Proulx Jessica, Ghaly Maria, Park In-Woo, Borgmann Kathleen
Department of Microbiology, Immunology and Genetics, University of North Texas Health Science Center, Fort Worth, TX 76107, USA.
Biomedicines. 2022 Mar 25;10(4):768. doi: 10.3390/biomedicines10040768.
With the advent of combination antiretroviral therapy (cART), overall survival has been improved, and the incidence of acquired immunodeficiency syndrome (AIDS)-defining cancers has also been remarkably reduced. However, non-AIDS-defining cancers among human immunodeficiency virus-1 (HIV-1)-associated malignancies have increased significantly so that cancer is the leading cause of death in people living with HIV in certain highly developed countries, such as France. However, it is currently unknown how HIV-1 infection raises oncogenic virus-mediated cancer risks in the HIV-1 and oncogenic virus co-infected patients, and thus elucidation of the molecular mechanisms for how HIV-1 expedites the oncogenic viruses-triggered tumorigenesis in the co-infected hosts is imperative for developing therapeutics to cure or impede the carcinogenesis. Hence, this review is focused on HIV-1 and oncogenic virus co-infection-mediated molecular processes in the acceleration of non-AIDS-defining cancers.
随着联合抗逆转录病毒疗法(cART)的出现,总体生存率得到了提高,并且获得性免疫缺陷综合征(AIDS)定义的癌症发病率也显著降低。然而,人类免疫缺陷病毒1型(HIV-1)相关恶性肿瘤中不属AIDS定义的癌症显著增加,以至于在某些高度发达国家,如法国,癌症是HIV感染者的主要死因。然而,目前尚不清楚HIV-1感染如何增加HIV-1与致癌病毒共同感染患者中致癌病毒介导的癌症风险,因此阐明HIV-1如何加速共同感染宿主中致癌病毒引发的肿瘤发生的分子机制对于开发治愈或阻碍致癌作用的疗法至关重要。因此,本综述聚焦于HIV-1与致癌病毒共同感染介导的加速非AIDS定义癌症的分子过程。