艾滋病合并丙型肝炎病毒感染者抗反转录病毒治疗效果和肝脏损伤

目的 评价对AIDS合并HCV感染患者抗反转录病毒治疗(ART)的临床疗效和肝损伤.方法 将患者按有无HCV合并感染分为HIV和HCV合并感染组(HIV/HCV组)65例,HIV感染组(HIV组)52例,应用两个核苷类反转录酶抑制剂(NRTI)联合一个非核苷类反转录酶抑制剂(NNRTI)的ART方案,疗程1年.随访并检测血浆HIV载量、外周血CD4细胞数、ALT.结果 治疗前,HIV/HCV组和HIV组的HIV载量均值分别为5.59和5.89 log10拷贝/mL,治疗1年后,分别降至2.91 log10拷贝/mL(P＜0.05)和2.88 log10拷贝/mL(P＜0.05),两组分别有83.1%和78.9%的患者HIV载量＜500拷贝/mL.HIV/HCV组和HIV组CD4细胞均值由治疗前的73.9和72.4/μL,分别增至215.1/μL和214.8/μL(P值均＜ 0.05).1年内,HIV/HCV组与HIV组肝功能异常率分别为24.6%与7.7%(P＜0.05),但无因发生严重肝损伤而终止ART者.结论 联合应用NRTI、NNRTI治疗AIDS合并HCV感染患者,短期内能有效抑制HIV复制,促进免疫功能重建.HCV感染虽可加重肝损伤,但对ART疗效无明显影响.     

乙型肝炎病毒感染对艾滋病患者联合抗反转录病毒治疗效果的影响

目的 了解HBV感染对AIDS患者联合抗反转录病毒治疗(cART)效果的影响.方法 对HIV、HBV合并感染者78例和AIDS患者156例定期进行CD4+T淋巴细胞、HIV RNA、HBV血清学标志物和肝功能检测,并记录其生存情况,比较两组患者cART期间免疫学和病毒学应答的差异.计数资料采用卡方检验,计量资料采用t检验,非正态分布的计量资料采用两独立样本非参数检验.结果 cART第42个月时,同一治疗时间的CD4+T淋巴细胞和HIV RNA水平在HIV、HBV合并感染者与单纯AIDS患者间比较,差异均无统计学意义;cART第48、54和60个月时,HIV、HBV合并感染者免疫学和病毒学应答水平均低于单纯AIDS患者.HIV、HBV合并感染者在cART后第12、24、36、48和60个月时,13例患者中有3例在各时间点均表现为HBeAg阴转;抗-HBe阳转率分别为32.1％(9/28)、50.0％(14/28)、53.6％(15/28)、64.3％(18/28)和71.4％(20/28),阳转率逐年增高(x2=10.189,P=0.037); HBV DNA阴转率分别为95.1％(39/41)、82.9％(34/41)、68.3％(28/41)、43.9％(18/41)和43.9％(18/41),阴转率逐年下降(x2=29.982,P=0.000);肝功能异常率分别为32.1％(25/78)、51.4％(38/74)、33.8％(22/65)、47.9％(23/48)及6.7％(3/45),各时间点差异有统计学意义(x2=28.053,P=0.000).HIV、HBV合并感染者及单纯AIDS患者的病死率分别为24.4％(19/78)和5.1％(8/156),差异有统计学意义(x2=18.841,P＜0.01),且HIV、HBV合并感染者84.2％死于HBV相关的终末期肝病.结论 合并HBV感染可影响cART的远期疗效,终末期肝病是HIV、HBV合并感染者接受cART后的首要死因.     

