新城疫病毒HBNU/LSRC/F3株与Mukteswar、LaSota株抗肿瘤效果的比较

目的： 研究新城疫病毒（Newcastle disease virus,NDV）弱毒力株HBNU/LSRC/F3对人食管癌ECA109细胞凋亡的影响,并与其他两株NDV（弱毒力株LaSota株、中等毒力Mukteswar株）的抗肿瘤作用进行比较。 方法： 体外培养ECA109细胞,不同NDV经扩增后分别感染ECA109细胞,CCK-8法检测各NDV对ECA109细胞增殖的抑制作用,激光共聚焦显微镜观察经各NDV感染后ECA109细胞的凋亡情况,流式细胞术检测其早期细胞凋亡,DNA琼脂糖凝胶电泳检测其晚期凋亡情况。 结果： HBNU/LSRC/F3株NDV能抑制ECA109细胞的增殖,且强于LaSota株,但稍弱于Mukteswar株（P<0.05）。ECA109细胞感染5×10-4Hu/ml NDV时,HBNU/LSRC/F3株、Mukteswar株、LaSota株对ECA109细胞的增殖抑制率分别为（31.43±157）%、（39.87±1.99）%和（19.89±0.99）%。流式细胞仪检测结果显示,HBNU/LSRC/F3株感染后ECA109细胞的早期凋亡率为（21.32±0.44）%,而Mukteswar株和LaSota株的早期凋亡率为（22.27±0.23）%和（14.32±0.61）%;激光扫描共聚焦显微镜和DNA琼脂糖凝胶电泳检测结果显示,Mukteswar株以诱导晚期凋亡为主,HBNU/LSRC/F3株以诱导ECA109细胞早期凋亡为主,且较LaSota株明显。 结论： 弱毒力HBNU/LSRC/F3株可有效抑制ECA109细胞增殖,诱导ECA109细胞早期凋亡,虽略低于中等毒力Mukteswar株,但远高于弱毒力LaSota株,因此HBNU/LSRC/F3株可能具有更高的抗肿瘤临床应用价值。     

新城疫病毒D90毒株致肺癌A549细胞死亡的方式

新城疫病毒(newcastle disease virus, NDV)属副黏病毒,可以引起禽类的新城疫.新城疫病毒在人类癌细胞中的复制效率是在正常细胞中的10 000倍, 因此,NDV可以选择性杀伤肿瘤细胞,这提示人们可将它作为潜在的抗癌因子.目前,已经应用于人癌症治疗的NDV毒株有73-T、MTH-68等溶癌毒株和Μlster等非溶癌毒株, 其中NDV73-T已经被证明可以在体外杀死人的多种肿瘤细胞,同时在体外试验中,该毒株被证明不会杀死正常的、增生性的白细胞或人的正常皮肤纤维原细胞,但是在于人的肿瘤细胞具有明显的杀伤作用.本研究在新城疫病毒D90株明显抑制肺癌A549细胞生长并导致细胞死亡的基础上,对其可能的致死亡作用方式进行了探讨.     

新城疫病毒D817株体外高效杀伤肝癌细胞及其作用机制

 目的 与NDV疫苗株LaSota对比研究一株NDV D817株对肝癌细胞高效特异性的杀伤效应和作用机制, 进一步筛选NDV溶瘤毒株。 方法 用MTT法对比病毒对三株传代肝癌细胞株SMMC-7721、Bel-7404和HepG-2及一株正常肝细胞株 HL-7702的杀伤效应,并用TUNEL法及透射电 子显微镜观察病毒诱导肿瘤细胞发生凋亡作用。 结果 NDV D817株对肝癌细胞株SMMC-7721、Bel-7404和HepG-2杀伤效应高达80％,显著高于疫苗 LaSota株（P<0.01）,而对人正常肝细胞HL-7702无明显影响;病毒在肝癌细胞中明显复制增 殖,对细胞的杀伤活性与病毒作用剂量和病毒作用时间成正比;NDV D817株有效诱导肝癌细胞 发生凋亡。 结论 NDV D817株有效诱导肝癌细胞发生凋亡, 对SMMC-7721、Bel-7404和HepG-2细胞具有高效杀伤 性,而对正常肝细胞HL-7702未见明显影响,推测为溶瘤株。     

