单纯疱疹病毒性角膜炎角膜组织病毒潜伏感染的PCR检测分析

 目的  探讨通过穿透性角膜移植获取的单纯疱疹病毒性角膜炎病变角膜组织中1型单纯疱疹病毒（HSV-1）DNA的表达情况及意义。设计 实验研究。研究对象  2010年5-12月北京同仁医院因病毒性角膜炎角膜白斑行穿透性角膜移植术后角膜标本20例,圆锥角膜、大泡性角膜病变和角膜营养不良等非感染性角膜病变的角膜标本20例。方法  对角膜组织标本中HSV-1 DNA进行聚合酶链反应（PCR）检测。 主要指标  HSV-1 DNA的阳性率。结果  单纯疱疹病毒性角膜炎静止期患者角膜组织中12/20例（60%）检出HSV-1 DNA,非感染性角膜组织中6/20例（30%）检出HSV-1 DNA（χ2=3.64,P=0.057）。结论  单纯疱疹病毒性角膜炎静止期角膜组织多数表达HSV-1 DNA,角膜内潜伏病毒是引起单纯疱疹病毒性角膜炎的可能原因,正常人角膜也可能有HSV-1的DNA存在。（眼科,2013,22：45-48）     

单纯疱疹病毒性角膜炎的研究新进展

单纯疱疹病毒性角膜炎是一种重要的致盲性眼病。它的致盲性和治疗上的困难性在于它的反复发作,从而引起角膜混浊,最终导致视力的丧失。随着分子生物学的发展,目前对于单纯疱疹病毒性角膜炎的诊断有着突飞猛进的发展,然而对于治疗复发性单纯疱疹病毒性角膜炎却没有有效药物,这将有待于分子生物学、病毒学、传统中医与现代西医的共同努力。     

角膜神经与单纯疱疹性角膜炎

角膜神经与单纯疱疹性角膜炎有密切的关系，角膜神经的基础和临床研究，为正确论断论断和治疗这一重要的致盲性眼病，提供了可靠的理论依据。本综述了角膜神经的中枢投射，角膜神经的变性与再生，角膜神经与单纯疱疹病毒的潜伏感染及复活，角膜知觉减退的关系。     

单纯疱疹病毒性角膜炎的免疫学

单纯疱疹病毒性角膜炎 (herpes simplex keratitis,HSK)是世界范围内角膜盲的最常见原因。单纯疱疹病毒 (herpes simplexvirus,HSV)不仅可直接导致角膜的感染性破坏 ,而且还可通过免疫病理机制诱导某些难以处理的疾病 ,如基质型角膜炎。1　免疫学机制1 .1　动物模型　目前 ,已有数种 HSK的动物模型 ,比较常用的是兔模型和小鼠模型。兔模型比较理想 ,因为兔眼球大小与人类相似易于观察 ;另外 ,存在有自发性病毒释放和疾病复发现象。而小鼠模型则缺乏病毒的自发性释放和疾病的复发 ,但在感染后经过一段时间才发生角膜的炎症反应 ,该特征类…     

诱导单纯疱疹病毒性角膜炎复发的研究进展

单纯疱疹病毒性角膜炎是重要的致盲眼病之一。它的致盲性和治疗上的困难性在于它的反复发作，从而引起角膜混浊。对其复发的研究已持续多年，动物实验研究证明，紫外线照射、电离子导入肾上腺素及６－羟基多巴胺、机械的、化学的、电的刺激、角膜手术、免疫抑制剂及皮质类固醇激素均可引起单纯疱疹性角膜炎的复发，临床观察也与动物实验研究相符。目前单纯疱疹病毒性角膜炎复发的确切机制仍不清楚，有赖于今后从病毒的基因水平，宿主     

无环鸟苷抑制小鼠单纯疱疹性角膜炎潜伏病毒激活作用的研究

目的 证实无环鸟苷能够作用于潜伏单郊病毒的激活阶段,抑制病毒活化。方法 以Ｂａｌｂ／ｃ小鼠作为潜伏感染模型,以紫外线Ｂ照射为激活条件,治疗组给予无环鸟苷口服,停药后１天处死动物检测活化病毒。结果 治疗组３０例中无１例,而对照组３０例中有１２例检测出活化病毒（Ｐ〈０．０１）;治疗至照射后２天的１０只鼠无１例,而相应对照组１０只中６例检出活化病毒（Ｐ〈０．０１）。结论 预防性应用ＡＶＣ特异作用于病毒激活期,有效的抑制病毒活化。     

单纯疱疹病毒性角膜炎实验室诊断技术

单纯疱疹病毒性角膜炎实验室诊断技术白求恩医科大学第一临床医院眼科杜鹃，徐杰锦州医学院附属第一医院眼科刘丹单纯疱疹病毒性角膜炎（ＨＳＫ）是目前世界上主要致盲疾病之一，诊断主要依据角膜病变形态及临床症状。但由于其反复发作的特点常致病变不典型，造成诊断上的...     

单纯疱疹病毒性角膜炎动物模型制备

单纯疱疹病毒性角膜炎(herpes simplex keratitis,HSK)是由单纯疱疹病毒Ⅰ型(herpessimplex virus type Ⅰ,HSV-1)感染引起的具有高复发率、高致盲率及难根治性特点的疾病,可导致角膜溶解、新生血管形成及溃疡穿孔,是目前角膜病中最常见的致盲眼病之一.本文参考目前国内外实验研究时使用的各种HSK动物模型建模方法来进行综述,如建立原发感染模型的划痕法、环钻法、外植体培养法以及潜伏感染模型和诱导复发模型的建立方法.力求探索如何建立一种可靠的HSK动物模型,在为研究人类HSK发病机制、药物治疗和对比以及角膜移植等方面均有重要意义.     