重视HIV合并HCV感染的诊断和治疗

HIV和HCV的传播途径相同,二者合并感染相当常见。高效抗反转录病毒治疗的广泛应用显著降低了HIV感染相关疾病的发病率和病死率,但HCV感染引起的终末期肝病已成为HIV/HCV合并感染者死亡的重要原因。因此,加强HIV合并HCV感染者的诊断和治疗对于降低HIV感染的病死率十分重要。本文就HIV合并HCV感染者病毒的相互影响、诊断和治疗进行概述。     

人类免疫缺陷病毒与重叠丙型肝炎病毒感染者免疫指标比较

目的 分析HIV/HCV重叠感染人群与HIV单独感染人群治疗前临床特征及免疫功能的差异,探讨其可能的影响因素.方法 以HIV/HCV重叠感染患者59例、HIV单独感染患者38例为研究对象,取患者治疗前外周血,检测其肝功能、血常规、外周血T细胞亚群(CD4+、CD8+)及HIV、HCV病毒载量,酶联免疫斑点法(ELISPOT)检测HIV特异性细胞毒性T淋巴细胞(CTL)的数量和功能.结果 HIV/HCV重叠感染率达60.8%.重叠感染组ALT、AST均明显高于HIV组(49.8 U/L比23.6 U/L,49.1 U/L比32.3 U/L,P值分别为0.000、0.013);重叠感染组PLT明显低于HIV组[(167.3±59.2)×109/L比(198.0±63.9)×109/L,P=0.040].外周血T细胞亚群检测结果两组间差异无统计学意义.重叠感染组HIV RNA定量为(4.046±0.541)lOglo拷贝/mL,低于HIV组的(4.394±0.507)log10拷贝/mL(P=0.018).重叠感染组对HIV-Gag全序列肽段的阳性孔斑点数(平均秩次30.85)较HIV组(平均秩次44.34)低,阳性孔数(4.60±5.52)低于HIV组(6.24±6.93),但两组比较差异无统计学意义.重叠感染组Alb与HCV病毒载量呈负相关(r=-0.540),CD4+与PLT呈正相关(P=0.000).结论 单采血浆感染HIV患者中,有较高的HIV/HCV重叠感染率和较低的细胞免疫功能.     

上海地区输血后丙型肝炎病毒感染者临床流行病学分析

目的 分析上海地区输血后HCV感染者的临床流行病学特点.方法 采用PCR检测HCV RNA载量、ELISA检测抗-HCV,分析输血后HCV感染者的年龄、原发病因、暴露年份、输血成分与输血量、潜伏期和肝功能损害等.计数资料采用x2检验,计量资料采用t检验和相关分析.结果 327例中的279例(85.3%)感染者HCV RNA载量≥3.0 log10拷贝/mL、中位数为5.99 log10拷贝/mL;19.7%病例为3.0～4.0 logl0拷贝/mL,69.9%为5.0～6.0 log10拷贝/mL.HCV RNA定性阳性率为81.6%(40/49),抗-HCV阳性率达99.7%(383/384),其阳性敏感度高于HCV RNA定量和定性检测(F=57.138,P=0.000;F=63.149,P=0.000).输血后HCV感染以30～60岁年龄段多见,84.4%病例暴露时间为1990年至1994年问,感染者中10%以上总病例数的疾病分别为妇产科、骨科疾病和胃肠道出血.输入全血者占80.0%,输血至临床诊断时间平均为(86.0±54.6)个月.89.0%感染者有肝功能损伤,但大多数ALT升高水平≤5×正常值上限(ULN).结论 输血后HCV感染以成年人居多,常伴有肝功能损伤,但ALT升高≤5×ULN;血清HCV RNA载量多为中等水平.     

北京地区人类免疫缺陷病毒感染者合并乙型肝炎病毒感染的流行病学特征及影响因素分析

目的分析北京市人类免疫缺陷病毒(HIV)感染者/艾滋病(AIDS)患者合并乙型肝炎病毒(HBV)感染的流行病学特征,并探索影响合并感染的相关因素。方法对北京地区HIV/AIDS定点治疗医院(北京协和医院、北京地坛医院、北京佑安医院)长期随访的接受抗反转录病毒治疗(ART)的13253例HIV感染者临床资料进行回顾性分析。结果排除未进行HBV标志物检测的患者1681例,共有11572例HIV感染者纳入研究,其中HIV合并HBV感染的患者532例(4.6%),主要为青壮年(28~48岁)男性,占85.9%,感染途径以同性性传播为主(74.8%)。87.4%的合并感染患者基线治疗接受了包含拉米夫定(3TC)、替诺福韦(TDF)两种抗HBV药物的治疗。2013—2018年,HIV合并HBV感染的年新增感染率呈波动性下降的趋势,年均增长率分别为6.37%、4.55%、3.92%、4.68%、4.24%和2.74%。HIV合并HBV感染的主要影响因素为年龄(28~48岁比<28岁,OR=2.807,95%CI 1.241~6.345)以及婚姻状况(已婚比未婚,OR=1.259,95%CI 1.004~1.579)。结论北京地区HIV合并HBV感染率为4.6%;2013—2018年HIV合并HBV的年新增合并感染率呈下降趋势。青壮年(28~48岁)已婚HIV感染者合并HBV感染的风险较高。     

