全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...

HBV逆转录酶区自然变异与不同阶段慢性肝病进展的关系

, PP. 738-742

Keywords: 乙型肝炎病毒,逆转录酶区,变异,初治,临床结局

Full-Text   Cite this paper   Add to My Lib

Abstract:

目的研究HBV逆转录酶区(reversetranscriptase,RT)自然变异情况,分析与不同阶段慢性肝病的关系。方法收集年龄和性别比例相匹配的三组患者(未接受抗病毒治疗)慢性乙型肝炎227例,肝硬化167例和肝癌121例,采用PCR后直接测序法检测HBV逆转录酶区变异,同时确定基因型。结果患者以HBV基因B型为主,分析全部418例B型患者(慢乙肝,173例;肝硬化,135例;肝癌,110例),发现了核苷(酸)类似物(Nucleos(t)ideanalogue,NA)相关耐药变异(rtL80I/V,rtI169T,rtV173L,rtL180M,rtA181T,rtS202C,rtM204I/V,rtN236T);HBV逆转录酶区rtS106C变异在慢乙肝和肝硬化组患者中的阳性率(13.3%和14.8%)高于肝癌组(5.5%)患者(χ2=4.494,P=0.034和χ2=5.598,P=0.018);rtD134E/G/N/S变异在慢乙肝和肝硬化组患者中的阳性率(21.4%和20.7%)高于肝癌组(10.0%)患者(χ2=6.191,P=0.013和χ2=5.224,P=0.022);HBV逆转录酶区A-B间域的变异频率在慢乙肝和肝硬化组患者中(5.4%和6.0%)高于肝癌组(3.4%)患者(χ2=11.188,P=0.001和χ2=16.325,P结论不同阶段慢性HBV感染者(未接受抗病毒治疗)确实存在核苷(酸)类似物耐药相关变异。HBV逆转录酶区的rtS106C变异、rtD134E/G/N/S变异和A-B间域变异可能与慢性肝病的炎症坏死、免疫反应和纤维化进展有关。

References

[1]  Lok AS, McMahon BJ. Chronic hepatitis B: update 2009[J]. Hepatology ,2009, 50: 661-662.
[2]  Locarnini S, Mason WS. Cellular and virological mechanisms of HBV drug resistance[J]. JHepatol, 2006, 44: 422-431.
[3]  Lok AS, Zoulim F, Locarnini S et al. Antiviral drug-resistant HBV: standardization of nomenclature and assays and recommendations for management[J]. Hepatology, 2007, 46: 254-265.
[4]  Huang ZM, Huang QW, Qin YQ et al. YMDD mutations in patients with chronic hepatitis B untreated with antiviral medicines[J]. World J Gastroenterol, 2005, 11: 867-870.
[5]  Lee CZ, Lee HS, Huang GT et al. Detection of YMDD mutation using mutant-specific primers in chronic hepatitis B patients before and after lamivudine treatment[J]. World J Gastroenterol ,2006, 12: 5301-5305.
[6]  Akarsu M, Sengonul A, Tankurt E et al. YMDD motif variants in inactive hepatitis B carriers detected by Inno-Lipa HBV DR assay[J]. J Gastroenterol Hepatol, 2006, 21: 1783-1788.
[7]  Han Y, Huang LH, Liu CM et al. Characterization of hepatitis B virus reverse transcriptase sequences in Chinese treatment naive patients[J]. J Gastroenterol Hepatol, 2009, 24: 1417-1423.
[8]  Liu BM, Li T, Xu J et al. Characterization of potential antiviral resistance mutations in hepatitis B virus reverse transcriptase sequences in treatment-naive Chinese patients[J]. Antiviral Res, 2010,85: 512-519.
[9]  Borroto-Esoda K, Miller MD, Arterburn S et al. Pooled analysis of amino acid changes in the HBV polymerase in patients from four major adefovir dipivoxil clinical trials[J]. J Hepatol, 2007, 47: 492-498.
[10]  Stuyver LJ, Locarnini SA, Lok A et al. Nomenclature for antiviral-resistant human hepatitis B virus mutations in the polymerase region[J]. Hepatology, 2001, 33: 751-757.
[11]  Bartholomeusz A, Tehan BG, Chalmers DK. Comparisons of the HBV and HIV polymerase, and antiviral resistance mutations[J]. Antivir Ther, 2004, 9: 149-160.
[12]  Echevarria JM, Avellón A. Hepatitis B virus genetic diversity[J]. J Med Virol, 2006, 78 (Suppl. 1), S36-S42.
[13]  Ogura Y, Kurosaki M, Asahina Y et al. Prevalence and significance of naturally occurring mutations in the surface and polymerase genes of hepatitis B virus[J]. J Infect Dis, 1999, 180: 1444-1451.

Full-Text

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133