6株NDV鄱阳株对肝癌细胞杀伤作用的初步研究

目的：研究从江西鄱阳湖野鸭分离的6株NDV对肝癌细胞的杀伤效应，进-步筛选NDV溶瘤毒株。方法：用MTT法研究6株NDV鄱阳株对两株传代肝癌细胞株Novikoff和HepG-2及一株正常肝细胞株HL-7702的杀伤效应。结果：6株NDV鄱阳株对肝癌细胞株Novikoff和HepG-2有湿著杀伤效应，而对人正常肝细胞HL-7702无明显影响；病毒对细胞的杀伤活性与病毒作用剂量和病毒作用时间成正比；病毒在肝癌细胞中有明显复制增殖现象；Novikoff肝癌细胞对NDV敏感性强于HepG-2肝癌细胞。结论：6株NDV鄱阳株对Novikoff及HepG-2肝癌细胞产生显著的杀伤作用，而对正常肝细胞HL-7702未见明显影响。     

新城疫病毒感染体外诱导胃癌细胞热休克蛋白70的表达及意义

目的：观察NDV在体外抗胃癌细胞活性，研究NDV感染诱导胃癌细胞热休克蛋白70(HSP70)的表达及其意义。方法：应用倒置显微镜观察细胞形态，MTT法测细胞生长抑制状况，血凝试验检测：NDV在细胞中的增殖状况，免疫组化染色观察细胞中HSP70表达情况，流式细胞术检测胃癌细胞HSP70的表达。结果：NDV在体外可使BGC-823胃癌细胞形成明显的细胞病变效应及生长抑制作用，且这种抑制作用与肿瘤细胞被NDV感染后HSP70表达增加呈正相关。结论：NDV的抗BGC-823胃癌细胞活性显著，其杀伤机制之一为通过感染而诱导BGC-823产生过多的HSP70。     

微管促解聚与促聚合药物序贯使用对肿瘤细胞的抑制作用

目的：探讨细胞微管促解聚与促聚合药物序贯使用对肿瘤细胞的抑制作用。方法：采用四唑盐（MTr）比色法，检测化疗药物紫杉醇和长春瑞滨对肿瘤细胞株MCF-7、SK-OV3、A549的抑瘤效应。设定紫杉醇组、长春瑞滨组、紫杉醇加长春瑞滨组、先紫杉醇4小时后加长春瑞滨组和先长春瑞滨4小时后加紫杉醇组，药物浓度为100％血浆峰值浓度（PPC），50％PPC，25％PPC，12．5％PPC，6．25％PPC，培养72小时测定。结果：对三种肿瘤细胞株MCF-7，SK-OV3，A549，先加长春瑞滨4小时后加紫杉醇组抑瘤效应均明显优于其他各组（P〈0．01），先紫杉醇4小时后加长春瑞滨组抑瘤率并不优于其他组（P〉0．1）。结论：在联合使用微管解聚或聚合的化疗药物时，先使用促解聚药物，再使用促聚合药物，对肿瘤细胞的抑制有增效作用。     

新城疫病毒体外抗白血病作用的实验研究

 目的　通过体外实验研究探讨新城疫病毒（NDV）对人类急性单核细胞白血病的作用。方法　应用倒置显微镜观察NDV感染后白血病细胞形态和密度的变化,AO／PI染色后观察病毒对白血病细胞的生长抑制情况;甲基偶氮唑蓝（MTT）法测定不同浓度NDV作用于白血病细胞不同时间后对细胞增殖的影响。结果　倒置显微镜下,对照组细胞形态规则、分布密集;NDV感染组细胞形态不规则,聚集、融合现象明显,分布稀疏;AO／PI染色后对照组呈均匀明亮的绿色荧光,NDV原液组呈红、绿两色荧光,以红色为主,MTT检测结果显示不同浓度NDV对SHI-1细胞的增殖均有明显抑制作用（P＜0.01）,不同时间的抑制作用也有明显差异（P＜0.01）;增殖抑制作用呈现时间-浓度依赖关系。结论　NDV是一种有效的抗人类急性单核细胞白血病的病毒。     

