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.     

复方抗病毒制剂体外抗流感病毒和呼吸道合胞病毒作用及毒性研究

目的 测定复方抗病毒制剂体外对流感病毒和呼吸道合胞病毒的抗病毒作用. 方法 用鸡红细胞血凝素滴定法测定不同浓度复方抗病毒制剂在狗肾传代细胞（MDCK）中对流感病毒的抑制作用;用中和实验测定复方抗病毒制剂在Hep 2细胞中对呼吸道合胞病毒的活性. 结果 复方抗病毒制剂浓度＜1.5 mg•mL^-1时对MDCK细胞及Hep 2细胞无明显毒性. 浓度＞0.15 mg•mL^-1能抑制流感病毒的血凝活性和呼吸道合胞病毒对靶细胞的攻击作用. 结论 复方抗病毒制剂体外对流感病毒和呼吸道合胞病毒具有较强的抑制作用,且有较大的安全性.     

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。     

芪红胶囊对柯萨奇病毒黏附和穿入的抑制作用

目的观察芪红胶囊(QH)对柯萨奇病毒的抑制作用,并探讨芪红胶囊作用机制。方法首先在HeLa细胞水平研究芪红胶囊对柯萨奇病毒的抑制作用,以利巴韦林作为阳性对照药物。通过细胞活性测定(XTT)实验和空斑形成实验确定芪红胶囊的半数有效剂量(IC50)以及半数毒性剂量(CC50)。在病毒感染后的不同时间段加入芪红胶囊或利巴韦林,观察药物发挥作用的主要时间点。通过黏附实验和穿入实验观察芪红胶囊是否对病毒的吸附和穿入具有抑制作用。结果芪红胶囊具有显著抗病毒作用,XTT实验和空斑形成实验结果显示:芪红胶囊的IC50值分别是:(7.2±0.8)μg/ml和(2.6±0.5)μg/ml;芪红胶囊细胞毒性是利巴韦林的16倍(芪红胶囊的CC50值为:(1648±219)μg/ml,利巴韦林CC50值:(103±14)μg/ml。病毒抑制时程实验提示芪红胶囊主要在病毒感染后0～4h内发挥作用;黏附实验和穿入实验证实芪红胶囊的抗病毒作用主要通过抑制病毒吸附和穿入发挥作用。结论芪红胶囊能够在体外有效抑制病毒对细胞的入侵,且毒性较低,其抗病毒作用主要源于对病毒吸附和穿入的抑制作用。     

腔肠素抗流感病毒研究

目的 对海洋来源的化合物腔肠素进行体外抗流感病毒活性研究。方法 细胞病变效应(CPE)抑制实验评价腔肠素对不同流感病毒株的抗病毒作用。CPE实验检测腔肠素细胞毒性和抗病毒作用方式并结合血凝抑制实验、神经氨酸酶(NA)活性实验及微基因组实验初步探究腔肠素的作用靶点。结果 腔肠素体外对不同流感病毒株均有良好抗病毒作用,其中对PR8的抑制作用最强,IC₅₀为5.0μmol·L^-1且细胞毒较小,CC₅₀为144.1μmol·L^-1。通过不同作用方式以及不同作用时间的实验显示,腔肠素预先处理流感病毒以及在病毒感染后加入均有良好抗病毒作用,并且在病毒吸附后0～3 h的抑制效果较好。用腔肠素预处理病毒后可以呈剂量依赖性地抑制血凝素(HA)的活力。故腔肠素可能是通过与病毒HA相互作用来阻断流感病毒的进入,其作用位点可能为HA蛋白HA2链的72、74位谷氨酸。结论 腔肠素具有良好的体外抗甲型流感病毒效果,为海洋来源的小分子化合物的开发与改造提供了借鉴,为寻找新型抗流感病毒药物提供新思路。     