格卡瑞韦/哌仑他韦治疗HCV感染者和人类免疫缺陷病毒合并HCV感染者疗效及安全性研究

目的 评估应用格卡瑞韦/哌仑他韦治疗丙型肝炎病毒(HCV)感染和人类免疫缺陷病毒(HIV)合并HCV感染者的疗效及安全性。方法 2021年4月～2021年12月凉山彝族自治州越西县第一人民医院诊治的HCV感染者25例和HIV合并HCV感染者27例,均接受格卡瑞韦/哌仑他韦治疗8～12周,随访12周。结果 两组静脉注射毒品感染HCV的比率分别为60.0%和63.0%;HCV感染者实现持续病毒学应答(SVR)为92.0%,而HIV合并HCV感染者为88.9%,两组间差异无统计学意义(P=1.000);两组患者对该药耐受性良好,均未发生不良事件导致的治疗方案调整或中止。结论 应用格卡瑞韦/哌仑他韦治疗HCV感染者和HIV合并HCV感染者具有较好的近期疗效和较高的安全性。     

重庆地区192例HIV/HCV合并感染者的回顾性研究

目的分析重庆地区艾滋病病毒(HIV)/丙型肝炎病毒(HCV)合并感染的发生率及危险因素;了解HIV合并慢性HCV感染者HCV-IgG抗体的产生情况,分析部分病人不能产生HCV-IgG的可能危险因素。方法回顾性收集HIV/HCV合并感染者资料,分析合并感染的可能危险因素;统计HIV合并慢性HCV感染者HCV-IgG阴性发生率,分析其HCV-IgG阴性的可能危险因素。结果 3 013例HIV感染者/艾滋病病人中合并HCV感染192例(6.37%);合并感染HCV者的HIV病毒载量[(4.97±0.89)log拷贝/mL]低于单纯HIV感染者[(5.15±0.81)log拷贝/mL](P0.05);合并感染者中吸毒人数的比例(64.06%)高于单纯HIV感染者(0.92%)(P0.05)。合并感染者中13例(6.77%)HCV-IgG阴性。单因素分析显示,HCV-IgG阴性组较阳性组年龄偏大(P0.05),HCV-IgG阴性组通过性途径导致感染所占比例(92.31%)高于阳性组(31.84%)(P0.05);多因素分析显示,通过性途径导致合并感染者出现HCV-IgG阴性的风险,为通过静脉吸毒途径导致感染者的52.669倍。结论重庆地区HIV/HCV合并感染发生率较高,静脉吸毒是合并感染的高危因素;合并HCV感染可能抑制HIV复制;年龄、传播途径为HIV/HCV合并感染者产生HCV-IgG的危险因素,其中性传播为影响HCV-IgG产生的独立危险因素。     

