HBVM阳性肺结核患者HBVDNA检测的临床意义

目的探讨HBVDNA(乙型肝炎病毒DNA)、HBVM(乙型肝炎病毒标志物)阳性肺结核患者抗结核治疗时对肝损害的影响。方法肺结核患者HBVM阳性且HBVDNA阳性为观察组A,HB-VM阳性、HBVDNA阴性者为观察组B,HBVM阴性为对照组C,观察各组抗结核药物肝损害发生率、停药率及A组HBVDNA水平与肝损害发生率、停药率有无相关。结果各组肝损害发生率两两比较均有显著性差异(P<0.01);A组停药率与其他两组均有显著性差异(P<0.01),B组与C组无显著性差异(P>0.05);A组HBVDNA水平与肝损害发生率、停药率无相关(P>0.05)。结论HBVM阳性尤其HBVDNA阳性肺结核化疗应重视,HBVDNA阴性者可短程化疗,HBVDNA阳性者都应慎行短程化疗。     

短程化疗中乙肝病毒标志物阳性对肝功能影响及处理

目的探讨抗结核治疗中乙肝病毒感染对肝功能的影响及其对策。方法回顾性分析818例肺结核病人及其中150例药物性肝损害的相关临床资料。结果160例乙型肝炎病毒标志物（HBVM）阳性结核病人中有77例（48．1％）出现肝功能损害。HBVM阴性患者658例中出现肝损害73例（11．1％）,HBVM阳性与阴性的肝损害发生率差异极显著（P〈0．01）。结论抗结核治疗中HBVM阳性患者发生肝损比率明显增加,损害程度也明显增高,在抗结核治疗前检查HBVM及肝功能十分必要,之后密切监测肝功能的变化。     

合并慢性乙型肝炎对抗痨治疗肺结核患者疗效的影响

目的观察分析不同乙型肝炎病毒载量的肺结核患者在抗结核治疗过程中肝功能的变化，了解乙型肝炎病毒对抗结核治疗的影响。方法79例HBV M阳性的肺结核患者，根据HBV DNA大于或小于1×10^5 copies／ml分为A、B组，与23例HBV M阴性肺结核患者比较在接受抗结核治疗时药物性肝炎和重型肝炎发生的情况。结果A组和B组肝功能异常出现和复常时间，及肝损害程度差异无统计学意义（P〉0．05），但均较HBV M阴性组肝功能异常出现时间早而复常时间较长，且肝损害程度明显重于阴性组（P〈0．05）；A组和B组药物性肝炎和重型肝炎发生率差异无统计学意义（P〉0．05），但均明显高于阴性组（P〈0．05）。结论对于HBV M阳性的肺结核患者，在化疗期间一定要密切监测肝功能情况，病毒载量指标不是引起肝功能异常的最直接原因，而只是其中的原因之一。     

短程化疗方案治疗合并糖尿病肺结核的近期疗效分析

目的 了解短程化疗方案治疗合并糖尿病肺结核的效果，探讨合并糖尿病肺结核的抗结核疗程。方法回顾性分析1999--2004年在汕头市结核病防治所治疗的符合选例标准的78例合并糖尿病肺结核患者接受短程化疗的疗效。结果满疗程血糖控制良好组（Ⅰ组）痰菌阴转率92．3％，与同期接受短程化疗的单纯肺结核痰菌阴转率94．5％比较无显著性差异（P〉0．05）。血糖控制不良组（Ⅱ组）痰菌阴转率为66．7％，Ⅰ组与Ⅱ组痰菌阴转结果比较，有显著性差异（P〈0．05）。满疗程Ⅰ组与Ⅱ组病灶吸收好转率分别为89．5％和52．4％（P〈0．01），空洞闭合率分别为67．6％和15．4％（P〈0．01），2组病灶吸收好转率、空洞闭合率结果分别比较均有显著性差异。结论合并糖尿病肺结核患者中血糖控制良好者采用短程化疗方案治疗，近期效果良好，血糖控制差者，疗效较差；对血糖控制不良者或满疗程肺结核仍呈活动性者，应考虑适当延长疗程；早期诊断、早期合理抗结核及合理降糖治疗，对提高治疗效果有积极的意义。     

