Human papillomavirus (HPV) infects epithelial cells on the skin or
mucosa. It is an important risk factor for cervical cancer and head and
neck cancers. A child may acquire HPV infection during childhood, even
before birth. However, our knowledge of HPV prevalence and
HPV‐specific immunity in children is limited.



In the present study, the prevalence of oral HPV infection among 331
infants was elucidated. Further, HPV 16‐specific cell‐mediated
immune response was studied in 56 children, aged from 10 to 16
years, who either 1) had a mother with a cervical intraepithelial
neoplasia or 2) had a HPV‐egative mother or 3) had HPV DNA detected in
placenta and/or cord blood or 4) had persistent oral HPV or 5) remained
constantly HPV‐negative during a six‐year follow‐up period.



HPV was detected in 18% of the 331 infants up to two months of age:
HPV 16 was the most prevalent genotype, followed by HPV 6, 11, 18, 33,
and 66. The HPV genotypes and the serum antibodies for HPV capsid
protein L1 were concordant between mother and newborn. HPV DNA
in the placenta was the most powerful predictor
(OR=14.0;95%CI,3.7‐52.2;P=.0001) of oral HPV in the newborn. A majority
of 56 children showed HPV 16‐specific proliferative T cell response.
The cytokine production of T cells indicated a more predominant Th2
response in children who had had HPV‐positive placenta and/or cord
blood.



These results support the view that an infected mother transmits HPV
to her newborn. The placenta is a substantive route for HPV
transmission and might also play a role in the development of
HPV‐specific immunity. HPV 16‐specific proliferative T cell
response was common in children, indicating a prior HPV 16 infection.