本期导读

肾综合征出血热(HFRS)是由汉坦病毒引起的一种自然疫源性疾病。我国是HFRS流行最严重的国家,每年发病人数占世界汉坦病毒感染病例的90%以上,且近10年新疫区不断出现,并时有暴发流行,老疫区的临床类型也有所变化。如何提高临床医师,尤其是非传染科医师对HFRS的认识,减少误诊、误治,进一步降低病死率?本期我刊特邀王贵强教授撰写专论“应重视肾综合征出血热的特殊临床表现和早期诊断线索”,指出降低HFRS病死率的关键是临床医生对该病早期特点的充分认识,掌握其临床特征并进行规范治疗。同期刊出了“第七次全国肾综合征出血热学术会议纪…     

肾综合征出血热病原学和疫苗研究进展

肾综合征出血热（HFRS）是由布尼亚病毒科（bunyaviridae）汉坦病毒属（hantavirus）中不同型汉坦病毒（HV）引起的一种由啮齿动物传播的自然疫源性疾病。因HV型别、传染源和分布地区不同,HFRS病人的临床类型也都不一致,因此对HFRS病原学研究,对诊治和预防本病有重要意义,本文就引起HFRS的汉坦病毒基因结构、分型、实验动物模型和疫苗等方面的研究进展作一综述。     

汉坦病毒及其所致的疾病

人感染汉坦病毒后能导致2种严重的疾病:肾综合征出血热(Hemorrhagic fever with renal syndrome, HFRS)和汉坦病毒肺综合征(Hantavirus pulmonary syndrome, HPS).在我国流行的是HFRS,并通常将HFRS称为流行性出血热(Epidemic hemorrhagic fever, EHF).     

宜春市1999-2009年肾综合征出血热流行病学分析

肾综合征出出热（HFRS）又称流行性出血热,是一种由汉坦病毒感染引起的。以发热、出血及肾损害为特征的一类全球性的自然疫源性疾病。宜春市是江西省HFRS主要流行地区。     

肾综合征出血热发病机制的研究进展

肾综合征出血热(hemorrhagic fever with renal syndrome, HFRS)是由汉坦病毒感染引起的以发热、休克、出血和肾脏损害为主要特征的急性自然疫源性疾病。汉坦病毒主要感染人血管内皮细胞,引起小血管和毛细血管广泛损伤。血管通透性增加是HFRS临床表现的病理基础。国内外学者尽管在汉坦病毒致病机制方面开展了诸多研究,如病毒诱导的免疫病理反应、宿主遗传与细胞凋亡、血小板减少与功能障碍、血管内皮损伤等,但HFRS发病机制仍未完全阐明,也无特效治疗药物,深入探讨汉坦病毒致病的分子机制,寻找有效治疗药物仍是汉坦病毒/HFRS领域的研究热点。本文结合近年来国内外相关研究,阐述HFRS发病机制的研究进展。     

利巴韦林联合干扰素对肾综合症出血热的临床疗效分析

肾综合症出血热（HFRS）又称流行性出血热，是由汉坦病毒引起的、以鼠类为传染源的一种自然疫源性疾病，临床表现为发热、出血、肾损害症状^[1]。该病具有发病率高、病情凶险、死亡率高等特征，目前临床针对HFRS的治疗方法主要包括液体疗法、皮质激素疗法、止血抗凝疗法、抗病毒疗法、免疫疗法等，但究竟何种疗法为首选措施临床仍存在争议。为此，笔者选择以抗病毒治疗为主的药物利巴韦林、干扰素对患者进行了治疗，并取得了良好的疗效，现将治疗过程与结果报道如下。     

阿魏酸哌嗪联合血液透析对肾综合征出血热急性肾衰竭患者血清sICAM-1、E-选择素、L-选择素的影响分析

<正>肾综合征出血热(HFRS)主要由汉坦病毒感染导致,是一种急性传染病。病情严重且进展速度快,具有较高的病死率~([1])。病原体侵入人体后可引发血管内皮细胞受损,继而诱发小动脉、小静脉及毛细血管损伤,最终导致血管内皮变性、肿胀、坏死,出现全身各器官损伤甚至衰竭~([2])。急性肾衰竭是HFRS最常见的并发症,也是对患者预后影响最为严重的并发症之一。HFRS的常规治疗方案为血液透析,是减轻肾脏负担、     

