitymentioning

confidence: 99%

Varicella-zoster virus

1996

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Varicella-zoster virus (VZV) is a ubiquitous human alphaherpesvirus that causes varicella (chicken pox) and herpes zoster (shingles). Varicella is a common childhood illness, characterized by fever, viremia, and scattered vesicular lesions of the skin. As is characteristic of the alphaherpesviruses, VZV establishes latency in cells of the dorsal root ganglia. Herpes zoster, caused by VZV reactivation, is a localized, painful, vesicular rash involving one or adjacent dermatomes. The incidence of herpes zoster increases with age or immunosuppression. The VZV virion consists of a nucleocapsid surrounding a core that contains the linear, double-stranded DNA genome; a protein tegument separates the capsid from the lipid envelope, which incorporates the major viral glycoproteins. VZV is found in a worldwide geographic distribution but is more prevalent in temperate climates. Primary VZV infection elicits immunoglobulin G (IgG), IgM, and IgA antibodies, which bind to many classes of viral proteins. Virus-specific cellular immunity is critical for controlling viral replication in healthy and immunocompromised patients with primary or recurrent VZV infections. Rapid laboratory confirmation of the diagnosis of varicella or herpes zoster, which can be accomplished by detecting viral proteins or DNA, is important to determine the need for antiviral therapy. Acyclovir is licensed for treatment of varicella and herpes zoster, and acyclovir, valacyclovir, and famciclovir are approved for herpes zoster. Passive antibody prophylaxis with varicella-zoster immune globulin is indicated for susceptible high-risk patients exposed to varicella. A live attenuated varicella vaccine (Oka/Merck strain) is now recommended for routine childhood immunization.

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Section: Cell-mediated Immunitymentioning

confidence: 99%

Varicella-zoster virus

1996

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“…In addition, in some cases the effector cells were cytotoxic for target cells with which they shared no HLA-A or -B locus antigens. Restriction by antigens other than class I antigens was reported by Hayward et al [12]. Although we did not study surface characteristics of the effector cells, it is reasonable to assume that the HLA-restricted responses observed were mediated by cytotoxic T cells [7,9].…”

Section: Discussionmentioning

confidence: 99%

“…Cytotoxic T cell responses are of particular interest because their occurrence in renal and bone marrow transplant recipients correlates with the ability of patients to recover from cytomegalovirus infections [9,10]. Lymphocytes from immune donors have recently been reported to kill VZV-infected fibroblasts in a non-HLA-restricted fashion consistent with antibody-dependent, cellmediated cytotoxicity [11] and that lymphocytes from three immune donors, stimulated in vitro, could kill Downloaded from https://academic.oup.com/jid/article-abstract/158/4/780/897613 by guest on 17 October 2018 HLA-DR-matched, VZV-infected, Epstein-Barr virus-transformed B cell lines [12]. To define further the nature and significance of VZV-specific cytotoxic T cell responses, we developed a method to stimulate VZV-immune lymphocytes in vitro and measured their ability to lyse VZV-infected target cells.…”

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confidence: 99%

Varicella-Zoster Virus-Specific HLA-Restricted Cytotoxicity of Normal Immune Adult Lymphocytes After in Vitro Stimulation

Cooper

Vujcic

Quinnan

1988

The Journal of Infectious Diseases

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Varicella-zoster virus (VZV)-specific cytotoxic T cell responses were studied in 35 presumably immune and two nonimmune adult donors and in two patients with herpes zoster. Peripheral blood lymphocytes (PBLs) were stimulated for five or 12 days with autologous, irradiated, VZV-infected PBLs. Cytotoxicity was measured in a chromium-release assay. Target cells were usually cryopreserved, phytohemagglutinin-stimulated PBLs, either infected with VZV or uninfected. In testing the presumably immune adults, VZV-specific cytotoxicity was observed in 32 (91%) of 35 cases after five days and in 19 (90%) of 21 cases after 12 d of stimulation. Lysis of HLA-matched target cells was significantly greater than that of mismatched, VZV-infected target cells after both intervals. Responses were similar when PBLs from two patients with acute zoster were tested after in vitro stimulation and in one of those two tested without in vitro stimulation.

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“…Cytotoxicity assays. Lysis of uninfected, peptide preincubated, and VZV-superinfected Epstein-Barr virus (EBV)transformed lymphoblasts was measured as before (16). Briefly, autologous and unrelated lymphoblasts were either preincubated with or without 100 ,ug of peptide per ml for 18 h or superinfected with VZV for 3 days before they were washed and radiolabeled (100 ,uCi of [5"Cr]sodium chromate [CJS 1P; Amersham Corp., Arlington Heights, Ill.] per 106 cells) for use as targets in a 4-h chromium release assay.…”

Section: Methodsmentioning

confidence: 99%

T-cell responses to predicted amphipathic peptides of varicella-zoster virus glycoproteins II and IV

Hayward

1990

J Virol

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Four peptides from the predicted amino acid sequences of varicella-zoster virus (VZV) glycoproteins II and IV selected for potential amphipathicity and a terminal lysine residue were synthesized. The peptides elicited weak proliferative responses by T cells with the CD4+ UCHL1+ CD45Rphenotype from the blood of VZV-immune individuals. The frequency of responder cells in individuals with specific response to peptides was 1:80,000 or fewer blood mononuclear cells, and the number of peptides responded to did not correlate with the proliferative response to VZV antigen. Of 40 peptide-specific T-cell clones obtained by limiting dilution, 10 were restimulated by extracted VZV antigen in the presence of autologous antigen-presenting cells. A total of 50% of these clones lysed HLA class II-positive lymphoblasts which had been preincubated with the appropriate peptide, and 2 of 15 cytotoxic clones lysed lymphoblast targets superinfected with VZV. The data indicated that T cells with specificity for putative VZV peptides may readily be cultured from the subset of blood mononuclear cells which bears the phenotype associated with memory.

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Specific lysis of varicella zoster virus-infected B lymphoblasts by human T cells

Cited by 51 publications

References 16 publications

Varicella-zoster virus

Varicella-zoster virus

Varicella-Zoster Virus-Specific HLA-Restricted Cytotoxicity of Normal Immune Adult Lymphocytes After in Vitro Stimulation

T-cell responses to predicted amphipathic peptides of varicella-zoster virus glycoproteins II and IV

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