苦瓜提取液体外抗柯萨奇病毒的实验研究

目的:探讨苦瓜提取液体外抗柯萨奇病毒(CVB3)的作用及抗病毒作用的机制,从而为柯萨奇病毒感染的治疗提供新的手段。方法:根据病毒复制周期,设计2个药物抗病毒作用靶点,观察苦瓜提取液在不同靶点对柯萨奇病毒的作用。在H ep-2单层细胞上,通过观察细胞病变效应(CPE)、四甲基偶氮唑蓝(M TT)法检测细胞活性、病毒抑制率测定,以确定苦瓜提取液体外抗病毒活性。结果:苦瓜提取液对H ep-2细胞的半数毒性浓度(TC50)为1004.8μg.mL-1;苦瓜提取液抑制病毒组对柯萨奇病毒的抑制率随药物浓度的增加而增加,其半数抑制浓度(IC50)为35.4μg.mL-1,T I为7.82。苦瓜提取液直接灭活病毒组,各浓度组均出现典型CVB3所致的细胞病变,与病毒对照孔无显著区别。结论:苦瓜提取液可通过抑制病毒增殖发挥抗柯萨奇病毒作用。     

5-羟基-6-溴-1H-吲哚-3-羧酸酯类衍生物的合成及其体外抗病毒活性

目的 设计合成5-羟基-6-溴-1H-吲哚-3-羧酸乙酯类化合物,评价其抗流感病毒和抗呼吸道合胞病毒活性.方法 经1H-NMR和MS确证目标化合物结构,并经体外抗病毒试验测定其抗病毒活性.结果与结论 合成了11个未见文献报道的5-羟基-6-溴-1H-吲哚-3-羧酸乙酯类化合物.初步活性试验表明,11个目标化合物均具有一定的抑制流感病毒和呼吸道合胞病毒作用,其中,化合物X9的体外抗病毒作用与阳性对照药物金刚烷胺相当.     

苦参碱类生物碱抗病毒的临床药理作用研究进展

苦参碱类生物碱具有广谱的抗病毒作用,除抗肝炎病毒外,还能抗柯萨奇B3病毒、流感病毒、呼吸道合胞体病毒、猪繁殖与呼吸综合征病毒、肠道病毒71型、牛乳头状瘤病毒、新城疫病毒和巨细胞病毒等。苦参碱类生物碱可能是通过直接灭活病毒、阻滞病毒吸附和进入细胞以及抑制病毒在细胞内复制,产生抗病毒作用。通过上调病毒感染细胞的磷脂酰肌醇-3激酶/蛋白激酶B信号通路和下调把关受体-4/髓样分化因子-88/肿瘤坏死因子-α受体相关因子-6信号通路,促进干扰素表达和抑制炎性因子表达,抗病毒对细胞的伤害。综述苦参碱类生物碱抗病毒的临床药理作用文献,并对其研究进展做了分析。     

5-羟基-1H-吲哚-3-羧酸乙酯类化合物的合成及其抗流感病毒活性

目的设计合成5-羟基-1H-吲哚-3-羧酸乙酯类化合物,评价其抗流感病毒和抗呼吸道合胞病毒活性.方法经IR、1H-NMR和MS确证目标物结构,并经体外抗病毒试验进行活性筛选.结果与结论合成了9个5-羟基-1H-吲哚-3-羧酸乙酯类化合物,初步活性试验表明,具有一定的抑制流感病毒和呼吸道合胞病毒作用,其中,化合物Ⅷ1、Ⅷ2、Ⅷ5的抗病毒活性与利巴韦林和阿比朵尔相当.     

