痰热清对呼吸道合胞病毒体外抑制作用研究

目的研究中草药痰热清注射液对呼吸道合胞病毒体外抑制作用。方法以利巴韦林为阳性对照药,采用细胞培养技术及四氮唑蓝（MTT）比色法,观察在痰热清干预下,感染呼吸道合胞病毒Hep-2细胞的病变效应（CPE）及光密度值（D）,计算各组细胞的病毒抑制率。比较不同药物剂量及不同给药方式（预防给药、直接灭活及治疗给药）下痰热清对呼吸道合胞病毒的抑制作用。结果 3种给药方式下,CPE法及MTT比色法测得痰热清抗呼吸道合胞病毒的半数有效浓度（EC50）分别为0.735、0.815、0.766g/L和0.854、0.842、0.887g/L,治疗指数（TI）分别为11.32、10.21、10.86和9.74、9.88、9.38;3种方式给药下痰热清对呼吸道合胞病毒的抑制作用无差异（P〉0.05）。结论痰热清对呼吸道合胞病毒有直接灭活及抑制增殖作用,对其感染靶细胞有阻断作用,并呈明显量效关系。     

硫酸卡那霉素体外抑制呼吸道合胞病毒作用的研究

目的评价硫酸卡那霉素体外抗呼吸道合胞病毒作用机制。方法采用细胞培养技术观察硫酸卡那霉素对细胞的毒性和抗呼吸道合胞病毒作用。结果用空斑减数实验测得半数有效剂量(EC50)为(1.71±0.23)mg/ml,MTT法测定其半数中毒浓度(CC50)为(12.36±0.85)mg/ml,SI为7.2,SI>4(有意义);在不同时间给药对病毒的抑制实验中,呼吸道合胞病毒感染喉癌上皮细胞(Hep-2)细胞后1、2、4、6、8和10h给药均有抑制作用(P<0.05),穿入和吸附抑制实验表明其对病毒穿入过程有明显地抑制作用(P<0.05),但是对吸附过程没有抑制作用。硫酸卡那霉素对RSV病毒没有直接的灭活作用。结论硫酸卡那霉素在体外实验中对呼吸道合胞病毒穿入细胞及在细胞内复制的过程均有抑制作用。     

中药抗病毒合剂抑制呼吸道合胞病毒作用的实验研究

呼吸道合胞病毒(简称RSV)是引起婴幼儿肺炎的主要原因。由RSV引起的婴幼儿肺炎约占小儿肺炎病例总数的1/2～3/4,是婴幼儿的一种常见病、多发病,对婴幼儿的身体健康危害严重,也是引起婴幼儿死亡的重要原因之一。目前尚无有效的预防办     

双黄连颗粒体外抗呼吸道合胞病毒作用的实验研究

目的研究双黄连颗粒体外抑制呼吸道合胞病毒(RSV)的作用。方法通过细胞培养,观察细胞病变(CPE),观察双黄连颗粒在人喉癌上皮细胞株(Hep-2)中抑制RSV的作用。结果双黄连颗粒能抑制RSV复制,具有明显的抗病毒作用。结论双黄连颗粒具有抑制RSV在Hep-2细胞内复制的作用。     

败酱草多糖体外抗呼吸道合胞病毒作用的研究

目的: 了解败酱草多糖(AP4)对呼吸道合胞病毒的体外抑制作用.方法: 经提取、沉淀、离心、大孔吸附树脂两次层析后,得败酱草抗病毒多糖AP4.通过细胞培养法检测呼吸道合胞病毒对Hela细胞的致病变作用及AP4对呼吸道合胞病毒感染Hela细胞的治疗作用.结果: AP4半数中毒浓度(TC50)为11.07mg/ml,抑制呼吸道合胞病毒的半数有效浓度(EC50)为0.097mg/ml,治疗指数(TI)为114;病毒唑半数中毒浓度(TC50)2.087 mg/ml,抑制呼吸道合胞病毒的半数有效浓度(EC50)为0.0385 mg/ml,治疗指数(TI)为54.结论: 败酱草抗病毒有效部位AP4在Hela细胞中对呼吸道合胞病毒有明显的抑制作用.     

