Lack of Association of Cytomegalovirus Antibody Level with Carcinoma of the Uterine Cervix

Hart, H; Springbett, Anthea; Norval, Mary

doi:10.1159/000299470

Cited by 10 publications

(3 citation statements)

References 5 publications

(5 reference statements)

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“…Al though the proportion of patients with CIS who were sero-positive for CMV was greater than the proportions of sero-positive patients with dysplasia, the difference was not statisti cally significant. A larger study had pre viously shown no difference in the anti-CMV antibody status of patients with CIS when compared with other dysplasias [21 ], and our results confirm this.…”

Section: Discussionsupporting

confidence: 86%

Natural Killer Cell Activity in Patients with Abnormalities of the Uterine Cervix

Neill

Norval

1984

Gynecol Obstet Invest

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Peripheral blood lymphocytes from 105 patients with various degrees of cervical dysplasia (normal/mild, moderate and severe) up to carcinoma in situ were assayed for natural killer cell activity against K562 cells and Chang liver cells in vitro. No difference was found between the natural killer cell activities of any of the groups of patients studied. In addition, the K cell activity of the patients’ lymphocytes was assayed in an antibody-dependent cellular cytotoxicity assay on Chang liver cells with anti-Chang cell antiserum. No difference was found between patient groups. There was no correlation between the presence of antibodies in the patients’ serum to cytomegalovirus measured by anti-complement immunofluorescence and increased natural killer cell activity.

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Section: Discussionsupporting

confidence: 86%

Natural Killer Cell Activity in Patients with Abnormalities of the Uterine Cervix

Neill

Norval

1984

Gynecol Obstet Invest

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“…While HCMV has been isolated from cervical cancer biopsy specimens and their derived cell cultures (72,122), seroepidemiologic studies linking HCMV infection to cervical cancer have yielded conflicting results. Some investigators have found significantly higher levels of antibodies to HCMV in patients with cervical carcinoma than in controls (133,172,184), while other groups have found no correlation (53,62,94,162). Huang et al (71) and Fletcher et al (51) have detected HCMV DNA in cervical cancer specimens.…”

Section: Overviewmentioning

confidence: 99%

Human Cytomegalovirus and Human Herpesvirus 6 Genes That Transform and Transactivate

1999

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SUMMARY This review is an update on the transforming genes of human cytomegalovirus (HCMV) and human herpesvirus 6 (HHV-6). Both viruses have been implicated in the etiology of several human cancers. In particular, HCMV has been associated with cervical carcinoma and adenocarcinomas of the prostate and colon. In vitro transformation studies have established three HCMV morphologic transforming regions (mtr), i.e., mtrI, mtrII, and mtrIII. Of these, only mtrII (UL111A) is retained and expressed in both transformed and tumor-derived cells. The transforming and tumorigenic activities of the mtrII oncogene were localized to an open reading frame (ORF) encoding a 79-amino-acid (aa) protein. Furthermore, mtrII protein bound to the tumor suppressor protein p53 and inhibited its ability to transactivate a p53-responsive promoter. In additional studies, the HCMV immediate-early protein IE86 (IE2; UL122) was found to interact with cell cycle-regulatory proteins such as p53 and Rb. However, IE86 exhibited transforming activity in vitro only in cooperation with adenovirus E1A. HHV-6 is a T-cell-tropic virus associated with AIDS-related and other lymphoid malignancies. In vitro studies identified three transforming fragments, i.e., SalI-L, ZVB70, and ZVH14. Of these, only SalI-L (DR7) was retained in transformed and tumor-derived cells. The transforming and tumorigenic activities of SalI-L have been localized to a 357-aa ORF-1 protein. The ORF-1 protein was expressed in transformed cells and, like HCMV mtrII, bound to p53 and inhibited its ability to transactivate a p53-responsive promoter. HHV-6 has also been proposed to be a cofactor in AIDS because both HHV-6 and human immunodeficiency virus type 1 (HIV-1) have been demonstrated to coinfect human CD4+ T cells, causing accelerated cytopathic effects. Interestingly, like the transforming proteins of DNA tumor viruses such as simian virus 40 and adenovirus, ORF-1 was also a transactivator and specifically up-regulated the HIV-1 long terminal repeat when cotransfected into CD4+ T cells. Finally, based on the interactions of HCMV and HHV-6 transforming proteins with tumor suppressor proteins, a scheme is proposed for their role in oncogenesis.

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“…Serological studies on patients with grades of cervical dysplasia up to carcinoma in situ (CIS) have been equivo cal with regard to CMV antibody status [7][8][9][10], while CMI responses in such patients have not yet been examined.…”

Section: Introductionmentioning

confidence: 99%

Cell-Mediated Immune Responses to Cytomegalovirus in Patients with Dysplasia of the Uterine Cervix

Neill¹,

Norval²

1985

Gynecol Obstet Invest

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Peripheral blood lymphocytes from 172 women with various degrees of cervical dysplasia were assayed for responsiveness to cytomegalovirus-induced early and late antigens using lymphocyte stimulation tests. No evidence was found to suggest that any group of patients was specifically sensitized to either of the antigens tested. Neither was there any difference between the patient groups in respect of mitogen-induced stimulation. The concept that cytomegalovirus might be involved in cervical cell transformation leading to carcinoma has therefore not been strengthened as a result of this study.

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Lack of Association of Cytomegalovirus Antibody Level with Carcinoma of the Uterine Cervix

Cited by 10 publications

References 5 publications

Natural Killer Cell Activity in Patients with Abnormalities of the Uterine Cervix

Natural Killer Cell Activity in Patients with Abnormalities of the Uterine Cervix

Human Cytomegalovirus and Human Herpesvirus 6 Genes That Transform and Transactivate

Cell-Mediated Immune Responses to Cytomegalovirus in Patients with Dysplasia of the Uterine Cervix

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