PubMed · 10088340
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S Iino. 1999. [TTV hepatitis].. https://pubmed.ncbi.nlm.nih.gov/10088340/
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Infants born to serum HCV-positive 12 mothers were enrolled in the study. Nucleotide sequences amplified by primers deduced from a noncoding region were compared between mothers and their infants. The rates for detection of serum TTV in 12 mothers and their infants were 10/12 (83%) and 9/12 (75%), respectively. Serum TTV DNA was not detected in any infant at 1 month of age, but was detected for the first time between 1.5 and 8 months after birth. Positivity persisted thereafter throughout the follow-up period. In seven randomly selected mother-infant pairs, intrahost TTV heterogeneity was lower in infants than in mothers. Furthermore, one of seven mother-infant pairs showed a high degree of similarity (98.7-100%) in all clones, while in four infants, all nucleotide sequences differed by >10% from those of their mothers. However, the degree of homology in the two mother-infant pairs was 89-98.7% in family 2 and 88.1-99.4% in family 5. In the present study, with only one exception, it was shown that TTV from infants is not identical to TTV from mothers. The mechanism is discussed briefly in this paper.
Peripheral blood mononuclear cells (PBMC), plasma, saliva and urine samples were collected from 50 thalassaemic patients for TT virus (TTV) detection by two sets of PCR. The set B nested PCR was more sensitive than the widely used NG hemi-nested PCR with TTV positive rates approximately PBMC: 98% vs. 70%; plasma: 92% vs. 66%; saliva: 62% vs. 22%; urine: 22% vs. 6%. All 50 patients had TTV detected in one or more specimens, with 16% of patients being positive in all four specimen types: 40% positive in PBMC, plasma and saliva; 30% positive in PBMC and plasma. In 82 NG hemi-nested PCR-positive samples TTV genotype was identified, 68.3% had a single genotype, 25.6% had multiple genotypes and 6.1% were uncharacterized. The positive rates for genotypes by specimen were: G1 (36/82), G2 (49/82), G3 (2/82), G4 (7/82), G5 (1/82) and G6 (3/82). Among the 42 patients for whom the genotype was examined, 42.9% had single-type infection, 45.2% had co-infections and 11.9% had uncharacterized genotypes. Sixteen of them had TTV detected both in PBMC and plasma with seven having identical genotypes in both samples. Eight patients had TTV detected in PBMC, plasma and saliva; two of them harboured identical genotypes in all three samples. The results indicate that, apart from hepatocytes, PBMC is a major cell type for TTV infection occurs. Shedding of TTV in urine and saliva is common and may have a significant role in nonblood-borne transmission among the general population. TTV-infected patients often harbour multiple genotypes suggesting infection with one genotype does not necessarily confer protection against the others. No correlation between TTV infection and liver dysfunction was observed.
TT virus (TTV) was first described in 1997 by representational difference analysis of sera from non-A to non-G posttransfusion hepatitis patients and hence intensively investigated as a possible addition to the list of hepatitis-inducing viruses. The TTV genome is a covalently closed single-stranded DNA of approximately 3.8 kb with a number of characteristics typical of animal circoviruses, especially the chicken anemia virus. TTV is genetically highly heterogeneous, which has led investigators to group isolates into numerous genotypes and subtypes and has limited the sensitivity of many PCR assays used for virus detection. The most remarkable feature of TTV is the extraordinarily high prevalence of chronic viremia in apparently healthy people, up to nearly 100% in some countries. The original hypothesis that it might be an important cause of cryptogenic hepatitis has not been borne out, although the possibility that it may produce liver damage under specific circumstances has not been excluded. The virus has not yet been etiologically linked to any other human disease. Thus, TTV should be considered an orphan virus.