Superinfections in herpes simplex keratitis

We reviewed 15 cases of culture-proven corneal superinfections in 15 patients (eight men and seven women ranging in age from 41 to 86 years) with recurrent herpes simplex keratitis. The factors that appeared to increase the risk of superinfection were the presence of an epithelial defect (found in all 15 cases), a history of recurrent herpetic keratouveitis (found in ten cases), and the use of topical corticosteroids (found in 13 cases). Eight of the 15 patients were taking antibiotics at the time the superinfections were diagnosed, indicating that topical antibiotics do not provide sufficient protection. Gram-negative rods were found in six cases (Proteus mirabilis, Pseudomonas aeruginosa, Serratia marcescens, Klebsiella oxytoca, Enterobacter cloacae, and Achromobacter sp.). Gram-positive organisms, often in association with another infecting agent, were found in six cases (Staphylococcus epidermidis, three cases; S. aureus, two cases; and Streptococcus sp., two cases). Fungal superinfections were found in three cases (Cephalosporium acremonium, Candida albicans, and Aspergillus fumigatus, one case each). Mycobacterium cheloni was found in two cases.     

单纯疱疹病毒性角膜炎的发病机制

单纯疱疹病毒性角膜炎(herpes simplex keratitis,HSK)是一种常见的眼部疾病,由单纯疱疹病毒(herpes simplex virus,HSV)感染引起。人群中超过90%的人曾经感染过HSV。HSV可以在神经组织及角膜组织长期潜伏。在适宜的刺激下,如紫外线照射、发热、精神压力、高温、低温、手术等,病毒活化增殖导致HSK。HSV感染引起的免疫反应是造成角膜组织损害的主要机制。HSK的免疫反应主要是由CD4+细胞介导的,而CD8+细胞对病毒感染具有保护作用。     

单纯疱疹性角膜炎的免疫发病机制

相关的动物模型研究表明，单纯疱疹性角膜炎（HSK）的转归取决于3种相互作用的因素，即宿主固有免疫的基因组成、适应性免疫、病毒的种属。HSK的发病依赖于病毒复制。眼内自身抗原的分子模拟机制可引起自身免疫反应。此外，炎性分子可能通过旁活化的方式激活T细胞，Toll样受体对病毒抗原的免疫识别在炎症反应中发挥重要作用。不同种属的特定病毒基因组成也是影响角膜病变的重要因素。就单纯疱疹性角膜炎的多种免疫机制学说做一综述。     

Latanoprost-associated recurrent herpes simplex keratitis

PURPOSE/METHOD: We present a case of a patient who developed recurrent epithelial herpes simplex keratitis after starting treatment with latanoprost. Her ophthalmic history was only remarkable for a past episode of herpetic keratitis 21 years previously. RESULTS/CONCLUSIONS: Episodes of herpetic keratitis were under remission only when latanoprost was discontinued. No recurrences of herpes simplex keratitis have been observed since then. Latanoprost usage might be associated with recurrent episodes of herpes simplex keratitis in patients with previous history of ocular herpes simplex virus infection.     

Activated inflammatory infiltrate in HSV-1-infected corneas without herpes stromal keratitis

PURPOSE: To investigate herpes stromal keratitis (HSK) immunopathology by studying HSV-1-infected corneas that fail to develop HSK. METHODS: Plaque assay quantified HSV-1 in the tear film of infected mice. FACS analysis enumerated corneal leukocytic infiltrate and characterized infiltrate phenotypically after staining for activation and regulatory T cell (Treg) markers and for markers of antigen-presenting cell (APC) maturation. Treg cells were depleted in vivo using anti-CD25 mAb. Luminex analysis quantified the amount of cytokines and chemokines expressed in corneal tissue homogenate. RESULTS: Infected corneas without HSK exhibited a pronounced leukocytic infiltrate containing a significantly higher proportion and nearly identical absolute number of activated CD4+ T cells 15 days after infection when compared with those with HSK. Moreover, the frequency and absolute number of regulatory CD4+ T cells (Tregs) was lower in nondiseased corneas, and Treg depletion did not influence HSK incidence. The frequency of mature, immunogenic DCs and the ratio of mature DCs to CD4+ T cells were nearly identical in corneas with and without HSK. The authors observed a reduced population of neutrophils and reduced expression of neutrophil chemoattractants MIP-1beta and keratinocyte chemoattractant and the neutrophil-attracting cytokine IL-6 in corneas without HSK. CONCLUSIONS: These findings demonstrate that HSV-1-infected corneas can retain clarity in the presence of a substantial secondary leukocytic infiltrate, that activated CD4+ T cells, while necessary, are not sufficient for HSK development, that susceptibility to HSK is not determined by Tregs, and that clinical disease correlates with the accumulation of a critical mass of neutrophils through chemoattraction.     

单纯疱疹病毒侵入受体在单纯疱疹病毒性角膜炎发病机制中的作用

单纯疱疹病毒侵入受体(疱疹病毒侵入介质、连接素-1、连接素-2、3-O-硫酸化的硫酸乙酰肝素等)是单纯疱疹病毒(HSV)侵入细胞及在细胞间扩散所必需的物质.不同的受体对HSV在组织的感染和扩散中具有不同的作用.疱疹病毒侵入介质可介导HSV进入小梁网细胞、结膜上皮细胞和角膜成纤维细胞,连接素则介导HSV侵入神经组织和细胞...