6株NDV鄱阳株对肝癌细胞杀伤作用的初步研究

目的:研究从江西鄱阳湖野鸭分离的6株NDV对肝癌细胞的杀伤效应,进一步筛选NDV溶瘤毒株。方法:用MTT法研究6株NDV鄱阳株对两株传代肝癌细胞株Novikoff和HepG-2及一株正常肝细胞株HL-7702的杀伤效应。结果:6株NDV鄱阳株对肝癌细胞株Novikoff和HepG-2有显著杀伤效应,而对人正常肝细胞HL-7702无明显影响;病毒对细胞的杀伤活性与病毒作用剂量和病毒作用时间成正比;病毒在肝癌细胞中有明显复制增殖现象;Novikoff肝癌细胞对NDV敏感性强于HepG-2肝癌细胞。结论:6株NDV鄱阳株对Novikoff及HepG-2肝癌细胞产生显著的杀伤作用,而对正常肝细胞HL-7702未见明显影响。     

新城疫病毒Lasota 弱毒株对人肿瘤细胞的体外修饰作用

 目的 研究新城疫病毒（NDV）弱毒株Lasota对体外培养的人肿瘤细胞株免疫功能的影响。方法 以不同病毒滴度作用于肿瘤细胞，采用MTT染色法检测NDV对肿瘤细胞的杀伤作用，同时用NDV处理过的小鼠黑色素B16细胞免疫小鼠，检测其对小鼠NK细胞活性影响。结果 NDV Lasota株对4种癌细胞株均具有较强的杀伤作用，用其处理小鼠黑色素瘤细胞株后，再次接种可提高小鼠体内的NK细胞活性。结论 NDV能够抑制肿瘤细胞生长，诱导其凋亡，免疫接种小鼠后，可提高小鼠的细胞免疫功能。     

新城疫病毒7793株对结肠癌小鼠肝转移的抑制效果及其可能的机制

目的：以脾脏保留法建立结肠癌小鼠肝转移模型,评价新城疫病毒（Newcastle disease virus,NDV）7793株对小鼠结肠癌肝转移的抑制效果,并初步探讨NDV抑瘤的免疫激活机制。方法：经脾注入1×107/ml小鼠结肠癌细胞CT26的单细胞悬液0.1 ml,建立结肠癌CT26小鼠肝脏转移瘤模型;建模小鼠随机分3组（每组20只）: PBS阴性对照组、NDV7793给药组和5-FU给药组,于建模当天起连续5 d经腹腔分别注射PBS(0.1 ml/d)、NDV7793(512 HU/kg)和5-FU(20 mg/kg)。观察各组小鼠的生存状态,分析肝脏成瘤情况,计算抑瘤率和胸腺指数。ELISA法检测模型小鼠肝脏的IFN-γ水平。结果：成功构建小鼠结肠癌肝转移模型。NDV7793给药组小鼠未观察到明显的不良反应,生活状态好于PBS组和5-FU组。NDV7793组和5-FU组小鼠的肝转移瘤数量较PBS组均显著减少\[ (20.40±5.20) 、(205.50±19.21) vs (265.30±35.73)个,均 P <0.01\],NDV7793组的抑瘤率明显高于5-FU组（75.4% vs 48.0%, P <0.05）,NDV7793组小鼠的肝脏癌灶范围小,癌细胞以坏死或凋亡为主。NDV7793组和5-FU组小鼠的中位生存期明显长于PBS阴性对照组（30、22 vs 17 d, P <0.01）。NDV7793组小鼠肝脏IFN-γ的表达和胸腺指数均显著高于5-FU组和PBS组（均 P <0.05）。结论：NDV7793株对结肠癌小鼠的肝转移具有较强的抑制效果,并可能通过上调肝脏的IFN-γ以及提升胸腺指数来抑制结肠癌的肝转移。     

