Jung Woon-Won
(MyGene Bioscience Institute, Sungok Bldg)
,
Chun Taehoon
(Department of Microbiology and Immunology, School of Medicine, Hanyang University)
,
Sul Donggeun
(Environmental Toxico-Genomic and Proteomic Center, College of Medicine, Korea University)
,
Hwang Kwang Woo
(Department of Immunology, College of Pharmacy, Chung-Ang University)
,
Kang Hyung-Sik
(School of Biological Sciences and Technology, Biotechnology Research Institute, Chonnam University)
,
Lee Duck Joo
(Department of Family Medicine, Samsung Cheil Hospital, Sungkyunkwan University)
,
Han In-Kwon
(MyGene Bioscience Institute, Sungok Bldg, Department of Internal Medicine, Samsung Cheil Hospital, Sungkyunkwan University)
Papillomaviruses infect a wide variety of animals, including humans. The human papillomavirus (HPV), in particular, is one of the most common causes of sexually transmitted disease. More than 200 types of HPV have been identified by DNA sequence data, and 85 HPV genotypes have been well characteriz...
Papillomaviruses infect a wide variety of animals, including humans. The human papillomavirus (HPV), in particular, is one of the most common causes of sexually transmitted disease. More than 200 types of HPV have been identified by DNA sequence data, and 85 HPV genotypes have been well characterized to date. HPV can infect the basal epithelial cells of the skin or inner tissue linings, and are, accordingly, categorized as either cutaneous or mucosal type. HPV is associated with a panoply of clinical conditions, ranging from innocuous lesions to cervical cancer. In the early 1980s, studies first reported a link between cervical cancer and genital HPV infection. Genital HPV infections are now recognized to be a major risk factor in at least $95\%$ of cervical cancers. 30 different HPV genotypes have been identified as causative of sexually transmitted diseases, most of which induce lesions in the cervix, vagina, vulva, penis, and anus, as the result of sexual contact. There is also direct evidence demonstrating that at least four of these genotypes are prerequisite factors in cervical cancer. The main aim of this review was to evaluate the current literature regarding the pathovirology, diagnostics, vaccines, therapy, risk groups, and further therapeutic directions for HPV infections. In addition, we reviewed the current status of HPV infections in South Korean women, as evidenced by our data.
Papillomaviruses infect a wide variety of animals, including humans. The human papillomavirus (HPV), in particular, is one of the most common causes of sexually transmitted disease. More than 200 types of HPV have been identified by DNA sequence data, and 85 HPV genotypes have been well characterized to date. HPV can infect the basal epithelial cells of the skin or inner tissue linings, and are, accordingly, categorized as either cutaneous or mucosal type. HPV is associated with a panoply of clinical conditions, ranging from innocuous lesions to cervical cancer. In the early 1980s, studies first reported a link between cervical cancer and genital HPV infection. Genital HPV infections are now recognized to be a major risk factor in at least $95\%$ of cervical cancers. 30 different HPV genotypes have been identified as causative of sexually transmitted diseases, most of which induce lesions in the cervix, vagina, vulva, penis, and anus, as the result of sexual contact. There is also direct evidence demonstrating that at least four of these genotypes are prerequisite factors in cervical cancer. The main aim of this review was to evaluate the current literature regarding the pathovirology, diagnostics, vaccines, therapy, risk groups, and further therapeutic directions for HPV infections. In addition, we reviewed the current status of HPV infections in South Korean women, as evidenced by our data.
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제안 방법
In this review, the current literature regarding the pathovirology, diagnostics, risk groups, vaccines, therapy, and further therapeutic direction of HPV infection were evaluated. In addition, this study reviewed the current status of HPV infections in South Korean women, as evidenced by our data.
Three vaccinations were performed over 6 months, on a total of 1533 individuals. The volunteers were examined at 6-month intervals for 48 months after vaccination by a PCR reaction, to determine whether there was any evidence of persistent HPV 16 infections. The results of the HPV VLP vaccine trials were quite promising.
대상 데이터
High risk and low risk groups of HPV infection in South Korean women over the last four years. A total of 14, 264 specimens were screened. The upper panel shows the result of a high-risk group of HPV infection in South Korean women, and the lower panel shows a result of a low-risk group of HPV infection.
성능/효과
Recently, a novel technique for the detection of HPV infection was developed. Over the last four years, a total of 14, 264 samples were tested, and the HPV infections in South Korea were genotyped. The results of this study suggest that the targets for HPV protection in South Korea should be different than those in other countries.
