<i>In situ</i> polymerase chain reaction detection of transfusion‐transmitted virus in liver biopsy

Comar, Manola; Ansaldi, Filippo; Morandi, Luca; Molin, G. Dal; Foschini, Maria Pia; Croce, Saveria; Bonin, Serena; Stanta, Giorgio; Tiribelli, Claudio; Campello, Cesare

doi:10.1046/j.1365-2893.2002.00346.x

Cited by 14 publications

(11 citation statements)

References 16 publications

(16 reference statements)

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“…A number of studies have supported the hypothesis that TTV infection causes some of these diseases [Fujiwara et al, 1998;Okamoto et al, 1998b;Ikeda et al, 1999;Itoh et al, 1999;Shibata et al, 2000;Tuveri et al, 2000;Moriyama et al, 2001;Sugiyama et al, 2001;Tajiri et al, 2001;Comar et al, 2002]. In contrast, other studies have shown that TTV infection is not associated with non-A to non-E hepatitis or hepatocellular carcinoma [GimenezBarcons et al, 1999;Kanda et al, 1999;Matsumoto et al, 1999;Parquet et al, 1999;Tagger et al, 1999;Fabris et al, 2000].…”

Section: Introductionmentioning

confidence: 98%

TTV infection in children born to mothers infected with TTV but not with HBV, HCV, or HIV

Komatsu¹,

Inui²,

Sogo³

et al. 2004

Journal of Medical Virology

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The TT virus (TTV) was isolated recently from the serum of a patient with post-transfusion hepatitis. TTV infection is widespread in the general population, and its prevalence increases continuously with age. The pathogenic role of TTV in liver disease remains controversial, and the source of transmission is still unclear. We investigated the pathogenicity and epidemiology of TTV infection in infants born to TTV DNA-positive mothers. Enrolled in this study were 22 mother-child pairs testing negative for antibodies to hepatitis B, hepatitis C, and the human immunodeficiency viruses (HIVs). The children were followed for 30 months after birth. Serum TTV DNA was detected by N22-PCR, and the PCR products were cloned and sequenced. The prevalence of TTV infection in children increased with age. Of the 22 children, 13 (59%) became positive for TTV DNA during the follow-up period. Of these 13 children, 6 (46%) had elevated levels of serum alanine aminotransferase (ALT), although the elevations were transient and mild. TTV viremia was not associated significantly with the abnormal ALT levels. Children with TTV viremia developed neither severe liver disease nor fulminant hepatitis. Phylogenetic analysis showed that, in 11 (85%) of the 13 pairs, the mother and child had the same genotype at the first PCR-positive time point. Among those 11 mother-child pairs, 6 (55%) had identical TTV nucleotide sequences. However, the genotype of predominant clones changed in 5 (50%) of 10 children who were positive for TTV DNA at two or more time points during the follow-up period. In conclusion, this study did not provide evidence that TTV infection is related to liver disease in children. Although the main source of TTV infection in children is presumed to be their mothers, transmitted via non-parenteral routes in the course of daily contact, intrafamilial carriers may also be sources of TTV infection.

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Section: Introductionmentioning

confidence: 98%

TTV infection in children born to mothers infected with TTV but not with HBV, HCV, or HIV

Komatsu¹,

Inui²,

Sogo³

et al. 2004

Journal of Medical Virology

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“…Current data suggest that though TTV may account for only a small proportion of cryptogenic, non-A-E hepatitis, a pathogenic role in some cases cannot be excluded [Dai et al, 2001;Comar et al, 2002;Hu et al, 2002]. Considering that the virus shows a significant prevalence in the general population [Abe et al, 1999;Desai et al, 1999;Dai et al, 2001], a pathogenic role in only a few cases alludes to a role of host, viral, and environmental factors in determining the clinical course of the infection [Tuveri et al, 2000].…”

Section: Introductionmentioning

confidence: 99%

Replication of TT virus in hepatocyte and leucocyte cell lines

Desai

Pal

Deshmukh

et al. 2005

Journal of Medical Virology

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The TT virus (TTV) is a non-enveloped, single-stranded, circular, DNA virus, first isolated from a patient with hepatitis of unexplained etiology. The much deliberated pathological role of the virus continues to be conjectural in the absence of a suitable in vitro replication model. So far, the liver and the bone marrow have been shown to be the main sites of TTV replication. In this study, the human cell lines HepG2 and Chang Liver, the rat hepatoma cell line MH1C1, phytohemagglutinin (PHA)-stimulated TTV-negative peripheral blood mononuclear cell (PBMC) cultures and the B lymphoblast cell line, Raji were investigated as potential in vitro replication systems for TTV. The cell lines were infected with an inoculum prepared by pooling TTV genotype1 DNA positive sera and monitored for virus replication. Of the three hepatocyte cell lines, while the HepG2 and MH1C1 cell lines did not support TTV replication, the Chang Liver cell line showed clear morphological changes as a result of the in vitro infection, which included clumping and granular degeneration of the entire cell sheet over a period of 6 days. The infected cells also showed presence of virus-specific mRNA representative of viral transcription. The consistent presence of infectious viral particles in the supernatant culture fluid at 24-hr fluid replacement intervals indicated limited extra-cellular release of viral particles. The PHA-stimulated TTV-negative PBMC cultures and the Raji cell line were also able to support TTV replication and released significant levels of infectious viral particles into the supernantant culture fluid.

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“…71 Some recent evidence suggests that TTV might replicate in the liver. 72 However, there does not seem to be any link between TTV infection and HCC or chronic hepatitis. [73][74][75][76] Although this virus is thought at present to be completely apathogenic, 77 recent evidence suggests that TTV infection might be involved in respiratory complications in children.…”

Section: Other Parenterally Transmitted Virusesmentioning

confidence: 99%

Genotypic Variability of Hepatitis Viruses Associated With Chronic Infection and the Development of Hepatocellular Carcinoma

Pujol¹,

Devesa²

2005

Journal of Clinical Gastroenterology

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At least five hepatitis viruses are known to date. Infection by enterically transmitted viruses (HAV and HEV) is generally benign compared with the disease caused by parenterally transmitted viruses (HBV, HCV, and HDV). Chronic infection by HBV is common and may evolve to cirrhosis and hepatocellular carcinoma (HCC). Eight HBV genotypes (A-H) have been described, with the South American genotype F being the most divergent. Seven clades of HDV have been described; among them, the South American genotype III is associated to a high frequency of fulminant hepatitis. HCV infection leads to a high rate of chronicity and HCC. From the six HCV genotypes, infection with genotype 1 might have the worst prognostic. Chronic infection by HCV and HBV is the major risk factor for HCC, which occurs, in the majority of the cases, as a consequence of cirrhosis. However, there is growing evidence that some HBV and HCV proteins might contribute to the generation of HCC. Some HBV and HCV variants and specific mutations within the viral genomes might be more frequently associated with the evolution to HCC. Although more studies are needed, emerging evidence indicates that it might be important to address the genetic variability of these viruses and their contribution to the development of HCC.

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In situ polymerase chain reaction detection of transfusion‐transmitted virus in liver biopsy

Cited by 14 publications

References 16 publications

TTV infection in children born to mothers infected with TTV but not with HBV, HCV, or HIV

TTV infection in children born to mothers infected with TTV but not with HBV, HCV, or HIV

Replication of TT virus in hepatocyte and leucocyte cell lines

Genotypic Variability of Hepatitis Viruses Associated With Chronic Infection and the Development of Hepatocellular Carcinoma

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