Experimental Infection of Subpopulations of Human Peripheral Blood Leukocytes by Herpes Simplex Virus

Plaeger-Marshall, Susan; Smith, Jerry W.

doi:10.3181/00379727-158-40185

Cited by 22 publications

(24 citation statements)

References 2 publications

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“…Since some of the latter are believed to be selective for T cells, the assumption has been that T cells are the cell type in which virus replication takes place. However, this assump tion has not been proven, and several investi gators have claimed that B lymphocytes were also capable of HSV replication after mitogen stimulation [9]. The experience of our labora tory has been that B cells sufficiently depleted of T cells do not respond to the phytomitogens PHA or Con A with lymphocyte proliferation and do not replicate HSV [4], On the other hand, highly purified B cells -without the need for helper cells -do respond to EpsteinBarr virus (EBV) strain B95-8 with a lympho proliférative response, and these 'preactivated' cells are permissive for replication of HSV [6].…”

Section: Discussionmentioning

confidence: 99%

“…Since the mitogens used in the studies mentioned above predomi nantly stimulate T cells, investigators have as sumed that T cells are the cell type in leukocyte cultures that replicate HSV. However, the Tcell cultures investigated until now have not been highly purified, and some investigators have claimed that B cells also replicate HSV after mitogenic activation [9]. Therefore, it was necessary to determine the nature of the lymphocyte subset replicating HSV.…”

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confidence: 99%

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Replication of Herpes Simplex Virus in Human T Lymphocytes

et al. 1983

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The replication of herpes simplex virus (HSV) in cultures of human T lymphocytes was investigated. Virus replication occurred only in lymphocyte cultures prestimulated with mitogen. At least one of the factors responsible for this phenomenon is adsorption of the virus to the cells, which was 5 times less efficient in nonstimulated cells than in stimulated cultures. Growth of virus in infected cultures was restricted to lymphocytes of T origin. This was shown by successful infection of highly purified T-cell cultures and by virus replication in four continuous T-cell lines. No virus production was obtained in cultures of lymphocytes of other than T-cell origin. Virus titers in T-lymphocyte cultures reached 10⁷ PFU/ml, which was a four logio step increase over the input dose. Lymphocytes infected with a syn strain of HSV, HSV-ANG, induced polykaryocyte formation in the cultures and therefore generated a CPE visible by microscopic examination. Infection with syn+ strains of HSV (i.e., strains which do not cause cell fusion) did not lead to such phenomena. Not more than 1% of infected T cells was replicating HSV, as revealed by infectious center assays. In contrast, about 5% of these cells showed positive immunofluorescence with anti-HSV antibodies, indicating the presence of cells which express viral protein but do not actively produce infectious virus.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Replication of Herpes Simplex Virus in Human T Lymphocytes

et al. 1983

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“…Similar studies concerning the interactions between herpes simplex virus type 1 (HSV-1) and human leukocytes indicated that monocytes/macrophages were permissive for HSV-1 replication, whereas peripheral blood lymphocytes were non-permissive (Mintz et al, 1980;Plaeger-Marshall & Smith, 1978a). However, HSV-1 could replicate in all human T lymphocyte subsets when they had been activated by antigens, mitogens or interleukin 2 (IL-2) (Plaeger-Marshall, 1978b;Hammer et al, 1982;Hammer & Gillis, 1985).…”

Section: Introductionmentioning

confidence: 91%

The interaction between bovine herpesvirus type 1 and activated bovine T lymphocytes

Griebel

Ohmann²,

Lawman³

et al. 1990

Journal of General Virology

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The interaction between activated bovine T lymphocytes (BTLs) and bovine herpesvirus type 1 (BHV-1) was investigated. BHV-1 infection of BTLs reduced the amplitude of recombinant bovine interleukin 2-induced proliferative responses. This decreased proliferation was caused by a virus-induced lymphocytolysis which was dependent on viable virus and was not inhibited by recombinant bovine interferon-~xl. Furthermore, lymphocytolysis was not associated with virus replication or with the synthesis of detectable levels of viral proteins. Electron microscopic examination of virusinfected cells revealed that lymphocytolysis was characterized by early nuclear disintegration resembling apoptosis. These observations suggest that activated T cells, localized at the site of BHV-1 infection, may be susceptible to virus-induced cytolysis.

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“…The HSV genes involved in activation depended on the cell type used in the transfection experiments and on the presence of the viral trans-activator tat (reviewed in Laurence, 1990;Pitha, 1990). Monocytes, which are a recognized reservoir for latent HIV infection (Gartner et al, 1986;Koening et al, 1986), were not studied for HSVmediated activation, possibly because HSV does not replicate in monocytic cells (Plaeger-Marshall & Smith, 1978;Daniels et al, 1978;Albers et at., 1989;Tenney & Morahan, 1987. Efforts to identify the responsive cis-acting targets were largely unsuccessful (Laurence, 1990;Nable et al, 1988;Osborn et at., 1989;Pitha, 1990) and the possible role of the NRE remains unknown.…”

Section: Introductionmentioning

confidence: 99%

The GGTCA palindrome and cognate cellular factors in trans-regulation of human immunodeficiency virus long terminal repeat by herpes simplex virus

Feng

Kulka²,

Aurelian

1993

Journal of General Virology

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Molecular interactions between herpes simplex virus type 1 (HSV-1) and human immunodeficiency virus (HIV) were investigated in the promonocytic cell line U937. HSV-l-mediated activation was observed in transient expression assays with hybrid constructions containing the HIV long terminal repeat (LTR)-directed chloramphenicol aeetyltransferase gene. Comparison of constructions that differ in the GGTCA palindrome located within the negative regulatory region of the LTR revealed four-to eightfold lower activation levels for the wild-type as compared to the mutant sequence. Three protein species, 37K, 59K/64K and 75K, that bind to the wild-type GGTCA palindrome were resolved in nuclear extracts of uninfected U937 cells by gel retardation and u.v.-crosslinking experiments. The 37K protein did not bind to the mutant palindrome sequence. However, a distinct 120K protein was detected. The 37K and 59K/64K binding proteins were not resolved in similar experiments performed with nuclear extracts from HSV-l-infected U937 cells but there was a novel p50 species that binds only to the wild-type palindrome sequence. These findings raise the possibility that interaction of these proteins at the GGTCA palindrome is involved in HSV-l-mediated regulation of the HIV LTR in U937 cells.

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Experimental Infection of Subpopulations of Human Peripheral Blood Leukocytes by Herpes Simplex Virus

Cited by 22 publications

References 2 publications

Replication of Herpes Simplex Virus in Human T Lymphocytes

Replication of Herpes Simplex Virus in Human T Lymphocytes

The interaction between bovine herpesvirus type 1 and activated bovine T lymphocytes

The GGTCA palindrome and cognate cellular factors in trans-regulation of human immunodeficiency virus long terminal repeat by herpes simplex virus

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