红树林淡紫拟青霉胞外多糖分离提取及体外抗HSV-1活性初探

目的初步探讨红树林淡紫拟青霉胞外多糖体外抗单纯疱疹病毒Ⅰ型(HSV-1)感染的可能机制,为开发新型抗病毒药物提供基础研究。方法以非洲绿猴肾细胞(Vero细胞)为病毒感染靶细胞,以不同浓度多糖作用于HSV-1感染过程的各个阶段,以细胞病变程度(CPE)测定病毒半数感染量(TCID50),四甲基偶氮唑盐(MTT)法测得多糖对Vero细胞的毒性作用及多糖抗HSV-1的活性。结果淡紫拟青霉胞外多糖对Vero细胞的半数有毒浓度(CC50)为1 374.04μg/mL,多糖浓度在500μg/mL以下时,细胞存活率达80%以上,且对细胞无增殖作用;在25~800μg/mL浓度范围内该多糖可在一定程度上抑制病毒吸附和生物合成,并表现出一定的量效关系,其半数抑制浓度分别为414.98μg/mL和390.47μg/mL,当多糖浓度达800μg/mL时,对病毒吸附的抑制率为77.1%,对生物合成的抑制率为88.3%;未发现该多糖对HSV-1有直接灭活作用。结论淡紫拟青霉胞外多糖对Vero细胞毒性较小,是一种较安全的多糖;该多糖具有一定的抗病毒作用,在一定浓度范围内可抑制HSV-1吸附和生物合成,且对生物合成的抑制作用稍强于对吸附的抑制作用。     

Inhibition activities of polysaccharide (RG4-1) from Gentiana rigescens against RSV

Respiratory syncytial virus (RSV) is the most important cause of lower respiratory tract infection in infants and young children. With the emergence of drug-resistant strains of RSV, new antiviral agents are needed urgently. Gentiana rigescens is a kind of Chinese herb, belonging to Gentianaceae, which has long been used as a folk medicine for curing inflammation, bacterial infection, viral infection, and so on. In this research, polysaccharide designated RG4-1 was isolated from G. rigescens by hot water extraction, ethanol precipitation, and macroreticular adsorbing resin column chromatography, and its antiviral activity, cytotoxicity, and possible antiviral mechanisms were assayed by cytopathogenic effect inhibition assay, 3-(4,5-dimethythiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay, and plaque reduction assay. RG4-1 was a fructose-binding lectin. In host cell cultures, RG4-1 was found to be an effective antiviral component against RSV. It showed good inhibitory effect against RSV when it was added 2?h after virus infection with 50% effective concentration of 12.86?μg/ml. RG4-1 also displayed its direct inactivation, attachment inhibition effect, and penetration inhibition effect against RSV. A time-dependent experiment was set up to confirm that RG4-1 blocked RSV infection at early stages of the infection. But RG4-1 seemed to be ineffective against intracellular virus and viral biosynthesis.     

Inhibition activities of polysaccharide (RG4-1) from Gentiana rigescens against RSV

Respiratory syncytial virus (RSV) is the most important cause of lower respiratory tract infection in infants and young children. With the emergence of drug-resistant strains of RSV, new antiviral agents are needed urgently. Gentiana rigescens is a kind of Chinese herb, belonging to Gentianaceae, which has long been used as a folk medicine for curing inflammation, bacterial infection, viral infection, and so on. In this research, polysaccharide designated RG4-1 was isolated from G. rigescens by hot water extraction, ethanol precipitation, and macroreticular adsorbing resin column chromatography, and its antiviral activity, cytotoxicity, and possible antiviral mechanisms were assayed by cytopathogenic effect inhibition assay, 3-(4,5-dimethythiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay, and plaque reduction assay. RG4-1 was a fructose-binding lectin. In host cell cultures, RG4-1 was found to be an effective antiviral component against RSV. It showed good inhibitory effect against RSV when it was added 2 h after virus infection with 50% effective concentration of 12.86 μg/ml. RG4-1 also displayed its direct inactivation, attachment inhibition effect, and penetration inhibition effect against RSV. A time-dependent experiment was set up to confirm that RG4-1 blocked RSV infection at early stages of the infection. But RG4-1 seemed to be ineffective against intracellular virus and viral biosynthesis.     

