Although bacterial dysbiosis has been previously associated with carcinogenesis and HIV infection, the impact of the virome and these disease states has been less well studied. In this review, we will summarize what is known about the interplay between both the bacterial and the viral components of the microbiome on cancer and HIV pathogenesis. Bacterial dysbiosis has been associated with carcinogenesis such as colorectal cancer (CRC), hepatocellular carcinoma (HCC), lung cancer, breast cancer, and gastric cancer. The dysbiotic pathogenesis may be species-based or community-based and can have varying mechanisms of carcinogenesis. The human virome was also associated with certain cancers. Viruses, such as cytomegalovirus (CMV), Human herpesvirus 8 (HHV-8), human papilloma virus (HPV), hepatitis B virus (HBV), hepatitis C virus (HCV), and Epstein–Barr virus (EBV), all had associations with cancers. It was also reported that an altered bacteriophage community may lead to carcinogenesis by allowing opportunistic, oncogenic bacteria to proliferate in a gastrointestinal biofilm. This mechanism shows the importance of analyzing the bacteriome and the virome concurrently as their interactions can provide insight into new mechanisms in the pathogenesis of not only cancer, but other diseases as well. The enteric bacteriome was shown to be distinctly altered in immunocompromised HIV-infected individuals, and highly active antiretroviral therapy (HAART) was shown to at least partially reverse the alterations that HIV causes in the bacteriome. Studies have shown that the progression to HIV is associated with changes in the plasma concentration of commensal viruses. HIV also acts synergistically with multiple other viruses, such as HPV, EBV, varicella zoster virus (VZV), and HHV-8. Although it has been shown that HIV infection leads to enteric virome expansion in humans, most of the research on HIV’s effect on the virome was conducted in non-human primates, and there is a lack of research on the effect of HAART on the virome. Virome-wide analysis is necessary for identifying novel viral etiologies. There is currently a wealth of information on the bacteriome and its associations with cancer and HIV, but more research should be conducted on the virome’s associations and reaction to HAART as well as the bacteriome-virome interactions that may play a major role in pathogenesis and recovery.

尽管细菌生态失调之前已被认为与致癌和艾滋病毒感染有关，但病毒组和这些疾病状态的影响尚未得到充分研究。在这篇综述中，我们将总结已知的微生物组中细菌和病毒成分之间的相互作用对癌症和艾滋病毒发病机制的影响。细菌失调与结直肠癌（CRC）、肝细胞癌（HCC）、肺癌、乳腺癌和胃癌等癌症发生有关。生态失调的发病机制可能是基于物种或基于群落的，并且可以具有不同的致癌机制。人类病毒组也与某些癌症有关。病毒，如巨细胞病毒 (CMV)、人类疱疹病毒 8 (HHV-8)、人类乳头瘤病毒 (HPV)、乙型肝炎病毒 (HBV)、丙型肝炎病毒 (HCV) 和 Epstein-Barr 病毒 (EBV)，均具有与癌症的关联。另据报道，噬菌体群落的改变可能会导致机会性致癌细菌在胃肠道生物膜中增殖，从而导致致癌。这种机制显示了同时分析细菌组和病毒组的重要性，因为它们的相互作用不仅可以深入了解癌症发病机制，还可以深入了解其他疾病的发病机制。研究表明，免疫功能低下的 HIV 感染者的肠道细菌组发生了明显改变，并且高效抗逆转录病毒治疗 (HAART) 被证明至少可以部分逆转 HIV 在细菌组中引起的改变。研究表明，艾滋病毒的进展与共生病毒血浆浓度的变化有关。HIV 还与多种其他病毒协同作用，例如 HPV、EBV、水痘带状疱疹病毒 (VZV) 和 HHV-8。尽管已经证明HIV感染会导致人类肠道病毒组扩张，但大多数关于HIV对病毒组影响的研究都是在非人灵长类动物中进行的，缺乏HAART对病毒组影响的研究。全病毒组分析对于识别新的病毒病因是必要的。目前有大量关于细菌组及其与癌症和艾滋病毒的关联的信息，但应该对病毒组的关联和对HAART的反应以及可能在发病机制和恢复中发挥重要作用的细菌组-病毒组相互作用进行更多的研究。