Current evidence is strong enough to conclude that human papillomavirus (HPV) can be transmitted both sexually and non-sexually. The debate on HPV infections in children still continues but it is more focused on HPV prevalence than on transmission modes. HPV DNA detection in amniotic fluid, foetal membranes, cord blood and placental trophoblastic cells all suggest HPV infection in utero, i.e. prenatal transmission. Based on recent meta-analysis, vertical transmission occurs in approximately 20% of cases. Most of the mucosal HPV infections in infants are incident, persistent infections in oral and genital mucosa being found in less than 10% and 2% respectively. The mother seems to be the main transmitter of HPV to her newborn, but subsequent HPV infections are acquired horizontally via saliva or other contacts. Bimodal peak prevalence is seen for skin warts, oral papillomas and recurrent respiratory papillomatosis (RRP) in younger and older age groups, suggesting similar epidemiology. Of the clinical HPV diseases, juvenile-onset-RRP and genital condylomata are problematic; the former because of its life-threatening potential and the latter because of possible sexual abuse. HPV6 and 11 are the most common genotypes in both the lesions. Early in life, infections by the high-risk HPV genotypes may also remain persistent for a considerable period, and should be of considerable importance for HPV vaccination strategies.