Antiviral activity of Australian tea tree oil and eucalyptus oil against herpes simplex virus in cell culture

The antiviral effect of Australian tea tree oil (TTO) and eucalyptus oil (EUO) against herpes simplex virus was examined. Cytotoxicity of TTO and EUO was evaluated in a standard neutral red dye uptake assay. Toxicity of TTO and EUO was moderate for RC-37 cells and approached 50% (TC50) at concentrations of 0.006% and 0.03%, respectively. Antiviral activity of TTO and EUO against herpes simplex virus type 1 (HSV-1) and herpes simplex virus type 2 (HSV-2) was tested in vitro on RC-37 cells using a plaque reduction assay. The 50% inhibitory concentration (IC50) of TTO for herpes simplex virus plaque formation was 0.0009% and 0.0008% and the IC50 of EUO was determined at 0.009% and 0.008% for HSV-1 and HSV-2, respectively. Australian tea tree oil exhibited high levels of virucidal activity against HSV-1 and HSV-2 in viral suspension tests. At noncytotoxic concentrations of TTO plaque formation was reduced by 98.2% and 93.0% for HSV-1 and HSV-2, respectively. Noncytotoxic concentrations of EUO reduced virus titers by 57.9% for HSV-1 and 75.4% for HSV-2. Virus titers were reduced significantly with TTO, whereas EUO exhibited distinct but less antiviral activity. In order to determine the mode of antiviral action of both essential oils, either cells were pretreated before viral infection or viruses were incubated with TTO or EUO before infection, during adsorption or after penetration into the host cells. Plaque formation was clearly reduced, when herpes simplex virus was pretreated with the essential oils prior to adsorption. These results indicate that TTO and EUO affect the virus before or during adsorption, but not after penetration into the host cell. Thus TTO and EUO are capable to exert a direct antiviral effect on HSV. Although the active antiherpes components of Australian tea tree and eucalyptus oil are not yet known, their possible application as antiviral agents in recurrent herpes infection is promising.     

Inhibition of herpes simplex virus type 2 replication in vitro by 1-N-pentadecanoyl-3'-N-trifluoroacetyl kanamycin A

The in vitro antiviral activity as well as the mechanism of action of a new antiviral agent, a kanamycin analogue, 1-N-pentadecanoyl-3'-N-trifluoroacetyl kanamycin A (PTKA) against herpes simplex virus type 2 (HSV-2) was investigated. The drug showed excellent antiviral action with negligible cytotoxic effect on the culture cells. Based on plaque reduction assays the 50% inhibitory dose (ID50) of the drug was 1 microgram/ml, and at 20 micrograms/ml plaque formation was totally suppressed. The compound inhibited viral protein synthesis in infected cells without affecting RNA and DNA synthesis, when added to the cultures after virus adsorption. Moreover, pretreatment of the cells with PTKA before HSV-2 infection, increased the antiviral activity significantly. Dot-blot hybridization analysis revealed that the drug reduced the level of immediate early viral mRNA if applied before infection. There was no detectable action at the level of virus adsorption, penetration or uncoating. These results indicate that PTKA exerted its antiviral action at the early stage of viral replication as well as at the level of viral protein synthesis.     

In vitro inhibition of influenza A virus infection by marine microalga-derived sulfated polysaccharide p-KG03

The sulfated polysaccharide, p-KG03, purified from the marine microalga, Gyrodinium impudium, is a unique compound comprising homogenous galactose units conjugated to uronic acid and sulfated groups. Although previous studies showed that p-KG03 suppresses tumor cell growth and infection by encephalomyocarditis virus, its effect against enveloped virus infection and the biological mechanism of action have not been elucidated. In this report, the inhibitory activity of p-KG03 against influenza virus was examined and compared with that of other sulfated polysaccharides (fucoidan and pentosan polysulfate) and antiviral agents (oseltamivir phosphate, oseltamivir carboxylate, amantadine, and ribavirin). The results of a cytopathic effect reduction assay using MDCK cells demonstrated that p-KG03 exhibited the 50% effective concentration (EC(50)) values of 0.19-0.48 μg/ml against influenza type A virus infection (selectivity index >200) but not all influenza type B viruses. Mechanism studies showed that inhibition of influenza virus replication was maximized when p-KG03 was added during or within 6 h after viral infection, suggesting that mainly the viral adsorption and internalization steps are targeted by this compound. The results of influenza virus binding assay to p-KG03 and fluorescence microscopy indicate that the antiviral activity of p-KG03 is directly associated with its interaction with viral particles. The sulfated polysaccharide p-KG03 is a potent and specific influenza A viral entry inhibitor and may be a candidate for antiviral drug development.     

