FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2804670094> ?p ?o ?g. }

• W2804670094 endingPage "510" @default.
• W2804670094 startingPage "509" @default.
• W2804670094 abstract "To the Editor: Wolf, Ruocco, and Ruocco have raised an important point. Several issues need to be addressed. First, what exactly is the role of herpes simplex virus (HSV) in carcinogenesis? HSV DNA has been shown to induce point mutations, gene rearrangements, and gene amplification in cells. It can also switch on foreign DNA in cells such as that from latent type C retroviruses and HPV, and it may switch on genes that are not normally expressed.1Galloway DA McDougall JK Alterations in the cellular phenotype induced by herpes simplex viruses.J Med Virol. 1990; 31: 36-42Crossref PubMed Scopus (17) Google Scholar The transforming regions of the HSV genome have been identified, cloned, and inserted into cells.2Dhanwada KR Garrett L Smith P et al.Characterization of human keratinocytes transformed by high risk human papillomavirus types 16 or 18 and herpes simplex virus type 2.J Gen Virol. 1993; 74: 955-963Crossref PubMed Scopus (11) Google Scholar, 3Dhanwada KR Veerisetty V Zhu F et al.Characterization of primary human fibroblasts transformed by human papilloma virus type 16 and herpes simplex virus type 2 DNA sequences.J Gen Virol. 1992; 73: 791-799Crossref PubMed Scopus (13) Google Scholar, 4Cameron IR Park M Dutia BM et al.Herpes simplex virus sequences involved in the initiation of oncogenic morphological transformation of rat cells are not required for maintenance of the transformed state.J Gen Virol. 1985; 66: 517-527Crossref PubMed Scopus (20) Google Scholar HSV DNA and polypeptide products are generally not found in transformed cells or in tumors, and their absence has given rise to the “hit and run” theory of HSV-induced transformation.4Cameron IR Park M Dutia BM et al.Herpes simplex virus sequences involved in the initiation of oncogenic morphological transformation of rat cells are not required for maintenance of the transformed state.J Gen Virol. 1985; 66: 517-527Crossref PubMed Scopus (20) Google Scholar, 5Galloway DA McDougall JK The oncogenic potential of herpes simplex viruses: evidence for a ‘hit and run’ mechanism.Nature. 1983; 302: 21-24Crossref PubMed Scopus (220) Google Scholar Despite its transforming ability, HSV alone will not induce cancer in intact animals; in one in vitro study, insertion of the transforming region of HSV 1 into human oral keratinocytes did not induce a malignant phenotype.6Das CM Murrah VA Zhang S et al.The effect on cell phenotype of the mutagenic peptide of herpes simplex virus type-1.Eur J Cancer. 1995; 31B: 267-274Abstract Full Text PDF Scopus (1) Google Scholar, 7Park NH Li SL Xie JF et al.In vitro and animal studies of the role of viruses in oral carcinogenesis.Eur J Cancer. 1992; 28B: 145-152Abstract Full Text PDF Scopus (25) Google Scholar, 8Park NH Niukian K Shklar G Combined effect of herpes simplex virus and tobacco on the histopathologic changes in lips of mice.Oral Surg Oral Med Oral Pathol. 1985; 59: 154-158Abstract Full Text PDF PubMed Scopus (24) Google Scholar In animal studies involving the oral mucosa, inoculation of infectious HSV or UV-inactivated HSV did not induce epithelial malignancies.7Park NH Li SL Xie JF et al.In vitro and animal studies of the role of viruses in oral carcinogenesis.Eur J Cancer. 1992; 28B: 145-152Abstract Full Text PDF Scopus (25) Google Scholar, 8Park NH Niukian K Shklar G Combined effect of herpes simplex virus and tobacco on the histopathologic changes in lips of mice.Oral Surg Oral Med Oral Pathol. 1985; 59: 154-158Abstract Full Text PDF PubMed Scopus (24) Google Scholar Carcinogenesis is a multistep process involving the activation of protooncogenes and inactivation of tumor suppressor genes such as p53. Known carcinogens such as tobacco constituents initiate the process of carcinogenesis through direct effects on cellular genes, not indirectly through prolongation of the intracellular survival of HSV. HSV is not a primary carcinogen, but a cocarcinogen that enhances and augments the carcinogenic process once it is started. HSV alone is not sufficient to cause cancer. In a 1992 study by Park et al.,7Park NH Li SL Xie JF et al.In vitro and animal studies of the role of viruses in oral carcinogenesis.Eur J Cancer. 