联合应用新城疫病毒及其 HN基因对小鼠黑色素瘤抑制效应的研究

背景与目的:尽管新城疫病毒( Newcastle disease virus, NDV)对多种肿瘤具有抑制作用 ,但其抑瘤机制尚不完全清楚.以前的研究结果表明,该病毒的血凝素神经氨酸酶( hemagglutinin-neuraminidase,HN)基因在该病毒的抗肿瘤作用上发挥重要作用且 HN蛋白表达后能够定位于肿瘤细胞膜上,以 HN蛋白作为肿瘤细胞的外源抗原来研究其抑瘤作用尚未见报道.本研究拟探讨 HN蛋白作为外源抗原在新城疫病毒抗肿瘤的作用以及二者联合应用对小鼠黑色素瘤的抑制效应.方法:在 C57BL/6小鼠右后肢皮下接种 B16黑色素瘤细胞 2× 105个.荷瘤第 2天,左后肢肌肉注射含新城疫病毒 HN基因的重组质粒,荷瘤第 7天,瘤内注射新城疫病毒 2× 109pfu;同时设单独 HN基因或 NDV治疗组及注射 PBS的对照组.通过抑瘤率观察动物体内的抑瘤效果;通过特异性细胞毒 T淋巴细胞( cytotoxic T lymphocyte,CTL)实验, ICAM Ⅰ、 CD48及新城疫病毒 HN蛋白在肿瘤细胞表面表达检测,探讨 HN蛋白所介导的抑瘤作用.结果:联合应用新城疫病毒及该病毒 HN基因对肿瘤的抑制效果明显好于单独 HN基因及新城疫病毒,抑瘤率达 82.8%,特异性 CTL反应增强,对靶细胞的杀伤率为 18.4%;单独 HN基因及新城疫病毒治疗组的抑瘤率分别为 56.6%、 41.0%,特异性 CTL活性分别为 4.4%、 10.1%;瘤内注射 NDV的肿瘤细胞表面检测到 HN分子的表达, ICAM Ⅰ、 CD48分子表达上调.结论:定位于肿瘤细胞表面的 HN蛋白介导机体对肿瘤细胞的特异性杀伤,联合应用新城疫病毒及该病毒 HN基因显著增强了机体对肿瘤细胞的杀伤效应.     

Evaluation of Ultra-Microscopic Changes and Proliferation of Apoptotic Glioblastoma Multiforme Cells Induced by Velogenic Strain of Newcastle Disease Virus AF2240

Aim: Newcastle disease virus (NDV) is a member of genus Avulavirus within the family Paramyxoviridae. Interestof using NDV as an anticancer agent has arisen from its ability to kill tumor cells with limited toxicity to normal cells.Methods: In this investigation, the proliferation of brain tumor cell line, glioblastoma multiform (DBTRG.05MG)induced by NDV strain AF2240 was evaluated in-vitro, by using MTT proliferation assay. Furthermore, Cytologicalobservations were studied using fluorescence microscopy and transmission electron microscopy, DNA laddering inagarose gel electrophoresis assay used to detect the mode of cell death and analysis of the cellular DNA content byflowcytometery. Results: MTT proliferation assay, Cytological observations using fluorescence microscopy andtransmission electron microscopy show the anti-proliferation effect and apoptogenic features of NDV on DBTRG.05MG.Furthermore, analysis of the cellular DNA content showed that there was a loss of treated cells in all cell cycle phases(G1, S and G2/M) accompanied with increasing in sub-G1 region (apoptosis peak). Conclusion: It could be concludedthat NDV strain AF2240 is a potent antitumor agent that induce apoptosis and its cytotoxicity increasing while increasingof time and virus titer.     

新城疫病毒HN基因对肝癌细胞SMMC7721的细胞毒性研究

目的:探讨新城疫病毒HN基因对肝癌细胞SMNC7721的杀伤作用及其机制.方法:以脂质体介导方法在体外转染含新城疫病毒HN基因的质粒pVHN于细胞SMMC7721 24 h后,采用MTT法检测细胞活性;3,5-二羟基甲苯测定其唾液酸含量的变化;丫啶橙/溴化乙锭(AO/EB)染色,荧光显微镜观察细胞形态学改变;以及FCM检测病毒HN基因和HLA-A,B,C的表达.结果:体外转染pVHN能显著地降低细胞表面唾液酸含量(P＜0.05),有效地杀伤肿瘤细胞SMMC7721;荧光显微镜观察可见典型的细胞死亡形态学改变;实验组细胞与对照组比较HN表达差异显著,HLA-A,B,C表达上调.结论:HN基因在体外能够显著降低肿瘤细胞表面唾液酸含量,同时,使其高表达HN抗原,上调HLA-A,B,C表达,从而,可能增强了肿瘤细胞的抗原性和免疫识别,诱导了细胞SMMC7721死亡.     