夏桑菊抗呼吸道合胞病毒的实验研究

目的 评价夏桑菊抗呼吸道合胞病毒(RSV)的疗效.方法 以病毒唑为对照,通过体外观察病毒致细胞病变效应(CPE)、病毒滴度、抗病毒指数;在体内观察其对染毒小鼠的死亡保护作用以及对小鼠心、脑、肺内病毒增殖的影响,从而判定夏桑菊抗RSV作用.结果 夏桑菊能抑制RSV的增殖,其有效浓度为544.59 μg/ml,并显示出病毒的感染性滴度随药物浓度的增加而下降;治疗RSV感染鼠结果 发现夏桑菊对RSV感染鼠有保护作用,10 g/(kg*d)时,RSV感染鼠的存活率为50%,平均存活天数为(10.9±2.3)d,随着药物剂量增加,疗效增强,该药物还能降低组织内病毒滴度,阻止体内病毒复制,抗RSV作用类似于同剂量的病毒唑.结论 夏桑菊是一种抗呼吸道合胞病毒的有效药物.     

莪术油抗流感病毒和呼吸道合胞病毒作用的实验研究

莪术油为姜科植物蓬莪术、广西莪术或温郁金的根茎经水蒸汽蒸馏而得到的挥发油,主要含有莪术醇、莪术二酮等,具有明显的抗肿瘤[1]、抗病毒[2]等作用,莪术油葡萄糖注射液作为抗病毒药在临床应用多年,但对莪术油口服给药的有效性却未见报道,本文通过体内、外实验研究莪术油抗流感病毒(IV)和呼吸道合胞病毒(RSV)的作用.     

双黄连口服液抗呼吸道合胞病毒的实验研究

目的:评价双黄连口服液抗呼吸道合胞病毒(RSV)的活性。方法:以病毒唑为对照,通过体外观察病毒致细胞病变效应(CPE)、病毒滴度、抗病毒指数,在体内观察其对染毒小鼠的死亡保护作用,以及对小鼠心、脑、肺内病毒增殖的影响,从而判定双黄连口服液抗RSV作用。结果:双黄连口服液能抑制RSV的增殖,其有效浓度为12ug/mL,并显示出病毒的感染性滴度随药物浓度的增加而下降;治疗RSV感染鼠结果发现,双黄连口服液对RSV感染鼠有保护作用,6.7g.k-g 1.d-1时,RSV感染鼠的存活率为75%,平均存活天数为(12.9±2.8)d,随着药物剂量增加,疗效增强;该口服液还能降低组织内病毒滴度,阻止体内病毒复制,抗RSV作用类似于同剂量的病毒唑。结论:双黄连口服液是一种有效的抗RSV中药复方制剂。     

呼吸道合胞病毒化学治疗药物的研究进展

到目前为止，对呼吸道合胞病毒(RSV)感染的研究已经有了一定进展，但是尚无特异有效的治疗和预防方案。目前唯一允许用于化学疗法的药物仍是利巴韦林，因此人们加大力量开发研制新的有效防治RSV感染的药物。主要包括两方面：(1)人工合成的具有抗病毒活性的化合物；(2)源于天然药物的抗病毒活性物质。本文综述了近年来国内外人工合成的各种类型的抗病毒因子的结构特点、抗病毒效果和作用机制，以及已经从天然药物中分离出的各种有效的抗RSV成分。     

干扰素、病毒唑抗呼吸道合胞病毒的体外观察

目的　观察重组人干扰素、病毒唑单独及联合体外抗呼吸道合胞病毒(RSV)的效果。方法　细胞病变抑制法,即测定药物单独及联合应用对RSV所致细胞病变的抑制作用。结果　干扰素浓度≥5　IU     

