Immunofluorescent evidence of prior herpes simplex virus type-2 infection in prostate carcinoma

Haid, Max; Sharon, Nehama

doi:10.1016/0090-4295(84)90118-3

Cited by 19 publications

(13 citation statements)

References 6 publications

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“…It was reported that herpes virus plays an important role in the pathogenesis of cancer via the inhibition of cell apoptosis and stimulation of DNA synthesis, which may ultimately lead to cancer (12). Previous studies indicated that infection by herpes simplex virus type 2 (HSV-2) or human herpesvirus 8 (HHV-8) may be associated with a higher prostate cancer risk (12)(13)(14). However, other epidemiological studies failed to demonstrate such an association (15)(16)(17).…”

Section: Introductionmentioning

confidence: 82%

“…Previous studies detected herpes virus DNA (41,47) or anti-virus antibody in tissue samples (13). However, herpes virus detection in tissues was not frequently performed, since blood samples were easier to collect from the participants compared to tissue samples and the serological assays were more convenient to conduct compared to DNA detection.…”

Section: Discussionmentioning

confidence: 99%

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Herpes simplex virus type 2 or human herpesvirus 8 infection and prostate cancer risk: A meta-analysis

Wang

Shen

2013

Biomedical Reports

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Abstract. Prostate cancer is the second most frequently diagnosed type of cancer and the sixth leading cause of cancer mortality among males worldwide. The aim of this study was to investigate the association between the infection by herpes simplex virus type 2 (HSV-2) or human herpesvirus 8 (HHV-8) and the risk of prostate cancer. A systematic literature search was performed using PubMed, Cochrane Library, Web of Science, Scopus, CNKI and CBM. The association of HSV-2 or HHV-8 infection with the risk of prostate cancer was separately assessed. Estimates of the odds ratio (OR) with 95% confidence interval (CI) were pooled by the fixed-or random-effects model. A total of 11 articles with 2,996 cases and 3,875 controls were included in this meta-analysis. HSV-2 infection was associated with increased prostate cancer risk (OR=1.209; 95% CI, 1.003-1.456). Results of the stratified analysis suggested that such an association existed among participants from North and South America (OR=1.226; 95% CI, 1.000-1.503). No significant correlation was observed in the HHV-8 group (OR=1.106; 95% CI, 0.765-1.598). Further investigations and large-sample studies are required to elucidate the possible mechanism underlying viral carcinogenesis and the association between herpes virus infection and the risk of prostate cancer.

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Section: Introductionmentioning

confidence: 82%

Section: Discussionmentioning

confidence: 99%

Herpes simplex virus type 2 or human herpesvirus 8 infection and prostate cancer risk: A meta-analysis

Wang

Shen

2013

Biomedical Reports

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“…Thus, cases (and their matched controls) were apparently linked to sera sometime between 1991 and when the article was submitted for publication (2004). Other previous studies relied on self-report as a measure of exposure (17,18) or collected data on HSV-2 infection post-diagnosis of prostate cancer (19)(20)(21). Self-report of STIs is problematic with a high potential for underreporting especially among nondiseased subjects.…”

Section: Resultsmentioning

confidence: 99%

Sexually Transmitted Infections and Prostate Cancer among Men in the U.S. Military

Dennis

Coughlin

McKinnon

et al. 2009

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Studies of self-reported sexually transmitted infections (STI) suggesting an association with prostate cancer may reflect underreporting of such infections among nondiseased subjects. To reduce such bias, we studied archived sera in a cohort of U.S. military personnel known to have high rates of both STIs and prostate cancer. Using a nested case-control design, serum samples from 534 men who served on active duty between September 1, 1993 and September 1, 2003 were examined. Controls were individually matched to cases based on date of serum collection, date of birth, branch of service, military rank, marital status, and race. Each of the 267 case-control pairs had two serum samples: a recent serum sample, taken ∼1 year before the case's prostate cancer diagnosis, and an earlier serum sample, taken ∼8 years before diagnosis. Each serum specimen was studied for antibodies against human papillomavirus, herpes simplex virus-2 (HSV-2), and Chlamydia trachomatis. Logistic regression accounted for matching and potential confounding factors. Study data indicated no association between prostate cancer and serologic evidence of infections just before the reference date. However, a statistically significant association between prostate cancer and serologic evidence of HSV-2 infection was detected in the earlier sample (odds ratio, 1.60; 95% confidence interval, 1.05-2.44). The strength of this association increased when analyses were restricted to sera collected at least 60 months before diagnosis (odds ratio, 2.04; 95% confidence interval, 1.26-3.29; 204 pairs). If this association is causal, then our findings would suggest a long latency period for prostate cancer development after HSV-2 infection. (Cancer Epidemiol Biomarkers Prev 2009;18(10):2665-71)