Interestingly, conventional high-risk HPV genotypes, such as 16 and 18, were still dominant, but new HPV genotypes such as 33, 56, and 58 have appeared in the South Korean population during the past few years. The results for low-risk HPV genotypes revealed that HPV 6, 11, 53, 54 and 70 were dominant in South Korean women. After analyzing the regional incidence of HPV infection, the populations of Inchon and Busan were found to be more susceptible to HPV infection, which might indicate geological specificity, as Inchon and Busan are major international ports (Fig.
참고문헌 (64)
Adam, E., Z. Berkova, Z. Daxnerova, J. Icenogle, W.C. Reeves, and R.H. Kaufman. 2001. Papillomavirus detection: demographic and behavioral characteristics influencing the identification of cervical disease. Am. J. Obstet. Gynecol. 182, 257-264
Allen, M., M. Kalantari, A. Ylitalo, B. Pettersson, B. Hagmar, L. Scheibenplug, B. Johansson, U. Petterson, and U. Gyllensten. 1996. HLA DQ-DR haplotype and susceptibility to cervical carcinoma: indications of increased risk for development of cervical carcinoma in individuals infected with HPV 18. Tissue Antigens 48, 32-37
Andrei, G., R. Snoeck, J. Piette, P. Delvenne, and E. DeClercq. 1998. Antiproliferative effects of acyclic nucleoside phosphonates on human papillomavirus (HPV)-harboring cell lines compared with HPV-negative cell lines. Oncol. Res. 10, 523-531
Apple, R.J., T.M. Becker, C.M. Wheeler, and H.A. Erlich. 1995. Comparison of human leukocyte antigen DR-DQ disease associations found with cervical dysplasia and invasive cervical carcinoma. J. Natl. Cancer Inst. 87, 427-436
Baker, T.S., W.W. Newcomb, N.H. Olson, L.M. Cowsert, C. Olson, and J.C. Brown. 1991. Structures of bovine and human papillomaviruses. Analysis by cryoelectron microscopy and threedimensional image reconstruction. Biophys. J. 60, 1445-1456
Bonnez, W. and R.C. Richman. 1994. Papillomaviruses, p. 1630-1640. In G.L. Mandell, J.E. Bennett, and R. Dolin R (eds.), Nandell, Douglas, and Bennetts principles and practice of infectious diseases, 5th ed. Churchill Livingston, Philadelphia, Pennsylvania
Bontkes, H.J., M. Van Duin, T.D. deGruijl, M.F. Duggan-Keen, J.M. Walboomers, M.J. Stukart, R.H. Vereheijen, T.J. Helmerhorst, C.J. Meijer, R.J. Scheper, F.R. Stevens, P.A. Dyer, P. Sinnott, and P.L. Stern. 1998. HPV 16 infection and progression of cervical intraepithelial neoplasia: analysis of HLA polymorphism and HPV 16 E6 sequences variants. Int. J. Cancer 78, 166-171
Bontkes, H.J., T.D. deGruijl, J.M. Walboomers, J.T. Schiller, J. Dillner, T.J. Helmerhorst, R.H. Vereheijen, R.J. Scheper, and C.J. Meijer. 1999. Immune responses against human papillomavirus (HPV) type 16 virus-like particles in a cohort study of women with cervical intraepithelial neoplasia. II. Systemic but not local IgA responses correlate with clearance of HPV-16. J. Gen. Virol. 80, 409-417
Bosch F., M.M. Manos, N. Munoz, M. Sherman, A.M. Jansen, J. Peto, M.H. Shiffman, V. Moreno, R. Kurman, and K.V. Shah. 1995. Prevalence of human HPV in cervical cancer: a worldwide perspective. J. Natl. Cancer Inst. 87, 796-802
Breitburd F., R. Kirnbauer, N.L. Hubbert, B. Nonnenmacher, C. Trin-Dinh-Desmarquet, G. Orth, J.T. Schiller, and D.R. Lowy. 1995. Immunization with viruslike particles from cottontail rabbit papillomavirus (CRPV) can protect against experimental CRPV infection. J. Virol. 69, 3959-3963
Burd, E.M. 2003. Human papillomavirus and cervical cancer. Clin. Microbiol. Rev. 16, 1-17
Burk, R.D., P. Kelly, J. Feldman, J. Bromberg, S.H. Vermund, J.A. Deltovitz, and S.H. Landesman. 1996. Declining presence of cervicovaginal human papilllomavirus infection with age is independent of other risk factors. Sex Transm. Dis. 23, 333-341
Calore, E.E., S.M.M. Pereira, and M.J. Cavaliere. 2001. Progression of cervical lesions in HIV-seropositive women: a cytological study. Diagn. Cytopathol. 24, 117-119
Campo, M.S., G.J. Grindlay, B.W. O'Neil, L.M. Chandrachud, G.M. McGarvie, and W.F. Jarrett. 1993. Prophylactic and therapeutic vaccination against a mucosal papillomavirus. J. Gen. Virol. 74, 945-953.