Newcastle disease virus as an antineoplastic agent: induction of tumor necrosis factor-alpha and augmentation of its cytotoxicity

The oncolytic strain 73-T of Newcastle disease virus (NDV) has been reported to be beneficial in the treatment of cancer patients, but little is known about its mechanism of action. In this study, NDV strain 73-T and a wild-type isolate of NDV were found to be potent inducers of tumor necrosis factor (TNF) production by both human peripheral blood mononuclear cells (PBMCs) and rat splenocytes. Antibody inhibition experiments identified TNF-alpha as the major species of TNF induced by NDV in PBMCs. The effect of recombinant human TNF-alpha (rHuTNF-alpha) on human cancer cells was then examined. Neither rHuTNF-alpha nor supernatants from NDV-stimulated PBMCs were cytotoxic toward the TNF-resistant human malignant melanoma cell line MEL-14. However, when MEL-14 cells were treated with NDV strain 73-T, both rHuTNF-alpha and supernatants from NDV-stimulated PBMCs killed 48% and 55%, respectively, of these tumor cells. Treatment with NDV also conferred TNF susceptibility to the TNF-resistant human malignant melanoma cell line MEL-21 and the human myelogenous leukemia cell line K562. In contrast to its enhanced cytotoxicity toward NDV-treated cancer cells, rHuTNF-alpha had no effect on NDV-treated normal human PBMCs proliferating in response to concanavalin A. These results suggest two important mechanisms for the antineoplastic activity of NDV: (a) induction of TNF-alpha secretion by human PBMCs and (b) enhancement of the sensitivity of neoplastic cells to the cytolytic effects of TNF-alpha.     

Antitumor effects of Newcastle Disease Virus in vivo: local versus systemic effects

Newcastle Disease Virus (NDV) has interesting anti-neoplastic and pleiotropic immune stimulatory properties. The virus preferentially replicates in and kills tumor cells and appears to be safe and to varying degrees effective in phase II-clinical studies in the US and in Europe. Here we have compared various lytic and non-lytic strains of NDV with regard to their antitumor effects after local or systemic application. As tumor models we used human metastatic melanoma xenotransplants in nude mice and murine metastatic colon carcinoma (CT26), renal carcinoma (Renca) and lymphoma (ESb) cell lines. Intra or peri-tumoral application of NDV or NDV infected tumor cells showed more pronounced antitumor activity than systemic application even when in the latter case much higher dose ranges were used. In the CT26 colon carcinoma model the non-lytic strain Ulster showed stronger antitumor activity than the lytic strain 73T. In the human MeWo melanoma xentransplant model strong antitumor bystander effects were observed by 20% admixture of melanoma cells pre-infected in vitro with NDV (either strain Ulster or Italien). Virus therapy of pre-established human melanomas by intra-tumoral injection of NDV was effective with the lytic strain Italien but not with the non-lytic strain Ulster. Systemic anti-metastatic effects were never observed with NDV alone in contrast to previous results obtained with NDV modified tumor vaccines.     

Antiproliferative effect of newcastle disease virus strain D90 on human lung cancer cell line A549

Newcastle disease virus (NDV) and variants of this virus have oncolytic properties and are potential anticancer agents. The objective of this study was to compare the effect of NDV strain D90 and strain D93 isolated from natural sources on human non-small cell lung cancer (NSCLC) cell line A549. We determined the 50% embryo infective dose (EID50) and 50% tissue culture infective dose (TCID50) of the NDV strains. The MTT assay was used to evaluate the effects of NDV strains on cell viability. We determined the expression of Annexin V and Bcl-2 proteins in NDV-infected cells. Light microscopy and electron microscopy indicated that the D90 strain significantly altered cell morphology and reduced cell viability, while strain D93 had negligible effects. Neither strain had a significant effect on normal cultured fetal liver cells. We used acridine orange staining to show that strain D90 (but not strain D93) induced nuclear fragmentation of A549 cells. An Annexin V-based apoptosis assay indicated that strain D90 (but not strain D93) caused significant apoptosis of A549 cells. Moreover, strain D90 (but not strain D93) significantly repressed the expression of Bcl-2 (an antiapoptotic protein) in A549 cells. Taken together, our results indicate that NDV strain D90 (but not strain D93) had no significant effect on normal cultured cells, but induced apoptosis of cultured NSCLC cells via a caspase-dependent pathway. These results suggest that NDV strain D90 has potential as an anticancer agent.     

