Tue. Jul 5th, 2022

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has infected 270 million people worldwide and killed over 5.3 million people. According to studies, cancer patients are particularly vulnerable to SARS-CoV-2 infections. Apart from this, older age (≥60 years), a history of smoking, obesity, hypertension, cardiovascular disease and diabetes are all characteristics that have been consistently related to a higher risk of severe COVID-19 disease and / or death from cancer. patients.

Study: Immune mechanisms in cancer patients leading to poor outcomes of SARS-CoV-2 infection.  Image credit: creativeneko / ShutterstockStudy: Immune mechanisms in cancer patients leading to poor outcomes of SARS-CoV-2 infection. Image credit: creativeneko / Shutterstock

The severity of coronavirus disease 2019 (COVID-19) disease in cancer patients is determined in part by the etiology of the tumor, type (heat vs. cold tumors, where hot tumors have an immunologically active microenvironment), stage, and anatomical location. Together with treatment regimens, these factors play an important role in the diversification of the immune landscape for a malignancy. COVID-19 patients with hot tumors are more likely to develop severe COVID-19 disease, according to research.

Recent studies have shown that adverse outcomes in COVID-19 infected cancer patients may be due to changes in the expression of host proteins that promote SARS-CoV-2 penetration, an abnormal cytokine profile, lymph node thrombosis, impaired T / B cell responses and decreased inflammatory response – especially the NLRP3 inflammatory.

A review published in Translational research conducted by a team of Emory University researchers assessing the impact of “heat” vs. “Cold” immune / tumor environments (and associated therapies) on susceptibility and disease course in individuals with these two types of tumors and infected with SARS-CoV-2 suggest the mechanisms driving these adverse outcomes in COVID-19 infected cancer patients. The processes outlined below can help with the development of targeted therapies that increase anti-cancer responses while limiting the severity of COVID-19 disease.

The study

COVID-19 with ‘pre-existing diseases’, especially cancer, has been shown in several studies to have higher mortality rates than the “healthy” population. The predicted 19 million new cancers (with breast, lung, colorectal, prostate, skin and stomach cancer), ten million deaths and increased risk of infection by 2020 make the understanding of the immunological interaction between cancer and SARS-CoV-2 -infection essential.

In addition, significant signaling pathways affected by SARS-CoV-2 infection are elevated in cancer patients with COVID-19, including cytokine signaling, type-I interferon signaling, androgen receptor signaling, and immunological checkpoint signaling. Resolving the complex relationships between the immunological responses caused by different cancers and SARS-CoV-2 infection has been a persistent problem for the field and will be investigated further in the following sections.

To fully understand the impact of these different cancer etiologies on COVID-19 outcomes, it is necessary to first understand their impact on SARS-CoV-2 onset / infection and any existing or subsequent immune cascades. Angiotensin-converting enzyme 2 (ACE2) expression in pulmonary epithelial cells was higher in elderly people, smokers and / or people with smoking-related diseases, including chronic obstructive pulmonary disease (COPD).

Furthermore, expression of transmembrane serine protease 2 (TMPRSS2), a membrane-bound serine protease that works with ACE2 to increase SARS-CoV-2 entry, is high in prostate cancer where it is induced by androgen receptor (AR).

In two recent studies, patients with prostate cancer (cold cancer) who were not treated with androgen deprivation therapy (ADT) were more likely to develop SARS-CoV-2, suggesting an association between increased TMPRSS2 expression and the development of Severe COVID-19 in patients with cold tumors such as prostate cancer. Based on these results, it is possible that increased ACE2 and TMPRSS2 expression, primarily due to pro-inflammatory conditions, in patients with variables associated with lung cancer risk may lead to higher viral titers and the development of severe COVID-19.

There is very little information on SARS-CoV-2-specific innate immune responses in cancer patients. Patients with malignancies have a weakened innate immune response, making them more susceptible to SARS-CoV-2 infection. Due to the improved immunologically compromised environment of hot malignancies compared to cold tumors, higher rates of COVID-19 adverse outcomes caused by dysregulated congenital immune responses are more likely in patients with hot cancers than in patients with cold cancers.

Lung cancer (a hot cancer) has an active but weakened and / or tired lung tumor microenvironment (TME), resulting in a weakened congenital immune response to SARS-CoV-2 infection. TME in lung cancer, which is infiltrated with immune cells and chronically inflamed, has an immunological activation profile that can promote dysregulation of innate immune responses to SARS-CoV-2 in the lungs.

In addition, tumor cells may experience cytokine storms due to several underlying causes that may affect the innate immune responses generated against SARS-CoV-2 infection and the severity of COVID-19. On the other hand, dysregulation of the innate immune response due to SARS-CoV-2 infection may promote the growth of lung cancer and / or other cancers.


The current COVID-19 pandemic affects people with pre-existing immunocompromised profiles (eg cancer patients). Because cancer populations are so diverse (in terms of tumor type and treatment), inconsistent reports of adverse outcomes from SARS-CoV-2 infection have been reported. The development of treatments that can prevent adverse outcomes and promote healthy recovery will be aided by a mechanical knowledge of how infections develop in homogeneous cancer populations.


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