Department of Cell and Molecular Biology, Manipal School of Life Science, Manipal Academy of Higher Education, Manipal, Karnataka, 576104, India.
Chronic Disease Program, Ottawa Hospital Research Institute and Department of Obstetrics & Gynecology and Cellular and Molecular Medicine, University of Ottawa, Ottawa, Ontario, K1N 6N5, Canada.
J Ovarian Res. 2021 Feb 25;14(1):39. doi: 10.1186/s13048-021-00787-z.
Coronavirus disease 2019 (COVID-19) caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) worldwide is a major public health concern. Cancer patients are considered a vulnerable population to SARS-CoV-2 infection and may develop several COVID-19 symptoms. The heightened immunocompromised state, prolonged chronic pro-inflammatory milieu coupled with comorbid conditions are shared in both disease conditions and may influence patient outcome. Although ovarian cancer (OC) and COVID-19 are diseases of entirely different primary organs, both diseases share similar molecular and cellular characteristics in their microenvironment suggesting a potential cooperativity leading to poor outcome. In COVID-19 related cases, hospitalizations and deaths worldwide are lower in women than in males; however, comorbidities associated with OC may increase the COVID-19 risk in women. The women at the age of 50-60 years are at greater risk of developing OC as well as SARS-CoV-2 infection. Increased levels of gonadotropin and androgen, dysregulated renin-angiotensin-aldosterone system (RAAS), hyper-coagulation and chronic inflammation are common conditions observed among OC and severe cases of COVID-19. The upregulation of common inflammatory cytokines and chemokines such as tumor necrosis factor α (TNF-α), interleukin (IL)-1β, IL-2, IL-6, IL-10, interferon-γ-inducible protein 10 (IP-10), granulocyte colony-stimulating factor (G-CSF), monocyte chemoattractant protein-1 (MCP-1), macrophage colony-stimulating factor (M-CSF), among others in the sera of COVID-19 and OC subjects suggests potentially similar mechanism(s) involved in the hyper-inflammatory condition observed in both disease states. Thus, it is conceivable that the pathogenesis of OC may significantly contribute to the potential infection by SARS-CoV-2. Our understanding of the influence and mechanisms of SARS-CoV-2 infection on OC is at an early stage and in this article, we review the underlying pathogenesis presented by various comorbidities of OC and correlate their influence on SARS-CoV-2 infection.
由新型严重急性呼吸系统综合症冠状病毒 2（SARS-CoV-2）引起的 2019 年冠状病毒病（COVID-19）是全球主要的公共卫生关注点。癌症患者被认为易感染 SARS-CoV-2 感染，并且可能出现几种 COVID-19 症状。在这两种疾病中，免疫功能低下状态、慢性炎症环境持续存在以及合并症是共同的，这可能会影响患者的预后。尽管卵巢癌（OC）和 COVID-19 是完全不同原发性器官的疾病，但它们在微环境中具有相似的分子和细胞特征，表明存在潜在的协同作用，从而导致不良预后。在 COVID-19 相关病例中，全球女性住院和死亡人数低于男性；然而，与 OC 相关的合并症可能会增加女性 COVID-19 的风险。50-60 岁的女性患 OC 和 SARS-CoV-2 感染的风险更高。促性腺激素和雄激素水平升高、肾素-血管紧张素-醛固酮系统（RAAS）失调、高凝和慢性炎症是 OC 和 COVID-19 严重病例中常见的情况。常见的炎症细胞因子和趋化因子如肿瘤坏死因子-α（TNF-α）、白细胞介素（IL）-1β、IL-2、IL-6、IL-10、干扰素-γ诱导蛋白 10（IP-10）、粒细胞集落刺激因子（G-CSF）、单核细胞趋化蛋白-1（MCP-1）、巨噬细胞集落刺激因子（M-CSF）等在 COVID-19 和 OC 患者的血清中上调表明，在这两种疾病状态下观察到的高度炎症反应中可能存在潜在的相似机制。因此，可以想象 OC 的发病机制可能会显著影响 SARS-CoV-2 的潜在感染。我们对 SARS-CoV-2 感染对 OC 的影响和机制的理解处于早期阶段，在本文中，我们回顾了 OC 各种合并症所呈现的潜在发病机制，并将其对 SARS-CoV-2 感染的影响进行了关联。
