High-risk mucosal human papillomavirus infections during infancy &amp; childhood

Cason, John; Mant, Christine

doi:10.1016/j.jcv.2004.12.007

Cited by 67 publications

(94 citation statements)

References 70 publications

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“…The finding that punctate ISH signals are common in both juvenile-onset (7/10) and adult-onset (7/11) patients infected with low-risk HPV genotypes, suggests that HPV integration into the cell genome occurs at an early stage and may be an important factor contributing to the recurrent nature of these lesions. Possibly, if HPV integration occurs in a basal stem cell, HPV is then locked into the cell genome at the site of laryngeal infection and thereafter may support the recurrent papilloma phenotype and eventually the conversion of laryngeal papillomas to carcinomas, especially in juveniles [6,7]. In cervical tumors, high-risk HPV integration is associated with the loss of the HPV E2 gene that regulates the E6 and E7 oncogenes that promote abrogation of cell cycle control and cell division; low-risk HPV integration may support a parallel situation in recurrent papillomas.…”

Section: Discussionmentioning

confidence: 99%

“…Juvenile-onset RRP (JO-RRP) is generally considered to have a more aggressive clinical course than the adultonset (AO-RRP) [2,4,5]. Also, conversion to laryngeal carcinoma occurs more frequently in juveniles [6,7]. In addition to having a different clinical course, JO-RRP differs in its route of acquisition; while numerous studies have indicated that vertical transmission from maternal genital condylomas is the primary mode of juvenile papillomas, adult papillomas apparently spread secondary to oral-genital contact [8,9].…”

Section: Introductionmentioning

confidence: 99%

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In Situ Hybridization Signal Patterns in Recurrent Laryngeal Squamous Papillomas Indicate that HPV Integration Occurs at an Early Stage

Brooks

Evans

Adamson

et al. 2011

Head and Neck Pathol

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Laryngeal papillomas are benign tumors that frequently recur and can compromise airways. We investigated HPV genotype, physical status, and protein expression in juveniles versus adults. Thirty-five laryngeal papilloma specimens were obtained from ten juveniles (1-16 years) and eleven adults (24-67 years). In cases of recurrent papillomatosis (7 juveniles, 7 adults), the first and last papillomas were assayed. HPV type was determined by GP5?/6? PCR and dot blot hybridization. In situ hybridization (ISH) was performed on 34 specimens; the data were recorded in terms of diffuse (episomal HPV) and punctate (integrated HPV) signal patterns. Immunohistochemistry for the HPV L1 capsid protein, a marker of HPV productive status, was performed on 32 samples. All samples tested HPV positive: HPV 11 in 2/10 (20.0%) juveniles and 5/11 (45.5%) adults; HPV 6 in 7/10 (70%) juveniles and 5/11 (45.5%) adults; and HPV 6/11 double infection was noted in one juvenile and one adult. ISH signals (punctate ± diffuse) were detected among 7/10 (70.0%) juveniles and 7/11 (63.6%) adults. L1 staining was detected in 1/9 (11.1%) juveniles and 6/10 (60.0%) adults (P = 0.06). These data support the idea that integration of low-risk HPV types into the cell genome is an early and common event in the etiology of juvenile and adult recurrent laryngeal papillomas. Productive HPV infections may be more common in adults; accordingly, constant laryngeal re-infection by HPV shed from a productive lesion may contribute to adult recurrent lesions, whereas the mechanism of papilloma recurrence in juveniles may be more attributable to HPV integration.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

In Situ Hybridization Signal Patterns in Recurrent Laryngeal Squamous Papillomas Indicate that HPV Integration Occurs at an Early Stage

Brooks

Evans

Adamson

et al. 2011

Head and Neck Pathol

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“…Une voie de transmission par contact de surface infectée ou de sous-vêtements a été évoquée. La présence d'HPV sur les sous-vêtements de patientes avec lésions HPV induites a été authentifiée [6,7]. Dans le cas de ce patient, aucune autre localisation de condylomes associée (génitale ou anale) n'a été décelée.…”

Section: Discussionunclassified

Le condylome acuminé isolé de la cavité buccale : à propos d’un cas clinique

Mahroug

Maja

Allaoui

et al. 2015

Med Buccale Chir Buccale

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Isolated condyloma acuminatum of the oral cavity: a short case report. Introduction: A condyloma acuminatum is a benign tumor considered to be a sexuallytransmitted infection. The viruses responsible are 90 % the human papilloma viruses types 6 and 11. They present low risk of cancer. The aim of this short case report is to state the clinical, histological and therapeutic aspects of condyloma acuminata of oral localization, and also to examine the pathways of non-sexual transmission. Observation: A thirty-yearold patient without sexual oro-genital activities consulted for whitish millimeter-length lesions localized in the hard palate and the left labial corners which had appeared a year ago. The surgical excision of both lesions of the hard palate were performed, as well as a biopsy of the left labial commissure, completed by electrocoagulation. The histological exam concluded the diagnosis of condyloma acuminata. No recurrence was recorded during the ten months of post-operative follow-up. Discussion: Oral lesions of condyloma acuminatum are very seldom and often secondary to contamination through direct sexual contact. Meanwhile, other transmission pathways not related to direct sexual contact are described. The diagnosis of condyloma acuminatum is clinical and confirmed by a histological exam. Radical treatment based mainly on surgical excision or electrocoagulation is imperative because of the highly contagious character of this lesion. Conclusion: Condyloma acuminatum is very seldom localized in the oral cavity. Diagnosis is mainly based on medical history and a histological exam.

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“…At the age of 1-4 days, Smith et al in two studies found a low HPV incidence (from 0.9% to 1%) in the buccal swabs of neonates, whereas other studies showed a higher prevalence varying from 40% to 56% (Cason et al, 1995;Kaye et al, 1994;Pakarian et al, 1994;Tseng et al, 1998;Smith et al, 1995Smith et al, , 2004b. Similarly, the detection rate of HPV in infants between 6 weeks and 6 months after delivery varied between 0% and 62% (Cason et al, 2005;Fredericks et al, 1993;Pakarian et al, 1994;Watts et al, 1998) and among 3-year-old children varied between 10% and 40% (Kojima et al, 2003;Puranen et al, 1996Puranen et al, , 1997Szydlowski et al, 2004). Mant et al studied the acquisition and the clearance of HPV in the buccal mucosa of 4-to 9-year-old children and showed that, during a 30-month follow-up, 63% of 19 initially HPV-negative children acquired new HPV16 infection, while 40% of 22 initially HPVpositive children cleared the virus (Mant et al, 2003).…”

Section: Incidence Of Hpv In Normal Oral Mucosamentioning

confidence: 98%