Inhibition of influenza A virus replication by a kanamycin derivative

We studied the antiviral activity and the mechanism of action of a new antiviral agent and kanamycin derivative, 1-N-eicosanoyl-3"-N-trifluoroacetyl kanamycin A (ETKA), against influenza A virus. From yield reduction assays with VERO cells, ETKA showed a significant antiviral activity with negligible cytotoxic effect. In the presence of 20 micrograms/ml of ETKA at which VERO cell growth was not inhibited, virus titer was suppressed to 11.2% of control, and at 100 micrograms/ml virus production was suppressed to more than 99%. ETKA markedly inhibited viral protein synthesis when cells were pretreated with the drug before infection, but there was no inhibition when the drug was added 15 min post-infection. ETKA did not inhibit virus adsorption and penetration. Nor did it affect the activity of viral RNA polymerase in vitro. We found that the drug had a direct inactivating effect on influenza A virus under acidic conditions. These results suggest that ETKA exerts its antiviral action mainly in the early stage, prior to uncoating by direct inactivation of the virus due to the acidic environment of the endocytic vesicle. Aerosol treatment with the drug protected mice against a lethal influenza A virus infection.     

Antiviral activity of NMSO3 against respiratory syncytial virus infection in vitro and in vivo

NMSO3, a sulfated sialyl lipid was evaluated for its efficacy against respiratory syncytial virus (RSV) and other myxovirus infections in cell culture. The median effective concentration (50% effective concentration, EC(50)) of NMSO3 against replication of the Long strain of RSV in HEp-2 cells was 0.2 and 0.32 microM by optical ELISA and the plaque reduction method, respectively. On the other hand, the corresponding values for ribavirin were 10.5 and 11.2 microM, respectively. NMSO3 showed potent activity against other laboratory strains as well as fresh clinical isolates of RSV, and the average EC(50) was similar to that for Long strain. NMSO3 exhibited minimal cytotoxicity against HEp-2, MDCK, HMV-2 and Vero cells for which the median cytotoxic concentration (CC(50)) was more than 685 microM. The selectivity index [SI=(CC(50) for HEp-2/EC(50))] of NMSO3 for RSV exceeded 2978 and that of ribavirin was 6. The EC(50) of NMSO3 against influenza virus (FluV) A (H3N2) was 23.8 by the MTT method using HMV-2 cells, and 17.8 microM by the TCID(50) method using MDCK cells. NMSO3 did not inhibit replication of influenza B virus, parainfluenza virus type 2 and canine distemper virus at 103 microM. NMSO3 inhibited RSV infection of HEp-2 cells when it was added between 0 and 1.5 h after virus infection. By a temperature shift experiment during the period of contact between the virus and cells, NMSO3 inhibited both the binding of RSV to the cells and its penetration into the cells. Prophylactic and therapeutic efficacy of NMSO3 against RSV infection in cotton rats was examined. Intraperitoneal administration of 100 mg/kg per day of NMSO3 to cotton rats from 1 day before or 1 h after to 3 days after the RSV infection, once a day every day, decreased the RSV titer in lungs to 10(-1.26) to 10(-1.63) compared to the control rats which were infected with RSV and left untreated.     

