Available evidence suggests that BK virus (BKV) and JC virus (JCV) persist in the kidneys of healthy individuals after primary infection and may reactivate when the host's immune response is impaired. Data supporting this hypothesis are presented. A previous study had shown BKV to be present in the kidneys of eight (57%) of 14 subjects. In the present study, which extended the investigation to a total of 30 subjects, BKV DNA was found in the renal tissues of 10 (33%) subjects, and JCV DNA was found in the renal tissues of three (10%) subjects. The viral DNA detected appeared not to be integrated with host DNA and to be isolated in foci. Investigation of normal and diseased brain tissue, including tissue from six subjects with multiple sclerosis, failed to reveal the presence of either JCV DNA or BKV DNA.

Evidence has accumulated indicating that BK virus, following an inapparent primary infection, persists in the renal organs of normal healthy individuals and reactivates upon immunosuppression. Data to support this hypothesis are presented and suggest that BK virus DNA sequences are present at very low levels in the kidneys of more than 50% of the population and that this persistence is localized in several foci within these organs.

The frequency of human papillomavirus (I-IPV) type 16 in premalignant and malignant lesions of the cervix was investigated and compared with the detection of HPV type 6. In cervical intraepithelial neoplasia (CIN) grades 1-111 HPV bwas detcctcd in 28% and HPV 16 in 62Y0 of patients whereas 90% of malignant lesions contained HPV 16 only. In the CIN lesions there was an increase in HPV 16 detection as the severity of disease increased while the levcl of detection of HPV 6 decreased. Only three (18%) of the cervices that were colposcnpically and histologically normal contained HPV genomes: although two of these three women had either a history of genital warts or a sexual partner with penile warts.

Herpesvirus of turkey (HVT) is an alphaherpesvirus that is widely used as a live vaccine against Marek's disease because of its antigenic relationship with Marek's disease virus (MDV). In spite of a similar genome structure, HVT has several unique genes, the functions of which are not completely understood. As a first step in carrying out detailed analysis of the functions of the HVT genes, a full-length infectious bacterial artificial chromosome (BAC) clone of HVT was constructed. DNA from two independent BAC clones, upon transfection into chicken embryo fibroblasts, produced plaques similar to those produced by the wild-type virus. Viruses derived from the BAC clones were stable during in vitro passage, but showed differences in in vitro growth kinetics compared with the wild-type virus. Using a one-step mutagenesis protocol to delete the essential glycoprotein B gene from the HVT genome, followed by construction of the revertant virus, BAC clones of HVT were shown to be amenable to standard mutagenesis techniques. In spite of the difference in in vitro growth, viruses from both clones induced 100 % protection against infection by the virulent MDV strain RB-1B, indicating that the BAC-derived viruses could be used as vaccines with efficacies similar to that of the parental virus. The construction of HVT BAC is a major step in understanding the functions of HVT genes by exploiting the power of BAC technology. Furthermore, the availability of the BAC clones enables use of HVT as a vector for expressing foreign genes.

Results from Southern hybridization and PCR amplification experiments using a randomly synthesized reverse transcription-PCR product showed that peripheral blood leukocytes from horses showing no clinical signs of disease expressed a putative latency-associated transcript antisense to and overlapping the 3 end of the equid herpesvirus 1 (EHV-1) immediate-early gene (gene 64). A PCR product derived from this transcript has >96% identity with the published EHV-1 sequence. In situ hybridization studies of equine bronchial lymph nodes corroborated these findings and are consistent with reactivation data (D. A. Smith, A. Hamblin, and N. Edington, unpublished data), indicating that EHV-1 latency is established predominantly in CD5 ؉ /CD8 ؉ leukocytes.