Christensen, N.D., J.W. Kreider, N.M. Cladel, and D.A. Galloway. 1990. Immunological cross-reactivity to laboratory-produced HPV-11 virions of polysera raised against bacterially derived fusion proteins and synthetic peptides of HPV-6b and HPV-16 capsid proteins. Virology 175, 1-9
Chua, K.L. and A. Hjerpe. 1996. Persistence of human papillomavirus (HPV) infections preceding cervical carcinoma. Cancer 77, 121-127
Cubie, H.A., A.L. Seagar, G.J. Beattie, S. Monaghan, and A.R.W. Williams. 2000. A longitudinal study if HPV detection and cervical pathology in HIV infected women. Sex Transm. Infect. 76, 257-261
Da Silva D.M., G.L. Eiben, S.C. Fausch, M.T. Wakabayashi, M.P. Rudolf, M.P. Velders, and W.M. Kast. 2001. Cervical cancer vaccines: emerging concepts and developments. J. Cell Physiol. 186, 169-182
Dupuy, C., D. Buzoni-Gatel, A. Touze, D. Bout, and P. Coursaget. 1999. Nasal immunization of mice with human papillomavirus type 16 (HPV-16) virus-like particles or with the HPV-16 L1 gene elicits specific cytotoxic T lymphocytes in vaginal draining lymph nodes. J. Virol. 73, 9063-9071
Emeny, R.T., C.M. Wheeler, K.U. Jansen, W.C. Hunt, T.M. Fu, J.F. Smith, S. MacMullen, M.T. Esser, and X. Paliard. 2002. Priming of human papillomavirus type 11-specific humoral and cellular immune responses in college-aged women with a viruslike particle vaccine. J. Virol. 76, 7832-7842
Evander, M., I.H. Frazer, E. Payne, Y.M. Qui, K. Hengst, and N.A. McMillan. 1997. Identification of the alpha6 integrin as a candidate receptor for papillomaviruses. J. Virol. 71, 2449-2456
Evans, T.G., W. Bonnez, R.C. Rose, S. Koenig, L. Demeter, J.A. Suzich, D. O'Brien, M. Campbell, W.I. White, J. Balsley, and R.C. Reichman. 2001. A Phase 1 study of a recombinant viruslike particle vaccine against human papillomavirus type 11 in healthy adult volunteers. J. Infect. Dis. 183, 1485-1493
Favre, M. 1975. Structural polypeptides of rabbit, bovine, and human papillomaviruses. J. Virol. 15, 1239-1247
Franco, E.L. 1995. Cancer causes revisited:human papillomavirus and cervical neoplasia. J. Natl. Cancer Inst. 87, 779-780
Greenstone, H.L., J.D. Nieland, K.E. de Visser, M.L. De Bruijn, R. Kirnbauer, R.B. Roden, D.R. Lowy, W.M. Kast, and J.T. Schiller. 1998. Chimeric papillomavirus virus-like particles elicit antitumor immunity against the E7 oncoprotein in an HPV16 tumor model. Proc. Natl. Acad. Sci. USA 95, 1800- 1805
Giroglu, T., L. Florin, F. Schafer, R.E. Stre, and M. Sapp. 2001. Human papillomavirus infection requires cell surface heparin sulfate. J. Virol. 75, 1565-1570
Harro, C.D., Y.-Y.S. Pang, R.B.S. Roden, A. Hildesheim, Z. Wang, J.M. Reynolds, T.C. Mast, R. Robinson, B.R. Murphy, R.A. Karron, J. Dillner, J.T. Schiller, and D.R. Lowy. 2001. Safety and immunogenicity trial in adult volunteers of a human papillomavirus 16 L1 virus-like particle vaccine. J. Natl. Cancer Inst. 93, 284-292
Hines, J.F., S.J. Ghim, N.D. Christensen, J.W. Kreider, W.A. Barnes, R. Schlegel, and A.B. Jenson. 1994. Role of conformational epitopes expressed by human papillomavirus major capsid proteins in the serologic detection of infection and prophylactic vaccination. Gynecol. Oncol. 55, 13-20
Ho, G.Y., R. Bierman, L. Beardsley, C.J. Chang, and Burk RD. 1998. Natural history of cervicovaginal papillomavirus infection in young women. N. Engl. J. Med. 338, 413-428