抗呼吸道合胞病毒药物专利技术分析

呼吸道合胞病毒（简称RSV）是引起2岁以下儿童急性下呼吸道感染最常见与最重要的病原,属于国内外的研发热点。本文以抗呼吸道合胞病毒的专利申请文献为基础,对其技术发展现状、国内外专利申请态势、技术分布、重点申请人等情况进行梳理分析,表明欧美发达国家在抗呼吸道合胞病毒药物研究中处于绝对领先地位,我国近年来处于快速发展阶段。     

抗呼吸道合胞病毒候选药物的研究进展

呼吸道合胞病毒(RSV)感染是引发婴幼儿细支气管炎、肺炎的主要病因之一,会导致严重的呼吸系统疾病,会增加罹患哮喘的风险。帕利珠单抗和利巴韦林可用于预防和治疗RSV感染,两者均推荐用于RSV感染风险最高的患者,但其有益作用尚有争议。抗RSV药物的研究主要集中于不同的作用机制如抑制病毒融合、靶向非融合靶点和靶向病毒宿主的抑制剂。因此,预防或治疗呼吸道合胞病毒感染,深入研究抗病毒策略,指导候选药物筛选尤显突出,但是至今仍没有抗病毒药物或疫苗被批准用于RSV感染的治疗或预防。随着病毒学的深入研究,研究者将开发针对病毒靶点蛋白或宿主细胞因子的一系列的抗病毒药物,这些药物研发将为抗病毒提供新的途径。     

中药抗呼吸道合胞病毒实验研究进展

中药具有高效低毒的特点,分别从抗呼吸道合胞病毒(RSV)复方和单味中药提取物2个方面,总结中药对RSV的实验抑菌作用及其作用机制,期待为临床治疗提供理论依据,并为进一步挖掘和深入研究中药抗病毒成分提供新的思路。同时指出了单味中药提取物虽然可以较为清晰地说明治疗机制和作用靶点,但目前多数尚停留在物质分析、鉴定和少数动物细胞实验阶段。     

Respiratory syncytial virus (RSV) immune globulin and palivizumab for prevention of RSV infection.

The efficacy, safety, administration, and advantages and disadvantages of respiratory syncytial virus (RSV) immune globulin and palivizumab for preventing RSV infection are discussed. Prevention of RSV infection has attracted considerable attention because of its dinical and economic impact. Studies have shown respiratory syncytial virus immune globulin intravenous (RSV-IGIV) and palivizumab to be effective in decreasing the number of hospitalizations and hospital days attributable to RSV. The number of intensive-care-unit admissions and the severity of RSV infection in high-risk children decreased with the use of these agents. Both agents have been well tolerated, with few adverse effects; however, their high cost necessitates strict guidelines on use. The patient populations at greatest risk are those with bronchopulmonary dysplasia, those with congenital heart disease, those with a history of apnea or respiratory arrest, immunocompromised patients, those with pulmonary consolidation on chest radiography, and those born prematurely. American Academy of Pediatrics guidelines do not preferentially recommend use of either agent; each has advantages and disadvantages. Prophylactic therapy with RSV-IGIV or palivizumab may reduce the likelihood of RSV infection in high-risk patients.     

Perspectives for the chemotherapy of respiratory syncytial virus (RSV) infections

Respiratory syncytial virus (RSV) is the major respiratory pathogen in infants and young children. Ribavirin is the only antiviral agent approved for the treatment of RSV infections, but its efficacy has remained controversial. In the past few years several compounds have been described that in vitro exhibit marked activity against RSV at a 50% effective concentration that is significantly lower, and with a selectivity index that is significantly higher, than that of ribavirin. Among the most potent and selective RSV inhibitors are various polyanionic substances (polysulfates, polysulfonates and polyoxometalates), EICAR (an IMP dehydrogenase inhibitor), pyrazofurin (an OMP decarboxylase inhibitor) and cyclopentenylcytosine (Ce-Cyd, a CTP synthetase inhibitor). These compounds should be further explored for their therapeutic potential in the treatment of RSV infections, following systemic or, preferably, topical administration (i.e. as an aerosol), as topical application may better mimic the potency and selectivity exhibited in vitro by these compounds.     

