Mechanism for human papillomavirus transmission at birth

Sedlacek, Thomas V.; Lindheim, Steven R.; Eder, Catherine; Hasty, Lisa A.; Woodland, Mark; Ludomirski, Avi; Rando, Robert F.

doi:10.1016/0090-8258(89)91021-4

Cited by 29 publications

(34 citation statements)

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“…This finding is convincing evidence of vertical transmission of BPV and substantiates the hypothesis which suggests a virus-mediated aetiology for the reported chromosomal aberrations. Vertical transmission has also been suggested for HPV in a number of cases (Sedlacek et al, 1989). This is the first report of the transmission of BPV through blood and of the clastogenic action of BPV in vivo in the absence of bracken fern.…”

Section: Discussionmentioning

confidence: 83%

Bovine papillomavirus transmission and chromosomal aberrations: an experimental model.

Stocco

Lindsey

Ferraz

et al. 1998

Journal of General Virology

106

141

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Enzootic haematuria and urinary bladder cancer in cattle are associated with feeding on bracken fern and bovine papillomavirus (BPV) infection. An increased rate of chromosomal aberrations in peripheral blood lymphocytes from chronically affected haematuric cows raised in bracken fern pastures has been reported, suggesting the presence of BPV in the peripheral blood of afflicted animals. The purpose of the present investigation was to examine the role of peripheral blood as a potential BPVtransmitting agent and search for clastogenic effects in experimentally infected animals kept on a bracken fern-free diet. Healthy cows were inoculated with blood samples of haematuric animals every two weeks for 18 months. Recipient cows, their offspring, donor animals and a control group were kept on a bracken fern-free diet throughout the experiment. Clinical and molecular analyses for

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Section: Discussionmentioning

confidence: 83%

Bovine papillomavirus transmission and chromosomal aberrations: an experimental model.

Stocco

Lindsey

Ferraz

et al. 1998

Journal of General Virology

106

141

View full text Add to dashboard Cite

show abstract

“…We feel that our control group of women of a comparable age range represents a fair reflection of those exposed to HPVs in the population as a whole but cannot be regarded as either naive or virus-free for the following reasons. Firstly, HPV infections can also be transmitted from mother to child at birth or in early infancy (Sedlacek et al, 1989) and secondly, women tested for the virus by PCR on cervical swabs taken at regular 5 weekly intervals over a 12 month period could change from positive to negative and back to positive again (Schneider et al, 1992). Also, a biopsy from the cervix of a 'normal healthy individual' might fail to detect the presence of latent virus by PCR due to the local nature of the disease, its low copy number and the limitations of taking small punch biopsies.…”

Section: Discussionmentioning

confidence: 99%

Proliferative T cell responses to human papillomavirus type 16 L1 peptides in patients with cervical dysplasia

Shepherd

Rowe

Cridland

et al. 1996

Journal of General Virology

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Human papillomavirus type 16 (HPV-16) can cause genital warts, cervical dysplasias and carcinoma of the cervix. Cell-mediated immunity is thought to be important in protection against the virus and in its elimination, but little is known about the mechanisms involved. In a cross-sectional study we have demonstrated proliferative T cell responses to peptides representing the HPV-16 L1 capsid protein (aa 199-409) in the peripheral blood of 63% of patients (n = 41) with histological evidence of cervical dysplasia and in 45 % of healthy age-matched controls (n = 11). This was achieved by generating short-term T cell lines (STLs) from each individual in vitro against a fl-galactosidase-HPV-16 L1 (aa 199-409) fusion protein for 2 weeks, and then identifying the HPV epitopes they recognized with overlapping synthetic peptides (15-mers) spanning this region in 3 day specificity assays. Histological grading and HPV typing by PCR were performed on patients' cervical biopsies taken at the same clinical visit as the peripheral blood samples. An immunogenic region was identified between aa 311-345 in 73 % of patients (18 % in controls) who responded to HPV-16 L1 (aa 199-409). The number ofresponders to this region was significantly higher in patients with HPV-16-positive biopsies when compared to those with HPV-16-negative biopsies (P = 0.006), as was the number of responders to individual peptides 311-325 (NLASSNYFPTPSGSM; P = 0"04) and321-335 (PSGSMVTSDAQIFNK;P = 0.004)representing this region. The mean level of response to each individual peptide was also higher in the patient group than the controls (P < 0.05). The most significant finding was that all patients with evidence of a current HPV-16 infection responded to one or more L1 peptides (P = 0-0004) and 92 % had high grade cervical intraepithelial neoplasia (CIN III). We also found that the CIN III group was more likely to respond to any L1 peptide than either the atypical group (P = 0.04) or the controls (P = 0.05). Data from four individuals showed that the majority of peptide-specific STLs were CD4 + but some CD8 ÷ STLs were also detected.

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“…Vertical transmission was considered when the maternal HPV type matches the HPV type isolated from the newborn/child. In 1989, Sedlacek et al were the first to demonstrate HPV DNA in the nasopharyngeal secretions of infants delivered vaginally by mothers with genital HPV infection (Sedlacek et al, 1989). Since then, several authors evaluated the rate at which HPV is transmitted from mother to newborn/child, but this rate is extremely variable among studies.…”

Section: Nonsexual Mode Of Transmissionmentioning

confidence: 99%

“…According to the age studied, there are variations in the prevalence rate. In nasopharyngeal aspirates collected immediately after birth, the detection rate of HPV varies from 1.5% to 37% (Cason et al, 1995;Castellsague et al, 2009;Mazzatenta et al, 1996;Puranen et al, 1996Puranen et al, , 1997Rintala et al, 2005aRintala et al, , 2005bRombaldi et al, 2008;Sedlacek et al, 1989;Tenti et al, 1997Tenti et al, , 1999Watts et al, 1998). 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.…”

Section: Incidence Of Hpv In Normal Oral Mucosamentioning

confidence: 99%

Human Papillomavirus and Related Diseases - From Bench to Bedside - A Clinical Perspective

Broeck¹

2012

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Mechanism for human papillomavirus transmission at birth

Cited by 29 publications

References 0 publications

Bovine papillomavirus transmission and chromosomal aberrations: an experimental model.

Bovine papillomavirus transmission and chromosomal aberrations: an experimental model.

Proliferative T cell responses to human papillomavirus type 16 L1 peptides in patients with cervical dysplasia

Human Papillomavirus and Related Diseases - From Bench to Bedside - A Clinical Perspective

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