Holowaty, P., A.B. Miller, and T.T. Rohan. 1999. Natural dysplasia of the uterine cervix. J. Natl. Cancer Inst. 91, 252-258
Hummel, M., J.B. Hudson, and L.A. Laimins. 1992. Differentiation-induced and constitutive transcription of human papillomavirus type 31b in cell lines containing viral episomes. J. Virol. 66, 6070-6080
Jacobs, M.V., P.J. Snijders, A.J. van den Brule, T.J. Helmerhorst, C.J. Meijer, and J.M. Walboomers. 1997. A general primermediated PCR enzyme immunoassay method for rapid detection of 14 high-risk and 6 low-risk human papillomavirus genotypes in cervical scrapings. J. Clin. Microbiol. 35, 791-795
Jeon, S., B.L. Allen-Hoffman, and P.F. Lambert. 1995. Integration of human papillomavirus type 16 into the human genome correlates with a selective growth advantage of cells. J. Virol. 69, 2989-2997
Jin, X.W., J. Cash, and A.W. Kennedy. 1999. Human papillomavirus typing and the reduction of cervical cancer risk. Cleveland Clin. J. Med. 66, 533-539
Joyce, J.G., J.-S. Tung, C.T. Przysiecki, J.C. Cook, E.D. Lehman, J.A. Sands, K.U. Jansen, and P.M. Keller. 1999. The L1 major capsid protein of human papillomavirus type 11 recombinant virus-like particles interacts with heparin and cell-surface glycosaminoglycans on human keratinocytes. J. Biol. Chem. 274 5810-5822.
Kleter, B., L.J. van Doorn, L. Schrauwen, A. Molijn, S. Sastrowijoto, J. TerSchegget, J. Lindeman, B. Ter Harmsel, M. Burger, and W. Quint. 1999. Development and clinical evaluation of a highly sensitive PCR-reverse hybridization line probe assay for detection and identification of anogenital human papillomavirus. J. Clin. Microbiol. 37, 2508-2517
Kim, K.Y., L. Blatt, and M.W. Taylor. 2000. The effects of interferon on the expression of human papillomavirus oncogenes. J. Gen. Virol. 81, 695-700
Kiviat, N.B. and L.A. Koutsky. 1993. Specific human papillomavirus types as the causal agents of most cervical intraepithelial neoplasia: implications for current views and treatment. J. Natl. Cancer Inst. 85, 934-935
Koutsky, L.A., K.A. Ault, C.M. Wheeler, D.R. Brown, E. Barr, F.B. Alvarez, L.M. Chiacchierini, and K.U. Jansen. 2002. A controlled trial of a human papillomavirus type 16 vaccine. N. Engl. J. Med. 347, 1645-1651
Lizard, G., M.-J. De´mares-Poulet, P. Roignot, and P. Gambert. 2001. In situ hybridization detection of single-copy human papillomavirus on isolated cells using a catalyzed signal amplification system:GenPoint™. Diagn. Cytopathol. 24, 112-116
Liu, W.J., K.N. Zhao, F.G. Gao, G.R. Leggatt, G.J. Fernando, and I.H. Frazer. 2001. Polynucleotide viral vaccines: codon optimisation and ubiquitin conjugation enhances prophylactic and therapeutic efficacy. Vaccine 20, 862-869
Magnusson, P.K.E., P. Lichtenstein, and U.B. Gyllenstein. 2000. Heritability of cervical tumors. Int. J. Cancer 88, 698-701
Meyers, C., M.G. Frattini, J.B. Hudson, and L.A. Laimins. 1992. Biosynthesis of human papillomavirus from a continuous cell line upon epithelial differentiation. Science 257, 971-973
Moscicki, A.B., J. Palefsky, G. Smith, S. Siboshski, and G. Schoolnik. 1993. Variability of human papillomavirus DNA testing in a longitudinal cohort of young women. Obstst. Gynecol. 82, 578-585
Muller, M., J. Zhou, T.D. Reed, C. Rittmuller, A. Burger, J. Gabelsberger, J. Braspenning, and L. Gissmann. 1997. Chimeric papillomavirus- like particles. Virology 234, 93-111
