摘要
卡波西肉瘤相关疱疹病毒(Kaposi's sarcoma-associated herpesvirus,KSHV)引起艾滋病相关恶性肿瘤卡波西肉瘤(Kaposi sarcoma,KS)、B淋巴细胞增生性疾病原发性积液淋巴瘤和多中心的淋巴结增生症。KSHV感染会经历潜伏和裂解性复制两个互相转换的阶段,而裂解阶段病毒的复制造成感染在组织中的散播,加速肿瘤恶化。由KSHV开放阅读框ORF50编码的复制与转录激活子(replication and transcription activator,RTA)是控制KSHV从潜伏向裂解复制转变的开关,并影响KS的病理进程,有望成为治疗KSHV感染性疾病的新靶标。
Kaposi's sarcoma-associated herpesvirus (KSHV) is the pathogen of AIDS-related malignant Kaposi's sarcoma (KS),B-lymphocyte proliferation diseases and mulricentric Castleman's disease (MCD).Infection with KSHV includes latent infection stage and lytic replication stage.KSHV in lyric replication causes spread of infection in tissues and exacerbates the growth of KS.Replication and transcription activator (RTA) coded by KSHV open reading frame 50 (ORF50) is the key regulatory factor to control the switch of KSHV from latent infection into lytic replication and is involved in multiple aspects of KS pathological process.RTA is hoped to become a new target for the treatment of infectious diseases caused by KSHV.
出处
《解放军医学院学报》
CAS
2014年第6期641-645,共5页
Academic Journal of Chinese PLA Medical School
基金
美国国立卫生院海外项目(1R01)~~
关键词
卡波西肉瘤
疱疹病毒
复制与转录激活子
Kaposi sarcoma
herpesvirus
replication and transcription activator