In February of 1996 a human adenovirus (formerly known as Ad-Cor-96-487) was isolated from the stool of an AIDS patient who presented with severe chronic diarrhea. To characterize this apparently novel pathogen of potential public health significance, the complete genome of this adenovirus was sequenced to elucidate its origin. Bioinformatic and phylogenetic analyses of this genome demonstrate that this virus, heretofore referred to as HAdV-D58, contains a novel hexon gene as well as a recombinant fiber gene. In addition, serological analysis demonstrated that HAdV-D58 has a different neutralization profile than all previously characterized HAdVs. Bootscan analysis of the HAdV-D58 fiber gene strongly suggests one recombination event.

Objectives: This study was carried out in order to evaluate the efficacy of the recently developed picobirnavirus (PBV) sets of primers and to establish the phylogenetic relationships of Argentine strains with PBV strains isolated in China and the USA. Methods: Thirteen fecal specimens tested as positive for PBV by polyacrylamide gel electrophoresis were analyzed by reverse transcription-polymerase chain reaction assays using primers target to the genomic segments 2 of PBV strains isolated in China and the USA. The amplicons were sequenced and analyzed. Results: Primers derived from the China strain produced amplicons in only 4 of the 13 specimens (30.76%). No sample was revealed as positive with the primers derived from the US strain. DNA sequencing of polymerase chain reaction products differed in nucleic acid and amino acid sequences by 13.9–42.28% and 18.1–51.1%, respectively. Despite this strain diversity, three domains of conserved nucleotide sequences as well as the amino acid motif D-S-D typical of RNA-dependent RNA polymerase gene of double-strand RNA viruses were identified. Comparatively, these conserved regions were also identified in homologous PBV strains from the USA and China. Phylogenetic analysis showed no time or geographic clustering. Conclusions: These findings provide evidence that PBV may represent an emerging heterogeneous group of viruses.

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Viral transformation models may be useful to detect and map human tumor suppressor genes. BK virus (BKV), a human papovavirus, readily transforms rodent cells but is unable to transform human cells, suggesting that oncosuppressive functions expressed in human cells control BKV oncogenic activity. We have transferred human chromosome 6 to BKV-transformed mouse pRPcT1ss1 cells. The great majority of the colonies growing in selective medium degenerated by senescence. Only five hybrid pRPcT1ss1/H6 clones maintained the immortalized phenotype of the recipient cell line. All the immortalized clones had two common regions of deletion involving bands 6q21-22 and the SOD2 gene in 6q25. Senescent colonies carried an intact chromosome 6. A specific human sequence in 6q21-22 was amplified by PCR in senescent cells, suggesting that this region harbors a gene inducing senescence. The SOD2 deletion confirms recent data on the role of the Mn-dependent superoxide dismutase in inhibition of proliferation. The monochromosomic hybrids bearing a deleted chromosome 6 showed a reverted phenotype in vitro and a significantly longer latency period before they were tumorigenic in nude mice, indicating the presence of a tumor suppressor gene in the residual regions of chromosome 6. Molecular mapping suggests that this gene is located in 6q27. The BKV transformation model detects genes inducing senescence and tumor suppressor genes on human chromosome 6 and may represent a useful system to isolate and clone such genes.

The suppression of T-cell function by cyclosporin therapy can result in an increase of HPV infection, adding to the proliferative activity of cyclosporin in the oral mucosa.