Murray, P.R., K.S. Rosenthal, G.S. Kobayashi, and M.A. Pfaller. 2002. Papovaviruses, p. 460. In Medical Microbiology. Mosby Press, London, United Kingdom
Okamoto, A., C.D. Woodworth, K. Yen, J. Chun, S. Isonishi, T. Nikaido, T. Kiyokawa, H. Seo, Y. Kitahara, K. Ochiai, and T. Tanaka. 1999. Combination therapy with podophyllin and vidarabine for human papillomavirus positive cervical intraepithelial neoplasia. Oncol. Rep. 6, 269-276
Orth, G. and Favre, M. 1985. Human papillomaviruses. Biochemical and biologic properties. Clin. Dermatol. 3, 27-42
Papanicolaou, G.N. 1949. A survey of actualities and potentialities of exfoliative cytology in cancer diagnosis. Ann. Intern. Med. 31, 661-674
Philips, D.H., and M. NiShe. 1993. Smoking-related DNA adducts in human cervical biopsies. IARC Sci. Publ. 124, 327-330
Quint, W.G.V., G. Scholte, L.J. Van Doorn, B. Kleeter, P.H.M. Smits, and J. Lindeman. 2001. Comparative analysis of human papillomavirus infections in cervical scrapes and biopsy specimens by general SPF10 PCR and HPV genotyping. J. Pathol. 194, 51-58
Roden, R.B., D.R. Lowy, and J.T. Schiller. 1997. Papillomavirus is resistant to dessication. J. Infect Dis. 176, 1076-1079
Roden, R.B., W.H. Yutzy, R. Fallon, S. Inglis, D.R. Lowy, and J.T. Schiller. 2000. Minor capsid protein of human genital papillomaviruses contains subdominant, cross-neutralizing epitopes. Virology 270, 254-257
Santin, A.D., P.L. Hermonat, A. Ravaggi, M. Chiriva-Internati, D. Zhan, S. Pecorelli, G.P. Parham, and M.J. Cannon. 1999. Induction of human papillomavirus-specific CD4(+) and CD8(+) lymphocytes by E7-pulsed autologous dendritic cells in patients with human papillomavirus type 16- and 18-positive cervical cancer. J. Virol. 73, 5402-5410
Solomon, D., D. Davey, R. Kurman, A. Moriarity, D. Oconnor, M. Prey, S. Raab, M. Sherman, D. Wilbur, T. Wright, and N. Young. 2002. The 2001 Bethesda System. Terminology for reporting results of cervical cytology. JAMA 287, 2114-2119
Syrjanen, K.J. 1996. Natural history of genital human papillomavirus infections, p.189-206. In C. Lacey (ed.), Papillomavirus reviews. Leeds University Press, Leeds, United Kingdom
Suzich, J.A., S.J. Ghim, F.J. Palmer-Hill, W.I. White, J.K. Tamura, J.A. Bell, J.A. Newsome, A.B. Jenson, and R. Schlegel. 1995. Systemic immunization with papillomavirus L1 protein completely prevents the development of viral mucosal papillomas. Proc. Natl. Acad. Sci. USA 92, 11553-11557
Tomas, M., D. Pim, and L. Banks. 1999. The role of the E6-p53 interaction in the molecular pathogenesis of HPV. Oncogene 18, 7690-7700
Torrisi, A., A. Del Mistro, G.L. Onnis, F. Merlin, R. Bertorelle, D. Minucci and D. Colposcopy. 2000. Cytology and HPV testing in HIV-positive and HIV-negative women. Eur. J. Gynecol. Oncol. 21, 168-172
Villa, L.L. 1997. Human papillomaviruses and cervical cancer. Adv. Cancer Res.71, 321-341
Walboomers, J.M.M., M.V. Jacobs, M.M. Manos, F.X. Bosch, J.A. Kummer, K.V. Shah, P.J.F. Snijders, J. Peto, C.J.L. Meijer, and N. Munoz. 1999. Human papillomavirus is a necessary cause of invasive cervical cancer worldwide. J. Pathol. 189, 12-19
Yang, X., G. Jin, Y. Nakao, M. Rahimtula, M. Pater, and A. Pater. 1996. Malignant transformation of HPV-16 immortalized human endocervical cells by cigarette smoke condensate and characterization of multistage carcinogenesis. Int. J. Cancer 65, 338-344
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