1992; 28B: 145-152Abstract Full Text PDF Scopus (25) Google Scholar DMBA (a tobacco-derived carcinogen), DMBA plus HSV, and HSV alone were applied to the mucosa of the buccal pouch of hamsters. Cancer developed in all the hamsters that received DMBA plus HSV. In half the animals that received DMBA alone cancer developed. In addition, none of the animals that received HSV alone developed cancer. These results support an important, but secondary, role for HSV in the pathogenesis of epithelial malignancy. The above schema is consistent with clinical facts. If HSV alone were a carcinogen, the incidence of lip, vulvar, cervical, and penile carcinoma would be much higher than is actually observed. These malignancies basically occur only in persons who have been exposed to carcinogens such as UV radiation, human papillomavirus, or tobacco. If HSV is present, the effects are synergistic and cancer is more likely to develop than if HSV is absent. Further confirmation of the secondary role of HSV in carcinogenesis comes from recent sero-epidemiologic studies that show a nonsignificant association between cervical cancer and HSV infection when smoking and the presence of HPV are taken into account and factored into statistical analysis.9Lehtinen M Dillner J Knekt P et al.Serologically diagnosed infection with human papillomavirus type 16 and risk for subsequent development of cervical carcinoma: nested case-control study.BMJ. 1996; 312: 537-539Crossref PubMed Scopus (142) Google Scholar, 10Lehtinen M Hakama M Ritva-Kaarina A et al.Herpes simplex virus type 2 infection and cervical cancer: a prospective study of 12 years of follow-up in Finland.Cancer Causes Control. 1992; 3: 333-338Crossref PubMed Scopus (17) Google Scholar, 11Jha PK Beral V Peto J et al.Antibodies to human papillomavirus and to other genital infectious agents and invasive cervical cancer risk.Lancet. 1993; 341: 1116-1118Abstract PubMed Scopus (61) Google Scholar, 12Munoz N Kato I Bosch FX et al.Cervical cancer and herpes simplex virus type 2: case-control studies in Spain and Colombia, with special references to immunoglobulin-G sub-classes.Int J Cancer. 1995; 60: 438-442Crossref PubMed Scopus (31) Google Scholar No clinical or epidemiologic data are available to support the assertion that the incidence of cancer of the cervix, vulva, penis, or lip is higher in patients with HSV who are receiving acyclovir suppression versus those not receiving such treatment. Although the process of carcinogenesis can take decades, there is not even the suggestion of a statistical trend for such an increase. When one looks into recent medical history, the experience with photodynamic inactivation (PDI) is instructive. PDI was in vogue in the years before the introduction of acyclovir. Warnings were sounded that this treatment produced defective transforming virus and therefore patients would be put at risk for cancer. Twenty years later, no excessive incidence of cancer has been reported in the thousands of patients who received this treatment. Given the enormous publicity PDI received in the medical and lay press, it is highly unlikely that any cancer in these patients would have passed unnoticed. Finally, it should be noted that in the course of reactivation and natural infection, at least 100 defective virus particles are produced for every one infectious virion. Natural infection alone is the biggest source of defective virus.13Jarratt MT Hubler WR Knox JM et al.Dye-photoinactivation and herpes simplex [letter].Arch Dermatol. 1974; 109: 570Crossref PubMed Scopus (1) Google Scholar Any treatment that significantly lessens the frequency and severity of recurrences would also lessen the number of these defective particles. If anything, acyclovir suppression should reduce cancer risk. In my opinion, it is entirely safe to prescribe acyclovir for long-term suppressive therapy. Is long-term continuous therapy for recurrent herpes simplex safe?Journal of the American Academy of DermatologyVol. 37Issue 3PreviewTo the Editor: We enjoyed reading the recent review article by Conant et al. on an integrated approach to management of genital herpes (J Am Acad Dermatol 1996;35:601–5) and the CME article by Pereira devoted to herpes simplex in the same issue (J Am Acad Dermatol 1996;35:503–20). In the two articles continuous therapy with acyclovir (over years) is considered effective and safe. We would like to present our long-term concern about the safety of using antiherpetic drugs over extended periods as a preventive therapy for recurrent attacks. Full-Text PDF" @default.