抗结核药物对乙肝病毒标记物阳性合并结核患者的肝功能影响

目的 观察分析220例抗结核药物对结核合并乙肝病毒标记物(HBVM)阳性患者肝功能的影响及肝损害与乙肝病毒载量水平(HBVDNA水平)的相关性.方法 88例HBVM阳性而HBVDNA阴性患者(Ⅰ组);132例HBVM阳性且HBVDNA阳性患者(Ⅱ组);与同期住院686例HBVM阴性患者作对照(Ⅲ组).HBVDNA阳性患者根据HBVDNA水平:在300拷贝/mL～ 105拷贝/mL之间的患者(Ⅱa组);HBVDNA水平﹥105拷贝/mL的患者(Ⅱb组).结果 肝损害发生率分别为:Ⅰ组10例(11.36%);Ⅱ组58例(43.94%);Ⅲ组84例(12.24%);Ⅱ组与Ⅰ组、Ⅲ组之间经统计学处理均有显著性差异,而Ⅰ组与Ⅲ组之间无明显差异;Ⅱa组18例(31.58%);Ⅱb组40例(53.33%),经统计学处理有显著性差异(P<0.05).结论 HBVM阳性而HBVDNA阴性合并结核的患者可予有效抗结核治疗,HBVM阳性且HBVDNA阳性患者在接受抗结核治疗时发生肝损害的危险性大,肝损害的危险性与HBVDNA水平成正相关.     

抗结核化疗对乙肝病毒标志物阳性者肝功能损害及对策

目的　探讨乙肝病毒标志物 (HBVM)阳性肺结核患者抗结核治疗中肝功能的损害及对策。方法　回顾性分析本院 6 91例痰菌阳性的初治肺结核中 ,97例 HBVM阳性 (A组 )与 5 94例 HBVM阴性 (B组 )抗结核治疗时肝功能损害的发生率。结果　 6 91例中发生药物性肝损害 73例 ,占总病例数的 10 .5 6 % ,其中 A组发生肝损者4 4例 (发生率 4 5 .36 % ) ;B组肝损者 2 9例 (4.88% ) ,二者有显著性差异 (P<0 .0 1)。治疗方案中含有利福平 (RFP)的 5 4 6例中 ,6 8例发生肝损 (发生率为 12 .4 5 % ) ,含有利福喷汀 (RFT)的 14 5例中 ,5例发生肝损 (3.5 4 % ) ,两者比较 ,肝损发生率有显著性差异 (P<0 .0 1)。 HBVM阳性患者 ,治疗方案含有 RFP的 88例中 ,4 3例发生肝损 (发生率4 8.86 % ) ,HBVM阴性患者 ,治疗方案含有 RFP的 4 5 8例中 ,2 5例发生肝损 (5 .4 6 % )。二者比较有显著性差异 (P<0 .0 1)。HBVM阳性者使用含 RFT方案治疗的 9例中 ,仅 1例发生肝损 ,肝损发生率降低为 11.1%。HBVM阳性患者治疗方案中含 RFP者与含 RFT者比较 ,肝损发生率也有显著性差异 (P<0 .0 5 )。结论　抗结核治疗中 HBVM阳性患者发生肝损比率明显增加 ,损害程度也明显增高。含 RFP的抗结核方案引起的肝功能损害明显大于含 RFT的抗结核方案。建     

西利宾胺预防板式抗痨药肝损害的临床效果观察

目的探讨西利宾胺对初治肺结核患者板式抗痨药物肝损害的预防效果。方法256例初治肺结核分为观察组和对照组,均应用“2H3R323E3／4H3R3”方案抗结核治疗,观察组加用西利宾胺,对照组加用肝泰乐。结果观察组药物性肝损害发生率为4．6％;中断抗结核化疗为0．8％;与对照组的17．5％、15．9％比较,均有显著性差异（P〈0．01）。结论西利宾胺可显著降低初治肺结核患者抗结核药物肝损害的发生率,提高肺结核病人规则化疗率。     

拉米夫定对乙肝合并肺结核病患者抗结核的临床观察

目的观察拉米夫定抗病毒治疗对乙型肝炎合并肺结核患者在抗结核化疗过程中的临床作用。方法选择45例乙型肝炎合并肺结核患者,随机分为两组：抗病毒治疗＋护肝治疗＋抗结核治疗组（A组）、护肝治疗＋抗结核治疗组（B组）,观察治疗前后肝功能和HBV DNA变化情况。结果 B组肝功能明显高于A组,差异有统计学意义（P〈0.05）;且B组停药率明显高于A组（P〈0.05）,B组HBVDNA水平明显较A组升高（P〈0.05）。结论拉米夫定抗病毒治疗能抑制乙肝病毒的复制,防止乙肝病情的加重,从而明显减轻乙肝合并肺结核患者抗结核过程中出现的肝脏功能损害情况。     

