TT virus. A review of the literature

In 1997, a new DNA virus was cloned by a Japanese team and designated TT virus (TTV). This virus seemed to be associated with non-A, non-G post-transfusion hepatitis. It was isolated by polymerase chain reaction (PCR) and was presumed to be human Circoviridae. The virus is heterogenous; 16 different genotypes are currently registered, and it can be classified as a "swarm" of at least 5 different viruses. Depending on the PCR technique used, the prevalence of infection ranges from 1.9 to 36% among blood donors, from 11.5 to 71% in hemodialysis patients, from 47 to 82% among patients with non-A, non-B or non-C fulminant hepatic failure, and the most elevated percentage is found in hemophiliacs. Epidemiological studies have established that the routes of TTV infection might be parenteral, oral-fecal, and possibly salivary. Mother-to-infant transmission is controversial. TTV may play a role in the pathogenesis of non-A, non-B or non-C fulminant hepatic failure. Patients co-infected with hepatitis C virus (HCV) and TTV have a significantly higher histological grade score than patients with isolated HCV infection. Treatment with interferon seems to decrease TT viremia, according to results obtained outside the context of clinical trials. TTV seems to be a light pathogenic virus. Its widespread presence in the blood of infected subjects contrasts with the apparent absence of pathological symptoms. PCR standardization is needed to clearly establish its real prevalence worldwide.