Herpes simplex virus and cancer of the cervix

Plummer, G.; Masterson, John G.

doi:10.1016/0002-9378(71)90929-x

Cited by 30 publications

(9 citation statements)

References 13 publications

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“…Although HSV-2 produced lower virus yields than HSV-1 [Plummer et al, 1968], HSV-2 spread more rapidly in cultured cells, as characterized by the larger ratio of plaque formation to virus production, than HSV-1. This efficient spread of HSV-2 may be reflected in the severity and sequelae of encephalitis caused by HSV-2 [Plummer and Hackett, 1966;Whitley et al, 1991;Kimura et al, 2002]. The difference in the ratio of plaque size to virus yield may be due to the interaction of cell-specific metabolism and a functional difference in viral proteins between HSV-1 and -2 rather than a difference in the cellular receptors for HSV infection [Spear, 2004].…”

Section: Discussionmentioning

confidence: 96%

Growth of herpes simplex virus in epidermal keratinocytes determines cutaneous pathogenicity in mice

Yoshida

Kurokawa

et al. 2005

J. Med. Virol.

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Herpes simplex viruses (HSV)-1 and -2 isolated from genital lesions were examined for cutaneous pathogenicity and its correlation with cellular tropism. HSV-1 caused vesiculation, erosion/ulcer, and zosteriform lesions successively, but skin lesions of HSV-2 developed without vesiculation in some mice, and with statistically significantly less frequent vesiculation than HSV-1. Thus, the virological type of HSV was correlated with its cutaneous pathogenicity. The growth characteristics of HSV-1 and -2 were compared in cultured human embryonic lung (HEL) fibroblasts, human lung cancer A549 cells, human neonatal epidermal keratinocytes, human neonatal dermal fibroblasts, HeLa cells, and Vero cells. HSV-2 produced plaques that were 72% times the size of HSV-1 plaques in epidermal keratinocytes but 230%-500% the size in the other cells. The difference between HSV-1 and -2 in the ratio of plaque size to virus yield in epidermal keratinocytes was much larger (502 times) than the ratio of the other cells (5.57-28.8 times). Keratinocytes are the major constituent of the epidermal layer of the skin and the cells in which vesiculation and erosion/ulceration occur histologically. Therefore, the smaller spread of HSV-2 in keratinocytes of the epidermal layer and the greater spread in other cells of the dermal layer might reflect its lesser invasiveness in the epidermal layer despite larger invasiveness in the dermal layer, which is reflected in the low incidence of erosion/ulcer of the skin compared to HSV-1. Thus, the growth of HSV in epidermal keratinocytes appeared to correlate with the cutaneous pathogenicity causing vesiculation in the skin.

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Section: Discussionmentioning

confidence: 96%

Growth of herpes simplex virus in epidermal keratinocytes determines cutaneous pathogenicity in mice

Yoshida

Kurokawa

et al. 2005

J. Med. Virol.

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“…Evidence for the relation of Type 2 infection to carcinoma of the cervix is based inainly on antibody studies in groups of patients with carcinoma, in situ and invasive, and without. Studies indicating that the incidence of infection is significantly greater in the carcinoma group have been made by Rawls et al (1970a), Royston and Aurelian (1970), Nahmias et al (1970b), and Plummer and Masterson (1971). The difficulty of finding a control group matched as regards race, social status and age is acknowledged by all the authors, particularly Rawls et al (1971).…”

Section: Herpeavirus Hominis (Hvh)mentioning

confidence: 99%

A Review of the Recent Literature on Diseases of the Vulva—part Ii.

1972

Br J Dermatol

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“…The subsequent discovery of HSV-2 in about 95% of genital infections, in contradistinction to herpes simplex virus type 1 (HSV-1) in mostly non-genital herpetic infections (Nahmias and Doodle, 1968), provided the foundation and stimulus for seroepidemiological studies to validate this association. Numerous retrospective studies (Rawls et al, 1970;Nahmias et al, 1970;Aurelian et al, 1970;Sprecher-Goldberger et al, 1970;Catalano and Johnson, 1971;Centifanto et al, 1971; Plummer and Masterson, 1971) have since shown a significant association between the HSV-2 infection and cervical cancer, but have not completely resolved either the chronological relationship between the infection and the cancer, or the association of HSV-2 infection with cervical cancer independently of both sexual promiscuity and exogenous estrogen. It must be acknowledged, however, that Catalano and Johnson (1971) have dealt with the chronological sequence between infection and cervical anaplasia in a small sample (14 cases) and the association of the HSV-2 infection with cervical cancer independent of sexual promiscuity has been reported by Adam and associates (1972).…”

mentioning

confidence: 99%

Herpesvirus infection and cervical anaplasia—a seroepidemiological study

Choi

Shettigara

Abu-Zeid

et al. 1977

Intl Journal of Cancer

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In a cohort of 23,146 pregnant females followed for 37-56 months subsequent to collection of prenatal sera, 57 cases of carcinoma of the cervix were encountered. Three controls were selected for each case from the residual cohort matched to cases for age, residence, number of prior cytology smears taken, and the data of entry to the study. The antibody activity to herpesvirus type 1 and type 2 was examined by the indirect hemagglutination test. The proportion of cases positive for HSV-2 infection was greater than that of the controls; however, the difference was not significant at the 5% level. The relative risk value for the association between HSV-2 infection and carcinoma of the cervix was found to be 2.33. The geometric mean titers of IHAT revealed that the cases of cervical cancer had a higher titer than the controls with respect to HSV-1 as well as HSV-2 antibodies. A sufficiently longer follow-up, yielding a larger sample size, is desired to assess the specific role of HSV-2 infection in development of cervical anaplasia.

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Herpes simplex virus and cancer of the cervix

Cited by 30 publications

References 13 publications

Growth of herpes simplex virus in epidermal keratinocytes determines cutaneous pathogenicity in mice

Growth of herpes simplex virus in epidermal keratinocytes determines cutaneous pathogenicity in mice

A Review of the Recent Literature on Diseases of the Vulva—part Ii.

Herpesvirus infection and cervical anaplasia—a seroepidemiological study

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