抗病毒治疗对乙肝患者抗结核药物肝损伤的作用观察

目的乙型肝炎合并肺结核的患者在抗结核化疗过程中,辅以抗病毒、护肝治疗的效果观察。方法将乙型肝炎合并肺结核患者56例,随机分为2组：抗结核＋抗病毒治疗＋护肝治疗组（A组）;抗结核＋护肝治疗组（B组）,观察肝功能情况。结果 B组ALT、AST和T-BIL、HBV-DNA高于A组,两者差异显著（P〈0.05）;B组肝功能异常率高于A组,两者差异显著（P〈0.05）;B组停药率高于A组,两者差异显著（P〈0.05）。结论抗病毒治疗能明显减轻乙型肝炎合并肺结核的患者抗结核治疗引起的肝功能损害,减少抗结核治疗的停药率。     

HBVM阳性肺结核病人用利福喷丁或利福平治疗肝功能损害观察

目的 观察利福喷丁?利福平对HBVM 阳性肺结核病人肝功能的影响?方法 对HBVM 阳性和阴性肺结核病人分别用利福喷丁和利福平治疗,观察治疗前后肝功能损害情况?结果 利福平组较利福喷丁组出现肝损害多( P< 0-01) ;HBVM 阳性较阴性病人易出现肝损害( P< 0-01) ;利福平组HBVM 阳性较阴性病人出现肝损害多( P< 0-01) ;利福喷丁组HBVM 阳性和阴性肝损害发生率无显著差异( P> 0-05) ?结论 抗结核治疗时HBVM 阳性比阴性病人更易发生肝损害,与其用药前即存在肝病理损害有关,治疗肺结核用利福喷丁比利福平疗效好且安全?     

Filovirus RefSeq Entries: Evaluation and Selection of Filovirus Type Variants,Type Sequences,and Names

Sequence determination of complete or coding-complete genomes of viruses is becoming common practice for supporting the work of epidemiologists, ecologists, virologists, and taxonomists. Sequencing duration and costs are rapidly decreasing, sequencing hardware is under modification for use by non-experts, and software is constantly being improved to simplify sequence data management and analysis. Thus, analysis of virus disease outbreaks on the molecular level is now feasible, including characterization of the evolution of individual virus populations in single patients over time. The increasing accumulation of sequencing data creates a management problem for the curators of commonly used sequence databases and an entry retrieval problem for end users. Therefore, utilizing the data to their fullest potential will require setting nomenclature and annotation standards for virus isolates and associated genomic sequences. The National Center for Biotechnology Information’s (NCBI’s) RefSeq is a non-redundant, curated database for reference (or type) nucleotide sequence records that supplies source data to numerous other databases. Building on recently proposed templates for filovirus variant naming [<virus name> (<strain>)/<isolation host-suffix>/<country of sampling>/<year of sampling>/<genetic variant designation>-<isolate designation>], we report consensus decisions from a majority of past and currently active filovirus experts on the eight filovirus type variants and isolates to be represented in RefSeq, their final designations, and their associated sequences.     

Nomenclature- and Database-Compatible Names for the Two Ebola Virus Variants that Emerged in Guinea and the Democratic Republic of the Congo in 2014

In 2014, Ebola virus (EBOV) was identified as the etiological agent of a large and still expanding outbreak of Ebola virus disease (EVD) in West Africa and a much more confined EVD outbreak in Middle Africa. Epidemiological and evolutionary analyses confirmed that all cases of both outbreaks are connected to a single introduction each of EBOV into human populations and that both outbreaks are not directly connected. Coding-complete genomic sequence analyses of isolates revealed that the two outbreaks were caused by two novel EBOV variants, and initial clinical observations suggest that neither of them should be considered strains. Here we present consensus decisions on naming for both variants (West Africa: “Makona”, Middle Africa: “Lomela”) and provide database-compatible full, shortened, and abbreviated names that are in line with recently established filovirus sub-species nomenclatures.     

