Neutralizing antibodies to SV40 were detected in 14 of 161 human sera from residents of Uttar Pradesh in North India. Antibody titers were low. The donors gave no history of immunization with any vaccine of monkey kidney origin, but lived in areas of high rhesus prevalence. Neutralizing antibodies were also detected in 10 of 37 individuals who cared for large numbers of juvenile rhesus collected for export. The prevalence of antibodies was related to length of service and titers were higher than in the positive sera from the residents of Uttar Pradesh.
A case is reported in which condylomata acuminata arose in a McIndoe neovagina. Histopathologic and virologic evidence are provided to support the characterization of these lesions as benign warty processes secondary to human papillomavirus-6. Factors influencing viral site specificity are discussed.
Nonimmune rhesus were readily infected by administration of SV40 by intranasal (i.n.), subcutaneous (s.c.), or intragastric (i.g.) route. Viremia, demonstrable in animals of all three groups, occurred earlier and with higher titers in the s.c. group. Neutralizing and viral CF antibodies appeared in all inoculated rhesus and T antibodies in 14 of 16. Viruria was detected in three of six of the s.c. group, most commonly in the third week after inoculation. Virus neutralizing activity occurred in the urine at or after 9 weeks postinoculation and was not confined to previously viruric animals. Virus was isolated from kidney of one rhesus from biopsy cultures performed 29–31 weeks after inoculation. Three rhesus fetuses which were given SV40 intracerebrally and subcutaneously at about 90 days of gestation had, at or soon after birth, high titers of antibodies and no tumors. In the single surviving infant, antibody titers did not fall in the first 11 weeks of life.
Sera from 517 laboratory-housed nonhuman primates representing five genera and from 13 laboratory workers were examined for the presence of neutralizing antibodies to SA12 virus. The antibody prevalences were as follows: baboons, 66%; patas and vervet monkeys, 24%; macaques, 8%, and chimpanzees, 2%. The serum of one laboratory worker had antibodies. These results suggest that SA 12 virus is a common infection of nonhuman primates in laboratory colonies, especially baboons.
In an examination of paired sera from pregnant women, 9 of 57 women who had JC virus antibodies in their first specimens exhibited virus reactivation, as judged by a fourfold or greater rise in JC virus hemagglutination-inhibiting antibodies; 43 women remained seronegative through pregnancy. JC virus-specific immunoglobulin M was not demonstrated in umbilical cord sera of six infants born to mothers showing reactivation or in 300 additional umbilical cord sera from normal pregnancies.
A human papillomavirus type 16 (HPV-16) virus-like particle (VLP)-based enzyme-linked immunosorbent assay (ELISA) was used to measure serum antibody to capsid proteins in 376 sexually active college women who were also screened for the presence of genital HPVs by PCR and interviewed for demographic and behavioral risk factors for HPV infection. The seroprevalence was 46% in women with HPV-16 DNA in the genital tract. The corresponding values for women who harbored other HPV types or no HPV in the genital tract were 30 and 19%, respectively (HPV-16 group versus no-HPV group; odds ratio [OR], 3.7; 95% confidence interval [CI], 1.5 to 8.9). The antibody response was significantly higher among women with a high viral load than among those with a low viral load (median optical density value, 0.838 versus 0.137, P = 0.009). Comparable levels of seroreactivity were observed among women infected with HPV types distantly or closely related genetically to HPV-16. Seroreactivity was significantly associated with an age of 25 to 30 years (OR, 2.3; 95% CI, 1.2 to 4.4), three or more lifetime sexual partners (OR, 2.9; 95% CI, 1.1 to 10), and history of a sexually transmitted disease other than HPV (OR, 3.1; 95% CI, 1.5 to 6.3). The percent seropositivity increased linearly with number of lifetime sexual partners until reaching a plateau at 35% for women with more than six partners (chi for linear trend, P < 0.001). The low sensitivity of HPV-16 VLP-based ELISA may limit the usefulness of the assay as a diagnostic test for HPV-16 infection. However, the assay appears to have adequate specificity and should be useful as an epidemiological marker of HPV-16 infection and sexual behavior.
SummarySA12, a newly recognized SV40-related primate papovavirus, transformed early passage hamster kidney cells. These cells, designated SAHK-1, were characterized by increased saturation density, altered morphology, loss of contact inhibition, increased growth rate, an indefinite life span, reduced serum requirements for growth, an ability to grow in soft agar, and the presence of SA12-specific T-antigen. Infectious virus was not rescued by Sendai virus-induced fusion of SAHK-1 cells with permissive cells. Inoculation of transformed hamster cells into syngeneic hosts produced adenocarcinomas, undifferentiated sarcomas, and mixed tumors containing both elements. SA12 T antibodies were demonstrated in all the tested sera from tumor bearing animals.
Serum samples from 194 cases and 217 controls participating in a case-control study of invasive cervical cancer in Brazil were examined for antibodies to human papillomavirus (HPV) 16 virus-like particles (VLPs) by ELISA. The prevalence of antibody in cases and controls was 47.4 versus 24.4% (P < 0.001). The prevalence was higher in women who had HPV-16 DNA in the genital tract (54.2%) than in those with other HPVs (36.8%) or no HPVs (44.8%), but the differences were not statistically significant. Among cases and controls, HPV-16 VLP antibodies were associated with a greater number of lifetime sexual partners (chi2 for trend, P < 0.001). Among controls, age was inversely associated with HPV-16 VLP seroreactivity (chi2 for trend, P = 0.019). The sera were previously tested for antibodies to HPV-16 E6 and E7 oncoproteins; there was no correlation between antibody titers to HPV-16 E6 or E7 and VLPs. The HPV-16 serological assays were compared as screening tests for invasive cervical cancer. The sensitivity and specificity estimates were 47.4 and 75.6% for HPV-16 VLP serology, 63.4 and 89.9% for either HPV-16 E6 or E7 serology, and 53.6 and 93.6% for high titers of either HPV-16 E6 or E7 or VLP antibodies. The utility of HPV-16 VLP ELISA as a screening test for invasive cervical cancer is limited by a high seroprevalence in women with probable prior exposure to HVP 16 but without disease.
We have chosen tumors of the uterine cervix as a model system to identify chromosomal aberrations that occur during carcinogenesis. A phenotype/genotype correlation was established in defined regions of archived, formalin-fixed, and hematoxylin/eosin-stained tissue sections that were dissected from normal cervical epithelium (n = 3), from mild (n = 4), moderate (n = 6), and severe dysplasias/carcinomas in situ (CIS) (n = 13), and from invasive carcinomas (n = 10) and investigated by comparative genomic hybridization. The same tissues were analyzed for DNA ploidy, proliferative activity, and the presence of human papillomavirus (HPV) sequences. The results show that an increase in proliferative activity and tetraploidization had occurred already in mildly dysplastic lesions. No recurrent chromosomal aberrations were observed in DNA extracted from normal epithelium or from mild and moderate dysplasias, indicating that the tetraploidization precedes the loss or gain of specific chromosomes. A gain of chromosome 3q became visible in one of the severe dysplasias/CIS. Notably, chromosome 3q was overrepresented in 90% of the carcinomas and was also found to have undergone a high-level copy-number increase (amplification). We therefore conclude that the gain of chromosome 3q that occurs in HPV16-infected, aneuploid cells represents a pivotal genetic aberration at the transition from severe dysplasia/CIS to invasive cervical carcinoma.