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Therapeutic potential of oncolytic Newcastle disease virus: a critical review

機(jī)譯：溶瘤新城疫病毒的治療潛力：嚴(yán)格的審查。

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Newcastle disease virus (NDV) features a natural preference for replication in many tumor cells compared with normal cells. The observed antitumor effect of NDV appears to be a result of both selective killing of tumor cells and induction of immune responses. Genetic manipulations to change viral tropism and arming the virus with genes encoding for cytokines improved the oncolytic capacity of NDV. Several intracellular proteins in tumor cells, including antiapoptotic proteins (Livin) and oncogenic proteins (H-Ras), are relevant for the oncolytic activity of NDV. Defects in the interferon system, found in some tumor cells, also contribute to the oncolytic selectivity of NDV. Notwithstanding, NDV displays effective oncolytic activity in many tumor types, despite having intact interferon signaling. Taken together, several cellular systems appear to dictate the selective oncolytic activity of NDV. Some barriers, such as neutralizing antibodies elicited during NDV treatment and the extracellular matrix in tumor tissue appear to interfere with spread of NDV and reduce oncolysis. To further understand the oncolytic activity of NDV, we compared two NDV strains, ie, an attenuated virus (NDV-HUJ) and a pathogenic virus (NDV-MTH-68/H). Significant differences in amino acid sequence were noted in several viral proteins, including the fusion precursor (F0) glycoprotein, an important determinant of replication and pathogenicity. However, no difference in the oncolytic activity of the two strains was noted using human tumor tissues maintained as organ cultures or in mouse tumor models. To optimize virotherapy in clinical trials, we describe here a unique organ culture methodology, using a biopsy taken from a patient’s tumor before treatment for ex vivo infection with NDV to determine the oncolytic potential on an individual basis. In conclusion, oncolytic NDV is an excellent candidate for cancer therapy, but more knowledge is needed to ensure success in clinical trials.
機(jī)譯：與正常細(xì)胞相比，新城疫病毒（NDV）具有在許多腫瘤細(xì)胞中復(fù)制的天然優(yōu)勢(shì)。觀察到的NDV的抗腫瘤作用似乎是腫瘤細(xì)胞的選擇性殺傷和免疫應(yīng)答誘導(dǎo)的結(jié)果。遺傳操縱改變病毒的向性并用編碼細(xì)胞因子的基因武裝病毒可以改善NDV的溶瘤能力。腫瘤細(xì)胞中的幾種細(xì)胞內(nèi)蛋白，包括抗凋亡蛋白（Livin）和致癌蛋白（H-Ras），與NDV的溶瘤活性有關(guān)。在某些腫瘤細(xì)胞中發(fā)現(xiàn)的干擾素系統(tǒng)缺陷也有助于NDV的溶瘤選擇性。盡管如此，盡管具有完整的干擾素信號(hào)傳導(dǎo)，NDV在許多腫瘤類型中仍顯示出有效的溶瘤活性。綜上所述，幾種細(xì)胞系統(tǒng)似乎決定了NDV的選擇性溶瘤活性。一些障礙，例如在NDV治療期間引起的中和抗體以及腫瘤組織中的細(xì)胞外基質(zhì)似乎會(huì)干擾NDV的擴(kuò)散并減少溶瘤作用。為了進(jìn)一步了解NDV的溶瘤活性，我們比較了兩種NDV株，即減毒病毒（NDV-HUJ）和病原性病毒（NDV-MTH-68 / H）。在幾種病毒蛋白中發(fā)現(xiàn)了氨基酸序列的顯著差異，其中包括融合前體（F0）糖蛋白，這是復(fù)制和致病性的重要決定因素。然而，使用維持為器官培養(yǎng)物的人類腫瘤組織或在小鼠腫瘤模型中，未觀察到兩種菌株的溶瘤活性的差異。為了在臨床試驗(yàn)中優(yōu)化病毒療法，我們?cè)诖私榻B一種獨(dú)特的器官培養(yǎng)方法，該方法是在對(duì)NDV進(jìn)行離體感染治療之前，使用取自患者腫瘤的活檢標(biāo)本確定個(gè)體溶瘤潛能?？傊?，溶瘤NDV是癌癥治療的極佳候選藥物，但是需要更多的知識(shí)來(lái)確保臨床試驗(yàn)成功。

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