The immune deficiency associated with human immunodeficiency virus (HIV) infection causes a distinct increased risk of developing certain cancer types. Kaposi sarcoma (KS), invasive cervical cancer and non-Hodgkin’s lymphoma (NHL) are the prominent malignancies that manifest as a result of opportunistic viral infections in patients with advanced HIV infection. Despite the implementation of antiretroviral therapy (ART), the prevalence of these acquired immunodeficiency syndrome (AIDS)-defining malignancies (ADMs) remains high in developing countries. In contrast, developed countries have experienced a steady decline in the occurrence of these cancer types. However, there has been an increased mortality rate attributed to non-ADMs. Here, we provide a review of the molecular mechanisms that are responsible for the development of ADMs and non-ADMs which occur in HIV-infected individuals. It is evident that ART alone is not sufficient to fully mitigate the potential for ADMs and non-ADMs in HIV-infected individuals. To enhance the diagnosis and treatment of both HIV and malignancies, a thorough comprehension of the mechanisms driving the development of such cancers is imperative.
人类免疫缺陷病毒(HIV)感染所引发的免疫缺陷状态,显著增加了罹患特定类型癌症的风险。卡波西肉瘤(KS)、浸润性宫颈癌和非霍奇金淋巴瘤(NHL)是晚期HIV感染者因机会性病毒感染而显现的主要恶性肿瘤。尽管抗逆转录病毒疗法(ART)已得到广泛应用,但在发展中国家,这些获得性免疫缺陷综合征(AIDS)相关恶性肿瘤(ADMs)的患病率依然居高不下。相比之下,发达国家中此类癌症的发生率已呈现稳步下降趋势。然而,非AIDS相关恶性肿瘤(non-ADMs)导致的死亡率却有所上升。本文综述了HIV感染者体内ADMs与non-ADMs发生发展的分子机制。显然,仅靠ART不足以完全消除HIV感染者发生ADMs与non-ADMs的潜在风险。为提升HIV及其相关恶性肿瘤的诊疗水平,深入理解驱动此类癌症发展的机制至关重要。