MOLLUSCUM CONTAGIOSUM VIRUS

传染性软疣病毒（MCV）是一种 痘病毒引起无症状皮肤肿瘤， 持续数月至数年的皮肤健康或 免疫缺陷个体，尤其是儿童。持久性 这种病毒的感染正在增加， 成人艾滋病患者的棘手并发症。现时 没有针对性的预防或治疗方法。所有尝试 培养病毒的方法都失败了，人们对此知之甚少。 该项目的目标是分析病毒的结构， 基因组，识别其基因，确定其表达模式， 复制，并寻找潜在的治疗靶点。病毒 抵抗人类免疫系统的药物是特别感兴趣的。在 在过去的几年里，我们成功地测序了 MCV和目前我们正在分析的几个功能 有趣的基因硒是人体必需的微量元素， 原核和真核抗氧化蛋白的组成部分。一 与谷胱甘肽过氧化物酶同源的候选硒蛋白是 根据MCV序列推断。硒被纳入 在生物合成过程中转化为这种蛋白质， 信使RNA末端附近的结构是必需的， 潜在UGA终止密码子的选择性硒代半胱氨酸解码 在开放的阅读框架内。硒蛋白保护人类 角质形成细胞对抗紫外线照射的细胞毒性作用， 过氧化氢，为病毒提供了一种防御机制 自身对抗环境压力。分泌型CC趋化因子 同源物，由MCV编码，有力地干扰了 人单核细胞、淋巴细胞和中性粒细胞的趋化性 对大量CC和CXC趋化因子的反应， 不同的受体特异性。有证据表明病毒蛋白 人趋化因子受体是通过竞争 结合和钙动员实验。广谱 这种MCV蛋白的趋化因子拮抗活性可以解释 在皮肤肿瘤中长期缺乏炎症反应， 港口复制基地车

Molluscum contagiosum virus (MCV) is a human poxvirus that causes asymptomatic cutaneous neoplasms that can persist for months to years in the skin of healthy or immunodeficient individuals, particularly children. Persistent infections with this virus are increasing and have become troublesome complications for adults with AIDS. At present there is no specific preventive or treatment for the disease. All attempts to culture the virus have failed and little is known about it. The objectives of the project are to analyze the structure of the viral genome, identify its genes, determine its mode of expression and replication, and find potential therapeutic targets. The way the virus resists the human immune system is of particular interest. In previous years, we succeeded in sequencing the entire genome of MCV and presently we are analyzing the functions of several interesting genes. Selenium, an essential trace element, is a component of prokaryotic and eukaryotic antioxidant proteins. A candidate selenoprotein homologous to glutathione peroxidase was deduced from the sequence of MCV. Selenium was incorporated into this protein during biosynthesis, and a characteristic stem-loop structure near the end of the messenger RNA was required for alternative selenocysteine decoding of a potential UGA stop codon within the open reading frame. The selenoprotein protected human keratinocytes against cytotoxic effects of ultraviolet irradiation and hydrogen peroxide, providing a mechanism for a virus to defend itself against environmental stress. A secreted CC chemokine homolog, encoded by MCV, potently interfered with the chemotaxis of human monocytes, lymphocytes, and neutrophils in response to a large number of CC and CXC chemokines with diverse receptor specificities. Evidence that the viral protein binds to human chemokine receptors was obtained by competition binding and calcium mobilization experiments. The broad spectrum chemokine antagonistic activity of this MCV protein can explain the prolonged absence of an inflammatory response in skin tumors that harbor replicating MCV.