慢性丙型肝炎患者肝组织学改变及其影响因素分析

目的探讨慢性丙型肝炎患者肝组织学改变及其影响因素。方法选择经皮肝组织活检的慢性丙型肝炎患者102例,记录患者年龄、性别、体质指数(BMI)、感染途径等,检测ALT水平、AST水平、HCV基因分型、病毒载量和肝脏组织学改变。统计学处理采用t检验和Logistic回归分析。结果肝脏炎症活动指数( HAI)≥4的慢性丙型肝炎患者的ALT、AST水平较高,PLT较低,与HAI＜4的患者相比差异有统计学意义(t=2.209、2.298、2.565,均P＜0.05)。纤维化分期评分(F)≥3的患者平均年龄、ALT水平、AST水平以及感染时间均高于F＜3的患者（t=2.340、3.497、2.758、2.570,均P＜0.05）,而PLT则较低(t=2.761,P=0.007)。女性、ALT＞1×正常值上限(ULN)、AST水平、F≥3、HCV RNA≥6 lgIU/mL和PLT计数是HAI≥4的单因素预测因子;经多因素分析后,Ishak纤维化分期评分是HAI≥4的唯一独立预测因子(OR 3.098,95％ Cl1.884～5.092,P＜0.01)。单因素分析F≥3的预测因子为年龄、BMI≥24 kg/m2、ALT＞1×ULN、AST水平、HAI≥4、PLT计数以及感染年限≥15年;多因素回归分析显示,年龄(OR 1.074,95％CI1.006～1.146,P=0.033)、ALT水平(OR 1.035,95％CI 1.015～1.055,P＜0.01)、AST水平(OR0.969,95％CI 0.948～0.990,P=0.005)、感染年限≥15年(OR 37.215,95％CI 5.816～238.127,P＜0.01)和HAI≥4(OR 1.939,95％CI 1.426～2.636,P＜0.01)是F≥3的独立危险因素。结论年龄、ALT水平、AST水平、感染年限≥15年和HAI≥4是肝组织学显著纤维化的独立预测因子。     

HCV、HIV混合感染的研究

当血清中抗-HIV/HIV RNA阳性,同时查出抗-HCV/HCV RNA阳性称之为。HIV、HCV混合感染。混合感染一般分重叠感染和合并感染。目前全世界约2亿HCV感染者,3400万HIV感染者。在HIV感染者中约30％混合感染HCV,而HCV感染者中感染HIV的百分率因传播途径、地区和人群的不同而变化较大,从(0-94)％,静脉毒瘾(IDHs)者中HIV合     

两种新发现的脑炎病毒

1994年爆发了两次能感染马和人类的一种新的病毒性疾病 ,引起昆士兰和澳大利亚 2 3匹马和 3人感染 ,其中一人死于爆发的呼吸道疾病 ,另一人死于脑炎 ,第三位患者出现流感样症状并完全康复 ,引起该病的病毒最初称为马麻疹病毒 (ｅｑｕｉｎｅｍｏｒｂｉｌｌｉｖｉｒｕｓ ,ＥＭＶ) ,后命名为Ｈｅｎｄｒａ病毒。 1998年 9月下旬至1999年 6月中旬在马来西亚爆发的一种病毒性脑炎 ,发病例数高达 2 65例 ,其中 10 5例死亡。绝大多数患者是养猪场或屠宰场工人。 1999年 3月 10日～ 19日在新加坡 1个屠宰场的 11名工人出现脑炎或不典型肺炎的临床表现…     

Dengue virus infections and anti-dengue virus activities of Andrographis paniculata

Dengue is a debilitating disease that poses a perpetual threat to human health and increases the global economic burden every year. Despite advances in medical sciences, dengue virus(DENV) infects approximately 200 million people every year. To date, no effective antiviral is valiable to treat DENV in individuals despite great efforts in accomplishing these goals. Numerous approaches have been used in the search for dengue antiviral like screening of combinatorial compounds against DENV enzymes and structurebased computational discovery. In recent years, investigators have turned their focus into medicinal plants, trying to identify compounds that can be used as dengue antiviral. Nature represents a great reservoir of potential substances that can be explored with the aim of discovering new drugs that can be either used directly as pharmaceuticals or can provide drug leads, which can be scrutinized further for the development of new anti-dengue natural product. Many previous investigations have dealt with numerous plant extracts or bioactive principles for their antiviral property as they normally considered being safer when compared to synthetic drugs. Andrographis paniculata belongs to family Acanthaceae and is generally known as ‘king of bitters'. Diverse bioactive compounds from this plant such as diterpenes, flavonoids, xanthones, noriridoides and other miscellaneous compounds have exhibited their potential as therapeutics for various chronic as well as infectious diseases. This review is based on literature review on scientific journals, books and electronic sources, which highlights the pathogenesis of DENV and describe an assortment of bioactive principles that have been possessing antiviral potential, which include dengue and discuss the therapeutic efficacy and mechanism of action of Andrographis paniculata. However, a detailed and more comprehensive clinical trial on mammalian tissues and organs is needed in future studies.     