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“…Results from these early studies were generally mixed; while some observed suggestive positive associations for HSV-2 [17] and CMV [19] seropositivity, others observed null or suggestive inverse associations for these viruses and EBV [8,16] (Table 1). A few additional small studies also investigated herpesvirus nucleic acids and antigens in prostate tissue with generally unstable results [17,18,20].…”

Section: Stis Assessed By Serology or Other Laboratory Methodsmentioning

confidence: 99%

“…Finally, other groups investigated herpesviruses, such as herpes simplex virus type 2 (HSV-2), cytomegalovirus (CMV) and Epstein-Barr virus (EBV), because they: 1) had been demonstrated to have transforming properties; 2) had been observed in malignant prostate tissue/cell lines; and 3) were believed to be involved in the development of other cancers, such as cervical cancer and Burkitt's lymphoma [8,[16][17][18][19][20]. Primitive serologic tests were available for these viruses as early as the 1970s, making it possible to assess histories of these infections by serology rather than or in addition to self-report or medical record abstraction.…”

Section: Viral Transformationmentioning

confidence: 99%

Sexually Transmitted Infections and Risk of Prostate Cancer: Review of Historical and Emerging Hypotheses

Sutcliffe

2010

Future Oncol.

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ABSTRACT/SUMMARYSince the early 1950s when sexually transmitted infections (STIs) were first proposed as a possible risk factor for prostate cancer, numerous epidemiologic studies have been conducted.Initially, these studies were primarily small case-control studies with retrospective, self-reported assessment of a narrow range of STIs, typically either any STIs, or gonorrhea and syphilis.However, as new STIs have been discovered/recognized, new and better tests to detect histories of STIs have been developed, and new resources for prostate cancer research have been created, epidemiologic studies have expanded to include a wider range of STIs, and have moved towards more rigorous, prospective study designs and serologic assessment of STI histories. The results of these studies are reviewed and discussed, as well as possible new avenues of research, such asTrichomonas vaginalis infection and infections not typically considered to be sexually transmitted. 3 EARLY HYPOTHESES FOR SEXUALLY TRANSMITTED INFECTIONS AND PROSTATE CANCEREarly hypotheses related to a sexually transmitted etiology of prostate cancer were initially motivated by contemporary, epidemiologic patterns of prostate cancer occurrence. In the early 1950s, Ravich and Ravich [1, 2] noted a higher prostate cancer prevalence among mainly uncircumcised non-Jewish than circumcised Jewish men, similar to patterns for penile cancer and cervical cancer among female partners of these men, leading them to propose that observed patterns might be explained by sexual transmission of a virus or other carcinogenic agent contained within the smegma of uncircumcised males. Subsequent investigators [3][4][5] further proposed additional hypotheses related to infection, sexual behavior, and sexual frustration to explain other contemporary patterns of prostate cancer occurrence by marital, paternal, and racial status. Together, these observations and hypotheses led to a series of investigations beginning in the early 1970s to examine possible associations between STIs and sexual behavior in relation to prostate cancer. Selection of STIs STI markers:Most early investigations of STIs and prostate cancer assessed either a history of any STIs or individual histories of gonorrhea and syphilis as markers or possibly vectors of the potentially causative STI or sexual behavior [6][7][8][9]. These STIs were likely selected because they were the most common, well-known, and symptomatic STIs at the time, making them also more readily assessed by self-report, medical record abstraction, or registry query. Prostate inflammation:Other early studies focused specifically on gonorrhea because it frequently led to 4 secondary gonococcal prostatitis in the pre-and early-antibiotic era, and because prostate inflammation had previously been hypothesized as a cause of atrophy and subsequent prostate cancer ([9-11] and references therein). This inflammation-atrophy-prostate cancer hypothesis has since gained further support with the observation of morphological and epigenetic transitions betwe...

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Immunofluorescent evidence of prior herpes simplex virus type-2 infection in prostate carcinoma

Cited by 19 publications

References 6 publications

Herpes simplex virus type 2 or human herpesvirus 8 infection and prostate cancer risk: A meta-analysis

Herpes simplex virus type 2 or human herpesvirus 8 infection and prostate cancer risk: A meta-analysis

Sexually Transmitted Infections and Prostate Cancer among Men in the U.S. Military

Sexually Transmitted Infections and Risk of Prostate Cancer: Review of Historical and Emerging Hypotheses

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