Anti-influenza virus activity of Ginkgo biloba leaf extracts

We examined the influence of Ginkgo biloba leaf extract (EGb) on the infectivity of influenza viruses in Madin–Darby canine kidney (MDCK) cells. Plaque assays demonstrated that multiplication of influenza viruses after adsorption to host cells was not affected in the agarose overlay containing EGb. However, when the viruses were treated with EGb before exposure to cells, their infectivity was markedly reduced. In contrast, the inhibitory effect was not observed when MDCK cells were treated with EGb before infection with influenza viruses. Hemagglutination inhibition assays revealed that EGb interferes with the interaction between influenza viruses and erythrocytes. The inhibitory effect of EGb was observed against influenza A (H1N1 and H3N2) and influenza B viruses. These results suggest that EGb contains an anti-influenza virus substance(s) that directly affects influenza virus particles and disrupts the function of hemagglutinin in adsorption to host cells. In addition to the finding of the anti-influenza virus activity of EGb, our results demonstrated interesting and important insights into the screening system for anti-influenza virus activity. In general, the plaque assay using drug-containing agarose overlays is one of the most reliable methods for detection of antiviral activity. However, our results showed that EGb had no effects either on the number of plaques or on their sizes in the plaque assay. These findings suggest the existence of inhibitory activities against the influenza virus that were overlooked in past studies.     

Antiviral effect of aqueous extracts from species of the Lamiaceae family against Herpes simplex virus type 1 and type 2 in vitro

Aqueous extracts from species of the Lamiaceae family were examined for their antiviral activity against Herpes simplex virus (HSV). Extracts from lemon balm (Melissa officinalis), peppermint (Mentha x piperita), prunella (Prunella vulgaris), rosemary (Rosmarinus officinalis), sage (Salvia officinalis) and thyme (Thymus vulgaris) were screened. Their inhibitory activity against Herpes simplex virus type 1 (HSV-1), type 2 (HSV-2) and an acyclovir-resistant strain of HSV-1 (ACV (res)) was tested in vitro on RC-37 cells in a plaque reduction assay. The 50% inhibitory concentrations (IC (50)) of the extracts for HSV plaque formation were determined in dose-response studies. All test compounds showed a high antiviral activity against HSV-1, HSV-2 and ACV (res). In order to identify the mode of antiviral action, the extracts were added to the cells or viruses at different stages of infection. Both types of Herpes virus including ACV (res) were considerably neutralized after treatment with the extracts prior to infection. At maximum non-cytotoxic concentrations of the extracts, plaque formation was significantly reduced by > 90% for HSV-1 and HSV-2 and > 85% for ACV (res). In time-response studies over a period of 2 hours, a clearly time-dependent activity was demonstrated. These results indicate that the extracts affect HSV before adsorption, but have no effect on the intracellular virus replication. Therefore, the extracts exert their antiviral effect on free HSV and offer a chance to use them for topical therapeutic application against recurrent HERPES infections.     

Efficacy of anise oil, dwarf-pine oil and chamomile oil against thymidine-kinase-positive and thymidine-kinase-negative herpesviruses

The effect of anise oil, dwarf-pine oil and chamomile oil against different thymidine-kinase-positive (aciclovir-sensitive) and thymidine-kinase-negative (aciclovir-resistant) herpes simplex virus type 1 (HSV-1) strains was examined. Clinical HSV-1 isolates containing frameshift mutations in the thymidine kinase (TK) gene, an insertion or a deletion, yield a non-functional thymidine kinase enzyme resulting in phenotypical resistance against aciclovir. The inhibitory activity of three different essential oils against herpes simplex virus isolates was tested in-vitro using a plaque reduction assay. All essential oils exhibited high levels of antiviral activity against aciclovir-sensitive HSV strain KOS and aciclovir-resistant clinical HSV isolates as well as aciclovir-resistant strain Angelotti. At maximum noncytotoxic concentrations of the plant oils, plaque formation was significantly reduced by 96.6-99.9%, when herpesviruses were preincubated with drugs before attachment to host cells. No significant effect on viral infectivity could be achieved by adding these compounds during the replication phase. These results indicate that anise oil, dwarf-pine oil and chamomile oil affected the virus by interrupting adsorption of herpesviruses and in a different manner than aciclovir, which is effective after attachment inside the infected cells. Thus the investigated essential oils are capable of exerting a direct effect on HSV and might be useful in the treatment of drug-resistant viruses. Chamomile oil did not reveal any irritating potential on hen's egg chorioallantoic membrane, demonstrated the highest selectivity index among the oils tested and was highly active against clinically relevant aciclovir-resistant HSV-1 strains.