Epstein-Barr virus and virus human protein interaction maps

A comprehensive mapping of interactions among Epstein-Barr virus (EBV) proteins and interactions of EBV proteins with human proteins should provide specific hypotheses and a broad perspective on EBV strategies for replication and persistence. Interactions of EBV proteins with each other and with human proteins were assessed by using a stringent high-throughput yeast two-hybrid system. Overall, 43 interactions between EBV proteins and 173 interactions between EBV and human proteins were identified. EBV-EBV and EBV-human protein interaction, or "interactome" maps provided a framework for hypotheses of protein function. For example, LF2, an EBV protein of unknown function interacted with the EBV immediate early R transactivator (Rta) and was found to inhibit Rta transactivation. From a broader perspective, EBV genes can be divided into two evolutionary classes, "core" genes, which are conserved across all herpesviruses and subfamily specific, or "noncore" genes. Our EBV-EBV interactome map is enriched for interactions among proteins in the same evolutionary class. Furthermore, human proteins targeted by EBV proteins were enriched for highly connected or "hub" proteins and for proteins with relatively short paths to all other proteins in the human interactome network. Targeting of hubs might be an efficient mechanism for EBV reorganization of cellular processes.     

Residual risk of transfusion transmitted human immunodeficiency virus, hepatitis B virus, hepatitis C virus and human T lymphotrophic virus

BACKGROUND: The risk of transfusion transmitted viral infection is now so low that mathematical modelling is required to estimate the residual risk. The first national viral risk estimates for hepatitis B virus (HBV), human immunodeficiency virus (HIV) and hepatitis C virus (HCV) were recently published by the Australian Red Cross Blood Service. Using several refinements to the original methodology, as well as an additional 2 years of data, new risk estimates have been derived. METHODS: Viral screening data for Australian donors for 2000/2003 were retrospectively analysed. The data were applied to three published models to estimate the residual risk of transmitting HIV, HBV, HCV or human T lymphotrophic virus (HTLV) by blood transfusion in Australia. RESULTS: Applying the three models to HBV, HIV and HCV, three point estimates of the residual risk per unit were calculated for each virus. The median point estimates were 1 in 1,339,000 for HBV, 1 in 1 in 7,299,000 for HIV, and 1 in 3,636,000 for HCV. Although the HTLV risk could not be equivalently calculated because of the lack of incident infection it was estimated to be considerably less than 1 in 1,000,000 using a separate method. CONCLUSIONS: The most current and accurate estimate of residual risk of viral transmission in Australia has been provided in the present study. The residual risk in Australia is exceptionally small, continuing to decrease and is generally less than European or US risk estimates. These new estimates demonstrate that for viral transmission the Australian blood supply is amongst the safest in the world, and provide a basis for evaluating the cost benefit of future viral testing methodologies.     

HBV/HCV重叠感染的抗病毒治疗

从全球范围看,乙型肝炎病毒(hepatitis B virus,HBV)和丙型肝炎病毒(hepatitis C virus,HCV)重叠感染估计约有700-2000万人口感染.重叠感染和单一HBV或HCV感染比较,更易发展为肝硬化、肝细胞癌甚至肝衰竭的比例也高,HBV和HCV重叠感染可有四种不同的临床模式,即HCV活动...     

Hepatitis B virus taxonomy and hepatitis B virus genotypes

Hepatitis B virus (HBV) is a member of the hepadnavirus family. Hepadnaviruses can be found in both mammals (orthohepadnaviruses) and birds (avihepadnaviruses).The genetic variability of HBV is very high. There are eight genotypes of HBV and three clades of HBV isolates from apes that appear to be additional genotypes of HBV. Most genotypes are now divided into subgenotypes with distinct virological and epidemiological properties. In addition, recombination among HBV genotypes increases the variability of HBV. This review summarises current knowledge of the epidemiology of genetic variability in hepadnaviruses and, due to rapid progress in the field,updates several recent reviews on HBV genotypes and subgenotypes.