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首页> 外文期刊>Hepatology research: the official journal of the Japan Society of Hepatology >TT virus of certain genotypes may reduce the platelet count in patients who achieve a sustained virologic response to interferon treatment for chronic hepatitis C.
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TT virus of certain genotypes may reduce the platelet count in patients who achieve a sustained virologic response to interferon treatment for chronic hepatitis C.

机译:某些基因型的TT病毒可能会减少对慢性丙型肝炎的干扰素治疗产生持续病毒学应答的患者的血小板计数。

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The platelet count increases after a sustained response to interferon (IFN) treatment for chronic hepatitis C (CH-C). However, the extent of the increase differs by patient. We investigated whether concurrent TT virus (TTV) infection interferes with the improvement of thrombocytopenia. Serial serum samples were obtained from 85 noncirrhotic CH-C patients who achieved a sustained virologic response for hepatitis C virus (HCV) upon IFN treatment, and tested for TTV DNA by three polymerase chain reaction (PCR) methods (UTR, N22 and TTV genotype-1). UTR PCR can detect essentially all TTV genotypes, whereas N22 PCR primarily detects four major TTV genotypes (1-4). Eighty-four patients (84/85, 99%) were positive for TTV DNA by UTR PCR, 27 (32%) by N22 PCR and 18 (21%) by TTV genotype-1 PCR just before IFN treatment was started (baseline). A sustained virologic response for TTV was observed in 6% (5/84) by UTR PCR, 52% (14/27) by N22 PCR and 56% (10/18) by TTV genotype-1 PCR. The platelet count was significantly lower in the N22 PCR-positive group than in the N22 PCR-negative group not only at baseline (14.9+/-3.8 vs. 18.1+/-6.4x10(4)/&mgr;l, P<0.05), but also at the non-HCV-viremic state one year after the completion of IFN treatment (15.5+/-2.8 vs. 18.6+/-5.5x10(4)/&mgr;l, P<0.05), the differences also being statistically significant by TTV genotype-1 PCR, but not by UTR PCR. These results suggest that certain TTV genotypes including genotype 1 may play a role in aggravating the thrombocytopenia of CH-C patients, either alone or in concert with HCV.
机译:对慢性丙型肝炎(CH-C)的干扰素(IFN)治疗产生持续反应后,血小板计数增加。但是,增加的程度因患者而异。我们调查了并发TT病毒(TTV)感染是否干扰血小板减少症的改善。从85名非肝硬化CH-C患者中获得系列血清样品,这些患者在IFN治疗后获得了持续的丙型肝炎病毒(HCV)病毒学应答,并通过三种聚合酶链反应(PCR)方法(UTR,N22和TTV基因型)检测了TTV DNA -1)。 UTR PCR基本上可以检测所有TTV基因型,而N22 PCR主要检测四种主要TTV基因型(1-4)。在开始干扰素治疗之前(基线),有84例患者(84/85,99%)通过UTR PCR检测TTV DNA阳性,通过N22 PCR检测27例(32%),通过TTV基因1型PCR检测18例(21%)。 。通过UTR PCR观察到TTV的持续病毒学应答率为6%(5/84),通过N22 PCR观察到52%(14/27),通过TTV基因型1 PCR观察到56%(10/18)。 N22 PCR阳性组的血小板计数显着低于N22 PCR阴性组,不仅在基线时(14.9 +/- 3.8与18.1 +/- 6.4x10(4)/&mgr; l,P <0.05 ),而且在完成IFN治疗后一年的非HCV病毒血症状态下(15.5 +/- 2.8与18.6 +/- 5.5x10(4)/ mg,1,P <0.05),差异也在TTV基因型1 PCR中具有统计学意义,而在UTR PCR中则没有统计学意义。这些结果表明,某些TTV基因型(包括基因型1)可能单独或与HCV一起加重CH-C患者的血小板减少症。

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