Potent anti-respiratory syncytial virus activity of a cholestanol-sulfated tetrasaccharide conjugate

A number of different viruses including respiratory syncytial virus (RSV) initiate infection of cells by binding to cell surface glycosaminoglycans and sulfated oligo- and polysaccharide mimetics of these receptors exhibit potent antiviral activity in cultured cells. We investigated whether the introduction of different lipophilic groups to the reducing end of sulfated oligosaccharides would modulate their anti-RSV activity. Our results demonstrate that the cholestanol-conjugated tetrasaccharide (PG545) exhibited ∼5- to 16-fold enhanced anti-RSV activity in cultured cells compared with unmodified sulfated oligosaccharides. Furthermore, PG545 displayed virus-inactivating (virucidal) activity, a feature absent in sulfated oligosaccharides. To inhibit RSV infectivity PG545 had to be present during the initial steps of viral infection of cells. The anti-RSV activity of PG545 was due to both partial inhibition of the virus attachment to cells and a more profound interference with some post-attachment steps as PG545 efficiently neutralized infectivity of the cell-adsorbed virus. The anti-RSV activity of PG545 was reduced when tested in the presence of human nasal secretions. Serial passages of RSV in the presence of increasing concentrations of PG545 selected for weakly resistant viral variants that comprised the F168S and the P180S amino acid substitutions in the viral G protein. Altogether we identified a novel and potent inhibitor of RSV, which unlike sulfated oligo- and polysaccharide compounds, could irreversibly inactivate RSV infectivity.     

注射用银黄体外抗呼吸道合胞病毒

目的:研究注射用银黄对呼吸道合胞病毒的体外抑制作用。方法:采用细胞培养技术,通过银黄直接抗病毒,病毒感染细胞同时使用银黄,先使用银黄再感染病毒3种给药方法,利用生物显微镜观察人喉癌细胞(Hep-2)和人宫颈癌细胞(Hela)发生病变的情况及观察实验组与病毒对照组病毒感染的滴度。结果:注射用银黄在Hep-2和Hela细胞上对呼吸道合胞病毒均有明显的抗病毒作用,注射用银黄对病毒的最小有效浓度(M IC)为0.016 g.L-1,而且毒性低,最大无毒浓度(TDO)为1.6 g.L-1,治疗指数(TI)为100。结论:体外实验注射用银黄对呼吸道合胞病毒具有抑制和直接杀灭的特异性。     

Comparison of the anti-respiratory syncytial virus activity and toxicity of papaverine hydrochloride and pyrazofurin in vitro and in vivo

Based on reports describing their broad antiviral activity, the toxicity and antiviral efficacy of papaverine hydrochloride and pyrazofurin against respiratory syncytial virus (RSV) infection were tested in vitro in tissue culture cells and in vivo in cotton rats. Papaverine inhibited RSV replication in vitro; however, the median minimal toxic dose-median minimal inhibitory concentration ratios (MTD50:MIC50) in vitro and in vivo for papaverine were less than 4. Further work with this compound was discontinued. In contrast, pyrazofurin inhibited RSV replication in vitro (a mean MIC50 of 0.04 microgram/ml was obtained) and in vivo (RSV pulmonary titers were significantly reduced consistently in cotton rats given daily 10 mg/kg doses compared to untreated control animals). However, some toxic effects were observed in both the in vitro and in vivo tests of this compound. The remaining potential of pyrazofurin as an anti-RSV compound is discussed.