Genetic Characterization of the Tick-Borne Orbiviruses

The International Committee for Taxonomy of Viruses (ICTV) recognizes four species of tick-borne orbiviruses (TBOs): Chenuda virus, Chobar Gorge virus, Wad Medani virus and Great Island virus (genus Orbivirus, family Reoviridae). Nucleotide (nt) and amino acid (aa) sequence comparisons provide a basis for orbivirus detection and classification, however full genome sequence data were only available for the Great Island virus species. We report representative genome-sequences for the three other TBO species (virus isolates: Chenuda virus (CNUV); Chobar Gorge virus (CGV) and Wad Medani virus (WMV)). Phylogenetic comparisons show that TBOs cluster separately from insect-borne orbiviruses (IBOs). CNUV, CGV, WMV and GIV share low level aa/nt identities with other orbiviruses, in ‘conserved’ Pol, T2 and T13 proteins/genes, identifying them as four distinct virus-species. The TBO genome segment encoding cell attachment, outer capsid protein 1 (OC1), is approximately half the size of the equivalent segment from insect-borne orbiviruses, helping to explain why tick-borne orbiviruses have a ~1 kb smaller genome.     

重型乙型肝炎患者血清乙型肝炎病毒全基因克隆及测序

目的建立重型乙型肝炎患者血清乙型肝炎病毒（HBV）DNA克隆并测序，从全基因水平分析HBV基因变异与重型乙型肝炎发病的关系。方法10例重型乙型肝炎患者血清提取HBV DNA，聚合酶链反应（PCR）扩增HBV全基因。PCR产物构建到PUCm-T载体上，转化至大肠杆菌感受态DH-5α细胞，经酶切鉴定，获得含3．2Kb HBVDNA的重组克隆菌，全基因测序，分析各读码框核苷酸和氨基酸变化。结果4例成功构建HBV DNA克隆，并完成全基因测序。其中3例在前C区发生G1896A变异，产生一个终止密码子，导致HBeAg缺失；1例在C启动子区1762、1764双位点出现突变；有多处点突变及缺失变异分布于PreS2区及C区已知细胞毒T淋巴细胞、B淋巴细胞和T淋巴细胞的细胞表位。结论该法可用于临床研究HBV病毒基因结构与重型乙型肝炎发病的关系，并为进一步研究其HBV基因功能奠定基础。     

Pan-Genome Analysis of Brazilian Lineage A Amoebal Mimiviruses

Since the recent discovery of Samba virus, the first representative of the family Mimiviridae from Brazil, prospecting for mimiviruses has been conducted in different environmental conditions in Brazil. Recently, we isolated using Acanthamoeba sp. three new mimiviruses, all of lineage A of amoebal mimiviruses: Kroon virus from urban lake water; Amazonia virus from the Brazilian Amazon river; and Oyster virus from farmed oysters. The aims of this work were to sequence and analyze the genome of these new Brazilian mimiviruses (mimi-BR) and update the analysis of the Samba virus genome. The genomes of Samba virus, Amazonia virus and Oyster virus were 97%–99% similar, whereas Kroon virus had a low similarity (90%–91%) with other mimi-BR. A total of 3877 proteins encoded by mimi-BR were grouped into 974 orthologous clusters. In addition, we identified three new ORFans in the Kroon virus genome. Additional work is needed to expand our knowledge of the diversity of mimiviruses from Brazil, including if and why among amoebal mimiviruses those of lineage A predominate in the Brazilian environment.     

Current risks of viral hepatitis from blood transfusions

The incidence of transfusion-associated hepatitis in the United States has fallen dramatically since the late 1960s. Where once the risks were so great that as many as one in three transfused patients contracted hepatitis, now they are infinitesimal. Many factors share responsibility for this accomplishment; however, two stand above the rest: (i) improved donor selection and screening criteria, especially elimination of paid blood donations; and (ii) major advances in testing for viral hepatitis carriers. Currently, four tests are used for the prevention of transfusion-associated hepatitis: (i) hepatitis B surface antigen; (ii) hepatitis C virus antibody; (iii) hepatitis B core antibody; and (iv) alanine aminotransferase. The first two tests are largely responsible for the current low risks of transfusion-associated hepatitis due to hepatitis B virus and hepatitis C virus of 1 in 63000 and 1 in 125000, per unit, respectively. To further reduce the risks of transfusion-associated hepatitis will require the enhanced sensitivity provided by nucleic acid amplification techniques (e.g. polymerase chain reaction). Currently, however, no such tests are licensed and practical, automated, or inexpensive enough for individual blood donor screening. We have made such great strides in the prevention of transfusion-transmitted hepatitis that background rates of viral hepatitis now greatly exceed the risk of transmission via transfusion. For this reason, while it may still be reasonable to consider a transfusion as a possible cause for hepatitis, it is imperative that many other possibilities (e.g., iatrogenic and other risk factors) be ruled out.     

