Methods and Technologies Branch, Epidemiology and Genomics Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, National Institutes of Health (NIH), 6130 Executive Boulevard, Suite 5100, Bethesda, MD 20892-7324, USA.
Technol Cancer Res Treat. 2014 Apr;13(2):177-94. doi: 10.7785/tcrt.2012.500366. Epub 2013 Aug 2.
Approximately 18% of the global cancer burden has been attributed to infectious agents, with estimates ranging from 7% in developed countries to about 22% in developing countries. Chronic infections caused by the hepatitis B and C viruses, human papilloma viruses (HPV), and Helicobacter pylori (H. pylori) are reported to be responsible for approximately 15% of all human cancers. Interestingly, although many of the infectious agents that have been associated with cancer--such as HPV, Epstein-Barr virus (EBV), and H. pylori--are highly prevalent in the world, most infected individuals do not develop cancer but remain lifelong carriers. Malignancies associated with infectious agents may result from prolonged latency as a result of chronic infections. Pathogenic infections are necessary but are not sufficient for cancer initiation or progression. Cancer initiation may require additional cofactors, including secondary infections. Therefore, in patients with chronic infection with one agent, secondary co-infection with another agent may serve as an important co-factor that may cause cancer initiation and progression. Additionally, opportunistic co-infections could significantly inhibit response to cancer treatment and increase cancer mortality. Co-infections are relatively common in areas with a high prevalence of infectious agents, especially in developing countries. These co-infections can cause an imbalance in the host immune system by affecting persistence of and susceptibility to malignant infections. Several articles have been published that focus on infectious agents and cancer. In this article, we discuss the role of infectious agents in malignancies, highlight the role of multiple/co-infections in cancer etiology, and review implications for cancer epidemiology.
约 18%的全球癌症负担归因于感染因子，估计从发达国家的 7%到发展中国家的约 22%不等。乙型肝炎和丙型肝炎病毒、人乳头瘤病毒 (HPV) 和幽门螺杆菌 (H. pylori) 等慢性感染据报道约占所有人类癌症的 15%。有趣的是，尽管许多与癌症相关的感染因子——如 HPV、Epstein-Barr 病毒 (EBV) 和 H. pylori——在世界范围内非常普遍，但大多数感染个体不会患上癌症，而是终身携带。与感染因子相关的恶性肿瘤可能是由于慢性感染导致的长期潜伏引起的。致病性感染是癌症发生或进展的必要条件，但不是充分条件。癌症的发生可能需要其他辅助因素，包括继发感染。因此，在慢性感染一种病原体的患者中，另一种病原体的继发感染可能是导致癌症发生和进展的重要辅助因素。此外，机会性合并感染会显著抑制癌症治疗的反应并增加癌症死亡率。在感染因子高发地区，合并感染相对常见，尤其是在发展中国家。这些合并感染通过影响恶性感染的持续存在和易感性，会导致宿主免疫系统失衡。已经发表了一些关于感染因子和癌症的文章。在本文中，我们讨论了感染因子在恶性肿瘤中的作用，强调了多重/合并感染在癌症病因学中的作用，并综述了对癌症流行病学的影响。