Tumor selective replication of Newcastle disease virus: association with defects of tumor cells in antiviral defence

To investigate tumor-selective viral replication, we compared several tumorigenic human cell lines to nontumorigenic human cells from the blood for the sensitivity to become infected by a recombinant lentogenic strain of Newcastle Disease Virus (NDV) with incorporated transgene EGFP (NDFL-EGFP). Although fluorescence signals in nontumorigenic cells were only weak or missing completely, a massive and long-lasting transgene-expression was observed in all tumor cell lines. The majority of tumor cells (50-95%) could be infected, and viral replication was associated with an increase in the cell surface density of viral antigens. To clarify the underlying mechanism of the observed difference in virus susceptibility we examined the kinetics of interferon-induced antiviral enzymes because NDV is a strong type-I interferon inducer. This analysis revealed several defects of tumor cells in their antiviral defence responses: They showed no response to UV-inactivated NDV, whereas nontumorigenic cells reacted with induction of high-levels of the antiviral enzymes PKR and MxA. Upon coincubation with live NDV, tumor cells showed a delayed response in the increased expression of the antiviral enzymes in comparison with PBMC. In nontumorigenic cells the replication cycle of NDV stopped after the production of positive-strand RNA, while tumor cells continued in the replication cycle and copied viral genomes 10-50 hr after infection. These results can explain the tumor selective replication behavior of this interesting antineoplastic virus.     

Prevention of metastatic spread by postoperative immunotherapy with virally modified autologous tumor cells. I. Parameters for optimal therapeutic effects

Effective anti-metastatic therapy was achieved in a mouse tumor model by combining surgery with post-operative immunotherapy using virus-modified autologous tumor cells. No therapeutic effect was observed when using for immunotherapy the nonmodified autologous tumor ESb, which is only weakly immunogenic and highly metastatic. The viral modification was achieved by infecting the tumor with an avirulent strain of Newcastle disease virus (NDV), which led to expression of viral antigens and to an increase in the tumor cells' immunogenicity. Parameters which were of decisive influence for success or failure of therapy were the time of operation of the primary tumor and the dose of virus which was admixed to a standard dose of irradiated tumor cells. There was a low dose optimum of NDV at about 100 hemagglutinating units per 25 X 10(6) tumor cells. The therapeutic effect observed was less pronounced if the virus was given separately from the tumor cells. Post-operative immunotherapy with NDV-modified tumor cells had the following therapeutic effects: (1) disappearance of micrometastases from visceral organs as ascertained by a sensitive bioassay; (2) life prolongation in virtually all animals when compared to controls (operated only); (3) cures in about 50% of the treated animals. The possible mechanism of this therapeutic effect and its potential for clinical application are discussed.     

Adhesive function of newcastle-disease virus hemagglutinin in tumor-host interaction

Infection of metastatic lymphoma cells (ESbL) by a low dose of a non-lytic strain of Newcastle disease virus (NDV) leads to viral replication followed by strong cell surface expression of viral antigens, especially hemagglutinin neuraminidase (HN). The expressed HN was functional and facilitated cell-cell interactions and cell attachment. This was shown for NDV infected tumor cells, lymphocytes, fibroblasts and endothelial cells. The interactions could be strongly inhibited by antibodies against the viral HN protein. Increased binding was also seen with HN c-DNA transfectants expressing the HN as the only viral protein. Viral infection did not influence proliferation and lysability of the infected tumor cells. Following intravenous injection of tumor cells, the number of hepatic metastases was significantly reduced when the cells had been pre-infected with NDV. This reduction of metastases correlated with an increased survival time of the animals. As potential mechanisms of these NDV effects we propose augmentation of cell-eel interactions and immune functions and reduction of invasive capacity of NDV infected, as compared to non-infected tumor cells.     

新城疫病毒7793株对人结肠癌细胞的杀伤作用

目的:研究新城疫病毒NDV7793对人结肠癌细胞的体外杀伤作用,为结肠癌的生物疗法奠定基础。方法:通过蚀斑实验纯化病毒并测定纯化的NDV7793株的感染力;用乳酸脱氢酶微量释放法测定纯化病毒对人LoVo和Ls174t结肠癌细胞株的杀伤作用并且通过血凝实验测定病毒在不同细胞中的增殖力。结果:NDV7793在感染细胞96h后出现直径约为0.5mm左右的空斑,PFU为1.25×107个/ml,为弱毒株;NDV7793对LoVo和Ls174t人结肠癌细胞株有明显的杀伤作用,而且杀伤作用的强度与病毒作用的时间和病毒的浓度呈正相关的关系;NDV7793可以在肠癌细胞中生长复制,该病毒株在人结肠癌细胞株LoVo的复制能力强于Ls174t。结论:NDV7793具有较强的选择性杀伤人结肠癌细胞的作用,且为弱毒株,这株病毒具备肿瘤生物治疗的潜能。