No abstract

Exfoliated cervical cells from 321 Japanese women were examined for human papillomavirus (HPV) DNA types 6, 11, 16, 18, 31, 33 and 35 using polymerase chain reaction (PCR) and dot-blot hybridization methods. HPV DNA was present in 9.3% of patients with normal cervixes, 72.7% of patients with cervical intraepithelial neoplasia (CIN) and 77.8% of patients with invasive carcinoma. Younger patients (/=50 years) had a 1.9% incidence, a significant difference (chi2= 6.478, P < 0.01). In the CIN I and II groups, an incidence of 11.1% of types 16 and 18 was found, while in the CIN III or invasive carcinoma group the incidence was 58.1%, again a significant difference (chi2 = 12.075, P < 0.01). Furthermore, persistence or progression of CIN showed a significant correlation with infections by types 16 and 33 (chi2= 4.904, P < 0.01). However, no significantly different incidence of HPV infection was found between the CIN and the invasive carcinoma groups. It is suggested that (a) younger patients with normal cervixes have a higher incidence of HPV infection than do older patients; (b) HPV types 16, 18 and 33 are important etiologic agents of CIN III and invasive carcinoma, as well as in the persistence and progression of CIN; (c) progression of CIN to invasive carcinoma may depend on factors other than HPV infection in the cervix.

The presence or absence of the anti-human T-cell leukemia virus type (HTLV-I) antibody and the HTLV-I proviral genome was examined in the offspring of inbred rabbits, which were born to HTLV-I carrier does. The results showed that not all offspring born to the carriers were infected and that not all the infected offspring seroconverted at the age of 10 weeks, which is similar to observations made in human carriers. The anti-HTLV-I antibody was assayed by indirect immunofluorescence in 55 offspring at the age of 10 weeks, which were born to B/J or (B/J x Chbb:HM)F1 seropositive HTLV-I carrier does. Twelve out of 31 offspring born from F1 x F1 mating were seropositive, whereas none of 24 offspring born from B/J x B/J mating, F1 x B/J mating, or F1 x Chbb:HM mating were seropositive. The polymerase chain reaction (PCR) method revealed the presence of the HTLV-I proviral genome in 18 out of 23 offspring born from F1 x F1 mating (F2 hybrids). In these 18 HTLV-I-infected F2 hybrids, 8 were seropositive and 10 were seronegative. The major histocompatibility complex (MHC) of these 23 F2 hybrids was analyzed by restriction fragment length polymorphism (RFLP) in southern hybridization. The results showed no close correlation of MHC with HTLV-I susceptibility or with seroconversion. Natural infection via mother-to-child transmission of virus seems to produce seronegative as well as seropositive carriers. This rabbit model may be useful for the study of seronegative virus carriers via mother-to-child transmission of HTLV-I.

Infection of human and rabbit cells with cell-free HTLV-I was studied by PCR analysis. Both human and rabbit PBL were infected similarly by cell-free virus of both human and rabbit cell origin. Cells were infected with the cell-free virus without prior treatment and regardless of the concentration of the culture supernatant containing the virus. Human and rabbit cell lines were also infected similarly by the cell-free virus, the proviral DNA persisting for more than two months. The culture supernatants of HTLV-I-producing cells could thus be a potential cause of laboratory infections.