• W2804670094 created "2018-06-01" @default.
• W2804670094 creator A5082637138 @default.
• W2804670094 date "1997-09-01" @default.
• W2804670094 modified "2023-09-25" @default.
• W2804670094 title "Is long-term continuous therapy for recurrent herpes simplex safe?: Reply" @default.
• W2804670094 cites W1992597559 @default.
• W2804670094 cites W2008748900 @default.
• W2804670094 cites W2020415912 @default.
• W2804670094 cites W2028373261 @default.
• W2804670094 cites W2028465552 @default.
• W2804670094 cites W2031140727 @default.
• W2804670094 cites W2047129067 @default.
• W2804670094 cites W2061172728 @default.
• W2804670094 cites W2086393748 @default.
• W2804670094 cites W2120461324 @default.
• W2804670094 cites W2124403381 @default.
• W2804670094 cites W2155052944 @default.
• W2804670094 cites W2169143877 @default.
• W2804670094 doi "https://doi.org/10.1016/s0190-9622(18)30766-7" @default.
• W2804670094 hasPublicationYear "1997" @default.
• W2804670094 type Work @default.
• W2804670094 sameAs 2804670094 @default.
• W2804670094 citedByCount "0" @default.
• W2804670094 crossrefType "journal-article" @default.
• W2804670094 hasAuthorship W2804670094A5082637138 @default.
• W2804670094 hasBestOaLocation W28046700941 @default.
• W2804670094 hasConcept C114614502 @default.
• W2804670094 hasConcept C121332964 @default.
• W2804670094 hasConcept C16005928 @default.
• W2804670094 hasConcept C33923547 @default.
• W2804670094 hasConcept C61797465 @default.
• W2804670094 hasConcept C62438384 @default.
• W2804670094 hasConcept C62520636 @default.
• W2804670094 hasConcept C71924100 @default.
• W2804670094 hasConceptScore W2804670094C114614502 @default.
• W2804670094 hasConceptScore W2804670094C121332964 @default.
• W2804670094 hasConceptScore W2804670094C16005928 @default.
• W2804670094 hasConceptScore W2804670094C33923547 @default.
• W2804670094 hasConceptScore W2804670094C61797465 @default.
• W2804670094 hasConceptScore W2804670094C62438384 @default.
• W2804670094 hasConceptScore W2804670094C62520636 @default.
• W2804670094 hasConceptScore W2804670094C71924100 @default.
• W2804670094 hasIssue "3" @default.
• W2804670094 hasLocation W28046700941 @default.
• W2804670094 hasOpenAccess W2804670094 @default.
• W2804670094 hasPrimaryLocation W28046700941 @default.
• W2804670094 hasRelatedWork W2317368154 @default.
• W2804670094 hasRelatedWork W2335344983 @default.
• W2804670094 hasRelatedWork W2375653280 @default.
• W2804670094 hasRelatedWork W2390068691 @default.
• W2804670094 hasRelatedWork W2410144786 @default.
• W2804670094 hasRelatedWork W2738981461 @default.
• W2804670094 hasRelatedWork W2773939186 @default.
• W2804670094 hasRelatedWork W3178036187 @default.
• W2804670094 hasRelatedWork W4234833016 @default.
• W2804670094 hasRelatedWork W4297184974 @default.
• W2804670094 hasVolume "37" @default.
• W2804670094 isParatext "false" @default.
• W2804670094 isRetracted "false" @default.
• W2804670094 magId "2804670094" @default.
• W2804670094 workType "article" @default.