The oncogenic and persistent Epstein Barr virus (EBV) is carried by more than 95% of the human adult population. While asymptomatic in most of these, EBV can cause a wide variety of malignancies of lymphoid or epithelial cell origin. Some of these are also associated with co-infections that either increase EBV-induced tumorigenesis or weaken its immune control. The respective pathogens include Kaposi-sarcoma-associated herpesvirus (KSHV),Plasmodium falciparumand human immunodeficiency virus (HIV). In this review, I will discuss the respective tumor entities and possible mechanisms by which co-infections increase the EBV-associated cancer burden. A better understanding of the underlying mechanisms could allow us to identify crucial features of EBV-associated malignancies and defects in their immune control. These could then be explored to develop therapies against the respective cancers by targeting EBV and/or the respective co-infections with pathogen-specific therapies or vaccinations.
致癌且持续存在的爱泼斯坦-巴尔病毒（EBV）在超过95%的成年人群中携带。尽管在大多数携带者中无症状，但EBV可引发多种源于淋巴细胞或上皮细胞的恶性肿瘤。其中部分肿瘤还与协同感染相关，这些感染可能增强EBV诱导的肿瘤发生或削弱其免疫控制。相关病原体包括卡波西肉瘤相关疱疹病毒（KSHV）、恶性疟原虫和人类免疫缺陷病毒（HIV）。本综述将探讨相关肿瘤类型，以及协同感染加重EBV相关癌症负担的可能机制。深入理解其潜在机制有助于识别EBV相关恶性肿瘤的关键特征及其免疫控制缺陷，进而通过靶向EBV和/或采用病原特异性疗法或疫苗接种干预协同感染，为开发针对相关癌症的治疗策略提供新方向。
Modulation of Epstein-Barr-Virus (EBV)-Associated Cancers by Co-Infections
肿瘤(癌症)患者之家