Molecular epidemiology of a hepatitis C virus outbreak in a leprosy sanatorium in Japan.

The hepatitis C virus (HCV) outbreak that occurred between 1940 and 1999 in a closed leprosy sanatorium located on a small island in Japan was analyzed. The analysis of 318 nucleotides in the NS5B region of HCV allowed us to establish the existence of at least three different HCV strains in this sanatorium.

Hepatitis C virus infection in a Japanese leprosy sanatorium for the past 67 years.

Oku-Komyo-En is one of the national leprosy sanatoria, located on a small island in Setouchi city, Okayama prefecture of Japan since 1938. Since autopsies were carried out routinely on almost all patients who had died in the sanatorium up to 1980, approximately 1,000 formalin-fixed autopsy tissue samples were available for analysis. When these samples were reviewed, the pathological data indicated a sharp rise in the death rate caused by cirrhosis of the liver and hepatocellular carcinoma (HCC) since 1960 and 1970, respectively.

Replication of chicken anemia virus (CAV) requires apoptin and is complemented by VP3 of human torque teno virus (TTV).

To test requirement for apoptin in the replication of chicken anemia virus (CAV), an apoptin-knockout clone, pCAV/Ap(-), was constructed. DNA replication was completely abolished in cells transfected with replicative form of CAV/Ap(-). A reverse mutant competent in apoptin production regained the full level of DNA replication.

Spliced mRNAs detected during the life cycle of Chicken anemia virus.

The existence of spliced mRNA in Chicken anemia virus (CAV) was investigated, as three proteins appeared to be derived from a single 2.0 kb mRNA species. Human Torque teno virus (TTV), which displays a number of genomic similarities to CAV, is known to transcribe three mRNA species, suggesting that CAV may also have multiple mRNAs.

Transcriptional regulation of TT virus: promoter and enhancer regions in the 1.2-kb noncoding region.

Since the discovery of TT virus (TTV) in 1997, its mechanism of transcriptional control has remained unsolved. Molecular analysis points at the 1.2-kb noncoding region (NCR) as being responsible for transcriptional control.