The novel hepatitis TT virus first described by a Japanese group has been reported to be parenterally transmitted and furthermore, to have been detected in patients with hepatitis of unknown etiology. Hence, in the present study its prevalence was investigated within groups at high risk for contracting blood-borne viruses, such as individuals with chronic liver disease, intravenous drug users and recipients of blood and blood products, as compared to voluntary blood donors and pregnant women. To that end, DNA was extracted from sera obtained from the respective patients and subjected to PCR using semi-nested primers. The frequency of TTV DNA detected within high risk groups, such as nine out of 50 patients with chronic non-A-to-G liver disease (18%), nine out of 98 hepatocellular carcinoma cases (9.2%), 17 out of 52 intravenous drug users (32.7%), 15 out of 80 thalassemia patients with multiple blood transfusions (18.8%) and three out of 31 prostitutes (9.7%) exceeded that among voluntary blood donors and pregnant women, which amounted to 14 out of 200 (7%) and seven out of 103 (6.8%), respectively. Additional molecular research should be performed in order to determine its short-, as well as long-term clinical significance.
In order to further elucidate the tropism of the novel hepatitis TT virus (TTV) we investigated 22 intravenous drug users (IVDU) for the presence of viral DNA in their peripheral blood mononuclear cells (PBMC) by means of seminested polymerase chain reaction using a set of primers specific for the conserved region of its genome. We detected TTV DNA in 63% of those individuals who had previously been found positive for the agent in their serum, whereas the three remaining ones not displaying TTV DNA in their serum and hence, serving as controls also proved negative in their PBMC. The results presented here further support earlier findings by other authors and their conclusion as to the virus employing a parenteral route of transmission. Further investigation will be required in order to clarify the mechanism of viral infection.
In Thailand, hepatitis B virus infection along with its fatal sequelae liver cirrhosis and hepatocellular carcinoma constitutes a public health burden of endemic proportions. The second phase of the infection is usually characterized by cessation of HBV DNA replication and seroconversion to anti-HBe. However, persistent viremia with active liver disease has been encountered in some anti-HBe positive patients, a discrepancy explained by mutations in the precore/core region of the viral genome. The resulting failure to synthesize HBeAg may help the virus evade immune clearance, while HBV replication and expression of HBcAg proceed unchecked. Discreet types of mutation in the precore/core region have been found at varying prevalence depending on the predominant HBV genotype in the respective geographical areas. The purpose of the present study has been to elucidate both prevalence and type along with the nucleotide positions of the mutations prevailing among Thai chronic hepatitis patients. We subjected 68 patients to serological tests for HBeAg, as well as semi-nested PCR with subsequent DNA sequencing. HBV DNA was detected in 87.5% of HBeAg positive and 40.9 % of HBeAg negative patients, respectively. Mutations in the core promoter amounted to 28.6 % in HBeAg positive and 75% in HBeAg negative patients, in the start codon of the precore gene to 37.5% and in codon 28 to 18.8% in HBeAg negative patients. Our results have shown mutations affecting the core promoter of HBeAg to be by far the most prevalent in Thai patients, followed by mutations of the start codon whereas those changing codon 28 into a stop codon are less frequently encountered than has been reported from other areas indicating a distinct HBV genotype prevailing in Thailand.
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