已知一些病毒与特定癌症的发作有关。这些微生物,致癌病毒或致癌病毒,可以通过调节中心代谢途径或阻碍基因组完整性机制将正常细胞转化为癌细胞,因此抑制凋亡机制和/或增强细胞增殖。已知七种致癌病毒可促进人类的肿瘤发生:人乳头瘤病毒(HPV),乙型肝炎和丙型肝炎病毒(HBV,HCV),EB病毒(EBV)人T细胞白血病病毒1(HTLV-1),卡波西肉瘤相关疱疹病毒(KSHV),和默克尔细胞多瘤病毒(MCPyV)。最近的研究表明,SARS-CoV-2感染和COVID-19进展可能会使康复患者易患癌症并加速癌症的发展。这一假设是基于关于SARS-CoV-2调节致癌途径的能力的越来越多的证据。促进慢性低度炎症并引起组织损伤。在这里,我们总结了迄今为止已知的病毒感染和癌症之间的主要关系,总结了细胞转化背后的生化机制。机械上,DNA病毒(如HPV,HBV,EBV,和MCPyV)编码其病毒癌基因。相比之下,RNA病毒(如HCV,HTLV-1)可以编码癌基因或通过顺式/反式激活引发宿主癌基因,从而导致不同类型的癌症。至于SARS-CoV-2,其作为致癌病毒的作用似乎是通过抑制抑癌因子或控制感染细胞中的代谢和自噬途径而发生的。然而,在某些特定情况下,如与严重COVID-19或长COVID相关的情况,这些影响可能是显著的。另一方面,从相反的角度来看SARS-CoV-2-癌症的关系,在某些情况下,SARS-CoV-2感染会引发溶瘤作用和抗肿瘤免疫反应。总之,我们的工作旨在唤起科学界的全面关注,以阐明SARS-CoV-2的影响,更一般地说,β-冠状病毒感染对癌症易感性的预防或支持癌症治疗方法。
Some viruses are known to be associated with the onset of specific cancers. These microorganisms, oncogenic viruses or oncoviruses, can convert normal cells into cancer cells by modulating the central metabolic pathways or hampering genomic integrity mechanisms, consequently inhibiting the apoptotic machinery and/or enhancing cell proliferation. Seven oncogenic viruses are known to promote tumorigenesis in humans: human papillomavirus (HPV), hepatitis B and C viruses (HBV, HCV), Epstein-Barr virus (EBV), human T-cell leukemia virus 1 (HTLV-1), Kaposi sarcoma-associated herpesvirus (KSHV), and Merkel cell polyomavirus (MCPyV). Recent research indicates that SARS-CoV-2 infection and COVID-19 progression may predispose recovered patients to cancer onset and accelerate cancer development. This hypothesis is based on the growing evidence regarding the ability of SARS-CoV-2 to modulate oncogenic pathways, promoting chronic low-grade inflammation and causing tissue damage. Herein, we summarize the main relationships known to date between virus infection and cancer, providing a summary of the proposed biochemical mechanisms behind the cellular transformation. Mechanistically, DNA viruses (such as HPV, HBV, EBV, and MCPyV) encode their virus oncogenes. In contrast, RNA viruses (like HCV, HTLV-1) may encode oncogenes or trigger host oncogenes through cis-/-trans activation leading to different types of cancer. As for SARS-CoV-2, its role as an oncogenic virus seems to occur through the inhibition of oncosuppressors or controlling the metabolic and autophagy pathways in the infected cells. However, these effects could be significant in particular scenarios like those linked to severe COVID-19 or long COVID. On the other hand, looking at the SARS-CoV-2─cancer relationship from an opposite perspective, oncolytic effects and anti-tumor immune response were triggered by SARS-CoV-2 infection in some cases. In summary, our work aims to recall comprehensive attention from the scientific community to elucidate the effects of SARS-CoV-2 and, more in general, β-coronavirus infection on cancer susceptibility for cancer prevention or supporting therapeutic approaches.