肠内营养干预对肾综合征出血热患者预后的影响研究

正肾综合征出血热(HFRS)又被称作流行性出血热(EHF),是一种自然疫源性疾病,在我国主要是由黑线姬鼠与褐家鼠所携带的汉坦病毒所致[1]。而我国是HFRS重灾区,由HFRS导致的病死率正在逐年升高[2]。HFRS患者常具有炎症反应、血小板下降、器官损害以及蛋白尿等临床症状,医师根据上述症状发生程度将患者分为轻、中、重、危重和非典型性型,其中重型以及危重型HFRS患者病情进展最快,病死率最     

肾综合征出血热生物标志物与病情预测模型研究进展

[摘要]　肾综合征出血热（hemorrhagic fever with renal syndrome, HFRS）是由汉坦病毒（Hantavirus, HV）感染引起的一种以发热、出血和急性肾损伤（acute kidney injury, AKI）为特征的自然疫源性疾病。HV感染可导致血管内皮细胞破坏,全身微血管弥漫性损伤,毛细血管通透性增加及血小板减少,部分患者可能产生细胞因子风暴并发展为毛细血管渗漏综合征,进而导致全身性水肿、低血容量性休克、AKI、凝血功能障碍甚至多器官功能障碍综合征。目前已有多项研究提出一些在HFRS病程中有实用价值的生物标志物,并构建了多种HFRS风险预测模型,部分生物标志物可能与HFRS的发病机制有关,且有助于临床医生早期预见性地评估病情,选择最佳治疗方案,提高HFRS的救治效果。     

白城市洮北区7例流行性出血热临床及流行病学调查分析

流行性出血热(HFRS)，临床上以发热，出血，肾功能损伤为特征，起病急，病情重，进展快，治疗不及时死亡率较高的一种自然疫源性疾病。为了进一步掌握HFRS的流行趋势和临床特征，本文对7例患者进行临床及流行病学调查分析，为提高防治水平提供科学依据。     

汉坦病毒感染致血小板减少的机制

汉坦病毒主要感染血管内皮细胞,引起两种人类疾病,即肾综合征出血热和汉坦病毒心肺综合征,它们的共同特点是毛细血管广泛损伤,通透性升高。汉坦病毒感染者血小板数量严重减少,不仅与“外周破坏增加”有关,而且还可能与“血小板生成和功能障碍”有关。尽管汉坦病毒感染引起血小板减少的机制尚不完全明确,但近年也取得了一些重要进展。本文主要围绕血小板减少相关的两种机制展开讨论,旨在阐明汉坦病毒感染发病机制,为治疗肾综合征出血热的药物设计提供指导。     

Emerging Zoonoses: Hantavirus-Infektionen

Among the emerging viruses, hantaviruses are being focused on more and more due to their increasing number and worldwide distribution. Transmission occurs via inhalation of aerosolized infected rodent excreta. The symptoms and course of disease vary with the infecting hantavirus species. The distribution of the different hantavirus species correlates with the geographical distribution of the virus-type-specific rodent host. Hantaviruses in Europe and Asia cause hemorrhagic fever with renal syndrome (HFRS). Infection with Puumala, the prevalent virus type in Germany, results in a more moderate form of HFRS, nephropathia epidemica. Infections with virus species on the American continents lead to a clinical picture with predominantly pulmonary pathology (hantaviral pulmonary syndrome). No specific antiviral therapy or approved vaccines are available for any hantavirus species. Controlling the rodent populations and avoiding contact with rodent excrement are the only measures that can be undertaken to contain and prevent infection.     

Severity Biomarkers in Puumala Hantavirus Infection

Annually, over 10,000 cases of hemorrhagic fever with renal syndrome (HFRS) are diagnosed in Europe. Puumala hantavirus (PUUV) causes most of the European HFRS cases. PUUV causes usually a relatively mild disease, which is rarely fatal. However, the severity of the infection varies greatly, and factors affecting the severity are mostly unrevealed. Host genes are known to have an effect. The typical clinical features in PUUV infection include acute kidney injury, thrombocytopenia, and increased vascular permeability. The primary target of hantavirus is the endothelium of the vessels of different organs. Although PUUV does not cause direct cytopathology of the endothelial cells, remarkable changes in both the barrier function of the endothelium and the function of the infected endothelial cells occur. Host immune or inflammatory mechanisms are probably important in the development of the capillary leakage. Several immunoinflammatory biomarkers have been studied in the context of assessing the severity of HFRS caused by PUUV. Most of them are not used in clinical practice, but the increasing knowledge about the biomarkers has elucidated the pathogenesis of PUUV infection.     

