Generalized cytomegalic inclusion disease

Wyatt, John P.; Saxton, Jennifer; Lee, R.S.; Pinkerton, Henry

doi:10.1016/s0022-3476(50)80097-5

Cited by 158 publications

(24 citation statements)

References 18 publications

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“…States, as well as in Finland and Germany (Farber & Wolbach, 1932; McCordock & Smith, 1934;Wyatt et al 1950;Ahvenainen, 1952;Seifert & Oehme, 1957). In other parts of the United States and also in Great Britain they seem to be very much less common (Potter, 1957;Symmers, 1960;Crome & France, 1959).…”

mentioning

confidence: 99%

The incidence of infection with cytomegalovirus in a normal population: A serological study in Greater London

Stern

Elek

1965

J. Hyg.

176

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A serological study of cytomegalovirus infection in London shows it to be prevalent. Under 5 years of age only 4% of children have antibodies, but this increases to 15% by 10 years of age and 21% by 15 years. The maximum incidence of 54% is reached by 25–35 years, and this is maintained in the older age groups of the population. In two mixed day schools the incidence of infection was significantly lower than in a boarding school, suggesting that close prolonged contact is required for spread of infection.Different strains of cytomegalovirus possess common group-specific complement-fixing antigens.It is suggested that clinical disease caused by cytomegaloviruses is more frequent and more varied than previously believed, although diagnosis may be difficult without virological help.

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mentioning

confidence: 99%

The incidence of infection with cytomegalovirus in a normal population: A serological study in Greater London

Stern

Elek

1965

J. Hyg.

176

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“…In infected persons HCMV replicates in a vari ety of cell types especially in epithelial cells of different origins [64], However, a substantial number of HCMVinduced diseases is caused by the reactivation of persis tent HCMV [65]. In HCMV carriers IE gene expression has been found in a wide variety of cell types including tubular and glomerular epithelial cells, cells of Bowman's capsule, hepatocvtes, Kupffer cells, bronchial and epithe lial cells, alveolar macrophages, fibroblasts, T lympho cytes, astrocytes and endothelial cells [66].…”

Section: H C M V Susceptibility Of Different Cell Types In Vivo and Imentioning

confidence: 99%

Modulatory Effects of Human Cytomegalovirus Infection on Malignant Properties of Cancer Cells

Činátl

Vogel²,

Rabenau³

et al. 1996

Intervirology

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Although there is no definitive evidence of the association of human cytomegalovirus (HCMV) infection with human cancers, the oncogenic potential of HCMV has been well established by in vitro studies demonstrating the ability of UV-irradiated or infectious virus to transform a variety of cells. After prolonged passaging the transformed cell type was maintained while HCMV DNA sequences were no more detectable. Three morphological transforming regions (mtr) of HCMV have been identified. The effects of HCMV on cellular functions which may be associated with the malignant phenotype include the expression of oncogenes and transcriptional activation of growth factors and interleukin synthesis. In infected cells, HCMV induces cytoskeletal alterations and changes in expression of cell surface receptors for extracellular matrix proteins which could result in increased motility and dissemination of cancer cells. Several human neuroblastoma cell lines undergo maturation in different neural crest derived cell types upon treatment with oncogenic potential agents, i. e. retinoic acid. The persistent HCMV infection of neuroblastoma cells (>1 year) is accompanied by the increased expression of oncoproteins (i.e. N-myc) and decreased expression of tyrosine hydroxylase and dopamine-β-hydroxylase. The activation of the cellular metabolism is due to HCMV binding to cellular receptors (prior to virus gene expression) and to the activity of HCMV immediate early (IE) gene products. IE proteins act directly as transcriptional activators or their activity is mediated by a variety of cellular transcription factors. HCMV infection may result in activation of promoters of cellular genes coding for cytokines, replication enzymes, protooncogenes and viral promoters. Recently it has been demonstrated that HCMV IE proteins block apoptosis probably by suppressing the ability of the antioncogene p53 to activate a reporter gene. The interactions of HCMV with tumor suppressor proteins such as p53 or retinoblastoma (pRb) susceptibility protein are reminiscent of those mediated by the oncoproteins of DNA tumor viruses. The acquisition of a fully malignant phenotype by normal cells is thought to require several mutations in a number of cellular genes. In this connection, HCMV may play the role of a nonobligate either direct or indirect cofactor for tumor genesis, e.g. by blocking apoptosis, which may be an essential requirement for tumor progression. Due to the stimulation of growth factors and/or inhibition of antioncogenes by its gene products, HCMV may modulate the malignant potential of tumor cells.

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“…The enlarged cells pathognomonic of cytomegalovirus (CMV) infection in vivo were first reported by JESIONEK and KIOLElV[ENOGL0C (5) in the kidneys, lungs and liver of an 8 month old foetus, and have since been found in numerous postmortem tissues including thyroid (13 ). Epithelial cells are most frequently infected but inclusions may also be found in cells of connective tissue, vascuIar endothetium and nervous tissue.…”

Section: Introductionmentioning

confidence: 96%

In-vitro cultivation of human cytomegalovirus in thyroid epithelial cells

Knowles¹

1976

Archives of Virology

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Several strains of human cytomegalovirus including recent isolates, were grown in epithelial cells derived from thyroid tissue. All the strains tested grew in these cultures without pre-treatment of the cells, and no difference in cytopathic effect was detected between strains of genital and non-genital origin. 4 strains of CMV were isolated directly from urine in thyroid cells; however the failure to isolate 6 further strains in these cultures from other specimens may indicate that a higher multiplicity of infection is required to infect epithelial than fibroblast cells.

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Generalized cytomegalic inclusion disease

Cited by 158 publications

References 18 publications

The incidence of infection with cytomegalovirus in a normal population: A serological study in Greater London

The incidence of infection with cytomegalovirus in a normal population: A serological study in Greater London

Modulatory Effects of Human Cytomegalovirus Infection on Malignant Properties of Cancer Cells

In-vitro cultivation of human cytomegalovirus in thyroid epithelial cells

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