Cytomegalovirus infection of peripheral blood mononuclear cells: effects on interleukin-1 and -2 production and responsiveness

Kapasi, K; Rice, George P.

doi:10.1128/jvi.62.10.3603-3607.1988

Cited by 79 publications

(35 citation statements)

References 24 publications

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“…The medical literature also reports on monocytes and macrophages being the main target cells of HCMV infection (18,32,35,37,52,76,79,87). HCMV infection can upregulate tumor necrosis factor-alpha and interleukin 1 (23,34,36,37) gene expression in monocytes and macrophages (37,47,72). Increased production of these pro-inflammatory cytokines is positively associated with the severity of destructive periodontal disease (31,80,81).…”

Section: Discussionmentioning

confidence: 99%

“…HCMV can infect and replicate in vivo in endothelial cells (29,30), epithelial cells (10,32,52,75), smooth muscle cells (51,57,75) and fibroblasts (10, 51-53, 57, 75). In addition, HCMV can reside in peripheral blood monocytes and lymphocytes during acute infection (20,27,37,48,51,53,57). Latent HCMV is mainly found in peripheral monocytes (20,86,87) and occasionally in bone marrowderived progenitor cells (10,45,57,74).…”

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confidence: 99%

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Herpesvirus infection of inflammatory cells in human periodontitis

Contreras

Zadeh

Nowzari

et al. 1999

Oral Microbiology and Immunology

118

135

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Human cytomegalovirus (HCMV) and Epstein-Barr virus type 1 (EBV-1) are frequently detected in human periodontitis lesions. However, no information is available on the types of gingival cells infected by herpesviruses. The present study determined the presence of herpesviruses in polymorphonuclear neutrophils, monocytes, macrophages and T and B lymphocytes in biopsies of periodontitis lesions from 20 adults. A nested polymerase chain reaction method was employed to detect HCMV, EBV-1, EBV-2, human herpes virus-6 and herpes simplex virus (HSV) in periodontal tissue biopsy and in gingival cell fractions separated by immunomagnetic cell sorting. Tissue specimens from 18 (90%) and cell fractions from 14 (70%) patients demonstrated herpesviruses. Periodontitis-derived monocytes and macrophages revealed HCMV in cell fractions from 11 (55%) patients and HSV in cells from 1 (5%) patient. T lymphocytes harbored HCMV in cell fractions from 4 (20%) patients and HSV in cell fractions from 4 (20%) patients. B lymphocytes showed EBV-1 in cell fractions from 9 (45%) patients. Periodontal polymorphonuclear neutrophils demonstrated no herpesviruses. This study suggests that HCMV mainly infects periodontal monocytes, macrophages and less frequently T lymphocytes and that EBV-1 infects periodontal B lymphocytes. The possible etio-pathologic significance of periodontal herpesvirus infection is discussed.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Herpesvirus infection of inflammatory cells in human periodontitis

Contreras

Zadeh

Nowzari

et al. 1999

Oral Microbiology and Immunology

118

135

View full text Add to dashboard Cite

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“…Viral infection may also activate destmctive host immune reactions and/or alter protective immune defense responses. For instance, cytomegalovims may infect lymphocytes and monocytes causing a significant reduction in both interleukin production and ability to proliferate in response to mitogens (23). In infectious mononucleosis, the expression of certain Epstein-Barr vims genes elicits a profound T cell response (cytotoxic T cells) and activates natural killer cells against proliferating B cells (31).…”

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confidence: 99%

Detection of human viruses in periodontal pockets using polymerase chain reaction

Parra

Slots

1996

Oral Microbiology and Immunology

172

220

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Even though viruses have been implicated in the etiology of several medical and dental disorders, little or no data are available on the possible involvement of human viruses in the pathogenesis of human periodontal disease. This study investigated the presence of human cytomegalovirus, Epstein-Barr virus, herpes simplex virus, human papillomavirus and human immunodeficiency virus (HIV) in crevicular fluid samples from 30 patients with advanced periodontitis and 26 subjects with gingivitis. Viral identification was performed on direct subgingival samples from 3 diseased sites in each patient using the polymerase chain reaction technique. Seventy-eight percent of advanced periodontitis patients were positive for at least one of the five test viruses. Cytomegalovirus was detected in 60% of the periodontitis patients, Epstein-Barr virus in 30%, herpes simplex virus in 20%, human papillomavirus in 17% and HIV in 7%. Forty percent of the periodontitis patients revealed coinfection by 2 to 5 viruses. Only 31% of the gingivitis subjects showed a positive viral identification in crevicular fluid, and infected individuals only revealed human cytomegalovirus. This study demonstrated that human viruses may occur in periodontitis lesions with relatively high prevalence. The pathogenetic significance of human viruses in destructive periodontal disease needs to be determined.

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“…Experimental CMV infection has also been shown to alter cytokine production, e.g. induction of the transforming growth factor-P (TGF-[3) production (Michelson et al 1994), and a reduction in the synthesis of interleukin-1 (IL-1) and IL-2 (Rodgers et al 1985, Kapasi & Rice 1988, Moses & Gamett 1990.…”

Section: Interference With Normal Cell Function As a Results Of Virus mentioning

confidence: 99%

A Novel Mechanism for Virus‐Induced Autoimmunity in Humans

Nauclér¹,

Larsson²,

Möller³

1996

Immunological Reviews

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A novel mechanism for virus-induced autoimmunity in humans is described. Infection of immunocompromised bone marrow-transplanted patients with human CMV results in the formation of autoantibodies specific for the cell-surface protein CD13 (aminopeptidase N). CD13 is present on all CMV-susceptible cells and infection can be specifically blocked by antibodies against CD13. CMV particles carry CD13, which is incorporated in the viral envelope during budding of viral nucleo-capsids into Golgi-derived vacuoles. Antibodies against CD13 are virus-neutralizing, in efficiency comparable to antibodies against viral envelope glycoproteins. Autoantibodies against CD13 are present in patients who develop chronic GVHD following allogeneic bone marrow transplantation. This lesion shows striking similarities to certain autoimmune diseases in humans, of which scleroderma is one example. In vivo binding of antibodies to tissue structures known to be targets for chronic GVHD has been demonstrated in patients with chronic GVHD. Finally, patient serum containing CD13-specific antibodies binds to skin and mucosa tissue sections in vitro, a binding which is inhibited by CD13-specific monoclonal antibodies. Thus a virus infection can activate an immune response against a specific autoantigen, providing possibilities for destruction of non-infected host cells, as originally proposed by Fujinami & Oldstone (1985), and also for the molecular mimicry model for induction of autoimmunity. Our findings lend support to the idea that inhibiting the transfer of CMV infection in bone marrow transplants will reduce morbidity and mortality from CMV infection but will also reduce the incidence of chronic GVHD. Elimination of CD13+ cells in bone marrow is not believed to interfere with the chance of recipient repopulation, and may be a way to decrease morbidity and mortality substantially following BMT. For all patients, every effort should be taken to prevent a post-BMT CMV infection in order to reduce the risk of the later development of chronic GVHD.

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Cytomegalovirus infection of peripheral blood mononuclear cells: effects on interleukin-1 and -2 production and responsiveness

Cited by 79 publications

References 24 publications

Herpesvirus infection of inflammatory cells in human periodontitis

Herpesvirus infection of inflammatory cells in human periodontitis

Detection of human viruses in periodontal pockets using polymerase chain reaction

A Novel Mechanism for Virus‐Induced Autoimmunity in Humans

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