High risk genital papillomavirus infections are spread vertically

Rice, Philip; Cason, John; Best, Jennifer M.; Banatvala, J. E.

doi:10.1002/(sici)1099-1654(199901/03)9:1<15::aid-rmv232>3.0.co;2-q

Cited by 46 publications

(34 citation statements)

References 45 publications

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“…Rice et al (1999) even reported that they were not aware of any sexually transmitted viruses that are not vertically transmitted. The presence of HPV has been found in amniotic fluid (Tseng et al, 1992;Armbruster-Moraes et al, 1994;Wang et al, 1998); thus, vertical transmission may be plausible.…”

Section: Discussionmentioning

confidence: 99%

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Transmission of carcinogenic human papillomavirus types from mother to child

Merckx

Liesbeth²,

Arbyn³

et al. 2013

European Journal of Cancer Prevention

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Currently, human papillomavirus (HPV) research focuses on HPV infection in adults and sexual transmission. Data on HPV infection in children are slowly becoming available. It is a matter of debate whether mother-to-child transmission of HPV is an important infection route and whether children born to HPV-positive mothers are at a higher risk of HPV infection compared with children born to HPV-negative mothers. The objective of this meta-analysis is to summarize the published literature on the extent to which genital HPV infection is vertically transmitted from mother to child. Medline, Web of Science, and CINAHL were searched for eligible reports published before January 2011. Differences in the risk of HPV infection between newborns from HPV-positive and HPV-negative mothers were pooled using a random-effects model. Twenty eligible studies, including 3128 women/children pairs, fulfilled the selection criteria. High heterogeneity could be found (I=96%). The overall estimated risk difference was 33% (95% confidence interval: 22-44%). On restricting to high-risk HPV-positive mothers only (n=4; women=231), the difference in risk was 45% (95% confidence interval: 33-56%). The heterogeneity was found to be low (I=15%). This meta-analysis indicates a significantly higher risk for children born to HPV-positive mothers to become HPV positive themselves. Plausible explanations include vertical transmission of HPV during pregnancy and/or birth or a higher infection rate during early nursing from mother to child. More research is required to gain an insight into the precise mode of transmission and the clinical effects of infection on the child.

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Section: Discussionmentioning

confidence: 99%

“…However, immune responses have not been tested in the studies included. It is therefore not known whether the early infection will result in the generation of virus-specific antibodies and cell-mediated immunity or specific immune tolerance (Rice et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Transmission of carcinogenic human papillomavirus types from mother to child

Merckx

Liesbeth²,

Arbyn³

et al. 2013

European Journal of Cancer Prevention

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“…These may include mother-to-child vertical transmission [39][40][41][42], nonsexual transmission in children prior to their sexual debut [43], or auto-inoculation. For example, respiratory papillomatosis occurs as a consequence of both peripartum and sexual transmission [44,45].…”

Section: Discussionmentioning

confidence: 99%

Oral Human Papillomavirus Infection in Adults Is Associated with Sexual Behavior and HIV Serostatus

et al. 2004

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The prevalence and risk factors for oral human papillomavirus (HPV) infection are unknown, despite evidence for an etiological role for HPV in oral cancers. Oral samples from human immunodeficiency virus (HIV)-seronegative (n=396) and HIV-seropositive (n=190) adults were tested for HPV DNA. High-risk HPV infections were present in 2.1% of tonsil and 6.3% of oral-rinse specimens. The prevalence of oral high-risk HPV infection was greater in HIV-seropositive individuals (13.7% vs. 4.5%; P<.001). In multiple logistic regression, odds of oral HPV infection increased with age, male sex, and herpes simplex virus (HSV)-2 seropositivity in HIV-seronegative individuals and with CD4 cell count <200 cells/mL, HSV-2 seropositivity, oral mucosal abnormalities, and >1 oral sex partner during the previous year (odds ratio, 12.8; 95% confidence interval, 3.1-52.7) among HIV-seropositive individuals. HPV type 16, which is present in most HPV-associated tonsillar cancers, was the most prevalent high-risk oral HPV infection.

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“…The presence of HPV in infants results in part from the passage of the infant through the infected birth canal. However, it is unclear whether the presence of HPV reflects passive contamination or is it a true perinatal infection of the infant [2][3][4][5]. Other possible modes of HPV transmission in infants are periconceptual transmission; prenatal transmission via placenta, amniotic fluid, and cord blood; horizontal transmission; and autoinoculation [1,5,6].…”

mentioning

confidence: 99%