Prevalence of Epstein‐Barr virus and human papillomavirus in oral mucosa of HIV‐Infected patients

Adler‐Storthz, Karen; Ficarra, Giuseppe; Woods, Kendra V.; Gaglioti, Domenico; DiPietro, Massimo; Shillitoe, Edward J.

doi:10.1111/j.1600-0714.1992.tb00095.x

Cited by 37 publications

(18 citation statements)

References 34 publications

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“…[75][76][77][78][79][80] In the population infected with HIV, hairy leukoplakia is seen with relative frequency, appearing either before or after an established diagnosis of AIDS. It represents an opportunistic EBV infection and presents as an asymptomatic white patch that may be flat, vertically corrugated, or papillate (hairy).…”

Section: Hairy Leukoplakia Clinical Characteristicsmentioning

confidence: 99%

Oral Cavity and Jaws

Weidner¹,

Matthews²,

Regezi³

2009

Modern Surgical Pathology

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Section: Hairy Leukoplakia Clinical Characteristicsmentioning

confidence: 99%

Oral Cavity and Jaws

Weidner¹,

Matthews²,

Regezi³

2009

Modern Surgical Pathology

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“…A review of seven studies indicated that group II and III lesions, a marker for HIV and disease progression, which includes viral lesions of the mouth, were definitely less common, and HPVassociated oral lesions were possibly associated with HIV infection, respectively (80). Even if HPV-induced oral lesions associated with HIV infection is less common, many studies suggest that the chances of HPV infection might increase in proportion to the immune suppression caused by HIV infection (81)(82)(83)(84)(85)(86)(87)(88). In a cervical infection study, the risk of HPV infection in HIV-positive females and males increased with lower CD4 levels and higher HIV viral load (85).…”

Section: Hpv Of the Oral Cavity In Immunosuppressed Patientsmentioning

confidence: 99%

“…However, the immunological effects of HAART could not provide sufficient protection against different kinds of HPV-induced lesions in some HIV-infected patients (75). The prevalence of HPV infection in the normal oral mucosa between HIV-positive and -negative females and males was not significantly different, but the spectrum of HPV genotypes in HIV-positive females and males could be wider than HIV-negative ones (81)(82)(83)(84). We also showed that prevalence in adults was similar among healthy individuals and HIV-positive females and males (Terai et al unpublished …”

Section: Hpv Of the Oral Cavity In Immunosuppressed Patientsmentioning

confidence: 99%

“…There might not be significant differences in HPV prevalence between HIV-positive and negative females and males (81)(82)(83)(84). Among HIVnegative females and males, the positive rate in the oral cavity of both adult groups was, however, higher than that in the elders and children (94).…”

Section: The Natural History Of Hpv In the Oral Cavitymentioning

confidence: 99%

“…The possibility of HPV transmission from another part of the body or another person should be considered. HPV transmission by sexual contact as a sexually transmitted disease is the present consensus (81)(82)(83)(84)(89)(90)(91)(92)(93). However, nonsexual routes, such as autoinoculation from one region to another in the same person (95) and vertical transmission during the perinatal period, were suggested or reported (96,97).…”

Section: The Natural History Of Hpv In the Oral Cavitymentioning

confidence: 99%

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Human Papillomavirus in the Oral Cavity

Terai

Takagi

2001

Oral Med Pathol

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Human papillomavirus (HPV) cannot be efficiently propagated in tissue cultures or animal models. However, molecular biological technology has made it possible to clone viral genomes, which can then be compared and also used as reagents in clinical and epidemiological studies.Today HPV infections are recognized as being responsible for inducing cancers worldwide and it is expected that HPV-based technologies will provide the tools to prevent and treat HPV-induced cancers. In this review, we focus on the association between oral lesions and HPV infection and the natural history of HPV infection of the oral cavity. We also evaluate the HPV detection methods in this important and fundamental matter for the HPV studies. We then discuss the potential targeted molecular therapies and prevention of a variety of HPVinduced diseases of the oral cavity, including oral cancers. Key words: HPV, human papillomavirus, oral cavityCorrespondence : Minoru Takagi, Molecular Pathology, Oral Restitution, Oral Health Science, Graduate School, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113- 8549, JapanPhone: +81-3-5803-5451, Fax: +81-3-5803-0188 IntroductionHuman papillomavirus (HPV) is a small, nonenveloped and double stranded circular DNA virus, about 8,000 bp in length, with a well-known physical structure and gene organization (1). HPV belongs in the subfamily papillomavirus (PV) of the papovavirus family, which are widely distributed in nature and infect many higher vertebrates including cattle, rabbits and dogs (1). It is thought that the viruses may have co-evolved with their hosts (2). They are highly species-specific species, having one or more of its own PVs, and viruses of one species do not infect other species (1).HPV is classified into more than 100 types, including 84 clones and others detected by PCR (3). To be recognized as a distinct HPV genome, the full genome should be cloned and the sequence of the L1 gene should be no more than 90% similar to previously assigned and referenced HPVs (4). HPVs naturally fall into two groups: mucosal HPVs and cutaneous HPVs according to the anatomic site of infection and/or phylogenetic analysis (5). Some HPV infections can lead to malignant lesions depending on HPV genotypes and infection persistence. HPV is also broadly categorized into low, intermediate and highrisk types in accordance with their potential to induce or their association with malignant lesions (6). In oral lesions 24 genotypes have been identified 2,3,4,6,7,10,11,13,16,18,30,31,32,33,35,45,52,55,57,59,69,72 and 73) (7-27) ( Table 1).The HPV genome is comprised of early (E) genes that function primarily in episomal replication and late (L) genes that encode the viral capsid proteins. HPV 16 genome map is shown in Fig. 1. The L1 and L2 genes code for proteins that make up the viral major and minor capsid. The capsid encloses the viral genome and mediates viral entry into susceptible cells (28). Much of the immune response to infection is directed at the capsid protein (29). Based on experi...

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Head and Neck Cancer Incidence Trends in Young Americans, 1973-1997, With a Special Analysis for Tongue Cancer

Schantz¹,

Yu²

2002

Arch Otolaryngol Head Neck Surg

302

196

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Objective: To examine the temporal changes in head and neck cancer in young adults in the United States.Methods: Using the cancer surveillance database from the National Cancer Institute Surveillance, Epidemiology, and End Results (SEER) Program, we calculated ageadjusted incidence rates for head and neck cancers. Using the joinpoint regression model, we described tongue cancer incidence trends and established the statistical significance of temporal changes. We also compared changes in 5-year survival rates for tongue cancer.Results: From 1973 to 1997, there were 63 409 patients with head and neck cancer in the 9 SEER registries. Of these, 3339 patients were younger than 40 years. The incidence of head and neck cancer remained stable in groups older than 40 years comparing the 1973-1984 and 1985-1997 data. In contrast, tongue cancer in adults younger than 40 years increased approximately 60% during the same period. We detected a significant increase (REPRINTED) ARCH OTOLARYNGOL HEAD NECK SURG/ VOL 128, MAR 2002 WWW.ARCHOTO.COM 268

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Prevalence of Epstein‐Barr virus and human papillomavirus in oral mucosa of HIV‐Infected patients

Cited by 37 publications

References 34 publications

Oral Cavity and Jaws

Oral Cavity and Jaws

Human Papillomavirus in the Oral Cavity

Head and Neck Cancer Incidence Trends in Young Americans, 1973-1997, With a Special Analysis for Tongue Cancer

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