Innate and adaptive immune responses against human Puumala virus infection: immunopathogenesis and suggestions for novel treatment strategies for severe hantavirus‐associated syndromes

Two related hyperinflammatory syndromes are distinguished following infection of humans with hantaviruses: haemorrhagic fever with renal syndrome (HFRS) seen in Eurasia and hantavirus pulmonary syndrome (HPS) seen in the Americas. Fatality rates are high, up to 10% for HFRS and around 35%–40% for HPS. Puumala virus (PUUV) is the most common HFRS‐causing hantavirus in Europe. Here, we describe recent insights into the generation of innate and adaptive cell‐mediated immune responses following clinical infection with PUUV. First described are studies demonstrating a marked redistribution of peripheral blood mononuclear phagocytes (MNP) to the airways, a process that may underlie local immune activation at the site of primary infection. We then describe observations of an excessive natural killer (NK) cell activation and the persistence of highly elevated numbers of NK cells in peripheral blood following PUUV infection. A similar vigorous CD8 Tcell response is also described, though Tcell responses decline with viraemia. Like MNPs, many NK cells and CD8 T cells also localize to the lung upon acute PUUV infection. Following this, findings demonstrating the ability of hantaviruses, including PUUV, to cause apoptosis resistance in infected target cells, are described. These observations, and associated inflammatory cytokine responses, may provide new insights into HFRS and HPS disease pathogenesis. Based on similarities between inflammatory responses in severe hantavirus infections and other hyperinflammatory disease syndromes, we speculate whether some therapeutic interventions that have been successful in the latter conditions may also be applicable in severe hantavirus infections.     

Severe pulmonary involvement in a case attributed to domestically acquired Seoul hantavirus in the United States

Hantavirus is known to cause 2 distinct clinical syndromes: hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome. Seoul virus is an Old World hantavirus known to cause HFRS. We report a case attributed to domestically acquired Seoul hantavirus with prominent pulmonary involvement and a fatal outcome.     

肾综合征出血热流行过程及其影响因素研究进展

肾综合征出血热（hemorrhagic fever with renal syndrome, HFRS）是由汉坦病毒（hantavirus）感染引起的一种乙类传染病,可引发急性肾损伤,病死率较高。汉坦病毒型别与选择性宿主转换和地区适应密切相关,并由此不断以基因重组等方式进化,不同型别汉坦病毒所致疾病严重程度不同。全球环境变化及宿主动物习性改变加速了汉坦病毒基因组变异;同时,我国大规模土地改造、基础设施建设也使人群与病毒宿主和疾病传播媒介的接触机会增加,一定程度上增大了人群患病风险。本文综述了肾综合征出血热流行过程的主要特征及其相关影响因素,为有效防控该疾病的发生和流行提供参考依据。     

肝功指标判断汉坦病毒所致肝损害的临床价值

目的探讨常用肝功能指标判断汉坦病毒所致肝损害的临床价值。方法回顾性分析367例肾综合征出血热(HFRS)患者肝功能指标、病情及治疗结局的关系。结果HFRS患者ALT、AST、TBIL及白蛋白异常分别占73.84%(271/367)、79.84%(293/367)、13.35%(49/367)和44.41%(163/367)。HFRS不同临床型间ALT、AST和TBIL差异有统计学意义(P<0.001),而白蛋白各型间差异无统计学意义(P>0.05)。结论汉坦病毒易于引起肝脏损害,肝损害程度与病情、预后有关;ALT、AST及TBIL是反映肝脏损害程度的重要指标;而白蛋白不能作为汉坦病毒肝损害程度的判断指标。     

Epidemic hemorrhagic fever with renal syndrome in Yugoslavia, 1986

An epidemic of hemorrhagic fever with renal syndrome (HFRS) occurred in Yugoslavia May-November 1986; all Republics and Provinces were involved. Serum samples were received from 260 of 276 persons with symptoms clinically compatible with a diagnosis of HFRS. Presumptive infection with a hantavirus was determined serologically for 161 of these. Many patients with serious clinical pictures, including severe renal insufficiency and shock, were hospitalized; 11 died. Indirect fluorescent antibody tests with antigens of 4 hantaviruses (Hantaan, Fojnica, Puumala, and the Vranica strain of Puumala virus) showed that greater than 1 serotype was circulating during this epidemic. Hantavirus antigens were detected in the lungs of 86 of 302 (28.5%) wild-caught small mammals.