A novel immunocompetent rat model of HCV infection and hepatitis

BACKGROUND & AIMS: Hepatitis C virus (HCV) infects millions of people worldwide. Therapy is limited, and treatment does not produce a sustained response in the majority of patients. Development of new agents has been hampered by the lack of a convenient animal model. The aim of this study was to determine whether an immunocompetent rat, tolerized and transplanted with a human hepatoma cell line (Huh 7 cells), could be used to sustain an HCV infection. METHODS: Fetal rats were tolerized in utero with 10(5) Huh 7 cells. One day after birth, rats were transplanted with 5 x 10(6) Huh 7 cells and, a week later, inoculated with HCV, genotype 1. RESULTS: In tolerized, transplanted, and HCV-infected rats, Huh 7 cells were found in the liver, and HCV viral replication was detected by the presence of negative strand HCV RNA. HCV levels in serum were measured at 11,000 copies/mL at week 4, peaked at 22,500 copies/mL by week 12. In tolerized, transplanted, inoculated rats, but not controls, serum alanine aminotransferase (ALT) values increased to 60 IU/L by week 4 and reached a peak of approximately 120 IU/L by week 13. Histology showed foci of mononuclear infiltrates in portal and central regions. CONCLUSIONS: HCV-inoculated immunocompetent rats tolerized and transplanted with Huh 7 cells support HCV gene expression, viral replication, and develop biochemical and histologic evidence of hepatitis.     

Herpesviruses and intermediate filaments: close encounters with the third type

Intermediate filaments (IF) are essential to maintain cellular and nuclear integrity and shape, to manage organelle distribution and motility, to control the trafficking and pH of intracellular vesicles, to prevent stress-induced cell death, and to support the correct distribution of specific proteins. Because of this, IF are likely to be targeted by a variety of pathogens, and may act in favor or against infection progress. As many IF functions remain to be identified, however, little is currently known about these interactions. Herpesviruses can infect a wide variety of cell types, and are thus bound to encounter the different types of IF expressed in each tissue. The analysis of these interrelationships can yield precious insights into how IF proteins work, and into how viruses have evolved to exploit these functions. These interactions, either known or potential, will be the focus of this review.     

Cross Talk between Viruses and Insect Cells Cytoskeleton

Viruses are excellent manipulators of host cellular machinery, behavior, and life cycle, with the host cell cytoskeleton being a primordial viral target. Viruses infecting insects generally enter host cells through clathrin-mediated endocytosis or membrane fusion mechanisms followed by transport of the viral particles to the corresponding replication sites. After viral replication, the viral progeny egresses toward adjacent cells and reaches the different target tissues. Throughout all these steps, actin and tubulin re-arrangements are driven by viruses. The mechanisms used by viruses to manipulate the insect host cytoskeleton are well documented in the case of alphabaculoviruses infecting Lepidoptera hosts and plant viruses infecting Hemiptera vectors, but they are not well studied in case of other insect–virus systems such as arboviruses–mosquito vectors. Here, we summarize the available knowledge on how viruses manipulate the insect host cell cytoskeleton, and we emphasize the primordial role of cytoskeleton components in insect virus motility and the need to expand the study of this interaction.     

Hepatitis G virus in multitransfused thalassaemics from India

Hepatitis G virus (HGV)/GB virus-C (GBV-C) has been identified as a blood-borne agent with disputed pathogenicity. This virus belongs to the flaviviridae with a distant relationship to hepatitis C virus (HCV). Genetically divergent HGV isolates have been reported from different parts of the world. This study describes the prevalence of HGV in multitransfused thalassaemic children in India and genomic sequence variations in 11 HGV isolates from the same geographical location. Hepatitis G virus RNA was detected in 39.7% multitransfused thalassaemic children. The seroprevalence of hepatitis B virus (HBV) and HCV was 23.8% and 17.1%, respectively, and 11.4% had dual infection. The nucleotide sequence of a 166 bp HGV genomic segment from the putative capsid-envelope region (nucleotide; nt 578–743) from 11 Indian isolates was compared to the sequences available in the nucleotide databases. The isolates from India were 81.3–94.5% homologous to the isolates from other parts of the world. On phylogenetic analysis, it was observed that HGV isolates from India may belong to two genetically divergent types.