Impact of tumor environments on susceptibility and disease progression in people infected with SARS-CoV-2


Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has infected 270 million people worldwide and killed more than 5.3 million people. Cancer patients are particularly vulnerable to infections with SARS-CoV-2, according to studies. Apart from this, advanced age (≥ 60 years), a history of smoking, obesity, high blood pressure, cardiovascular disease, and diabetes are all characteristics that have been consistently linked to a higher risk of COVID disease. -19 severe and / or death from cancer patients.

To study: Immune mechanisms in cancer patients that lead to poor outcome from SARS-CoV-2 infection. Image Credit: creativeneko / Shutterstock

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

Recent studies have shown that adverse outcomes in cancer patients infected with COVID-19 may be caused by changes in the expression of host proteins that promote entry of SARS-CoV-2, a cytokine profile abnormal, lymph node thrombosis, T / B cell damage and altered inflammasome response – especially NLRP3 inflammasome.

A review published in Translation search conducted by a team of researchers from Emory University is evaluating the impact of “hot” versus “cold” immune / tumor environments (and associated therapies) on susceptibility and disease course in subjects with these two types of tumors and infected with SARS-CoV-2 to decipher the mechanisms that lead to these adverse outcomes in cancer patients infected with COVID-19. The processes described below may aid in the development of targeted therapies that stimulate anti-cancer responses while limiting the severity of COVID-19 disease.

The study

It has been proven in numerous studies that COVID-19 with “pre-existing diseases”, especially cancer, has higher death rates than the “healthy” population. The 19 million new cases of cancer predicted (mainly breast, lung, colorectal, prostate, skin and stomach cancers), the ten million deaths and the increased risk of infection in 2020 makes understanding the immunological interaction between cancer and SARS-CoV-2 infection crucial. .

In addition, important signaling pathways affected by SARS-CoV-2 infection are elevated in cancer patients with COVID-19, including cytokine signaling, type I interferon signaling, receptor signaling androgens, as well as signaling immunological checkpoints. Unraveling the complicated links between the immune responses caused by various types of cancer and infection with SARS-CoV-2 has been an ongoing problem in the field and will be discussed in more detail in the following sections.

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

In addition, the expression of transmembrane serine protease 2 (TMPRSS2), a membrane-bound serine protease that acts in tandem with ACE2 to increase the entry of SARS-CoV-2, is elevated in cancer of the prostate, where it is induced by the androgen receptor (AR).

In two recent studies, patients with prostate cancer (cancer of the common cold) who were not treated with androgen deprivation therapy (ADT) were more likely to get SARS-CoV-2, suggesting a link between increased expression of TMPRSS2 and the development of severe COVID-19 in patients with cold tumors such as prostate cancer. Based on these results, it is possible that elevated expression of ACE2 and TMPRSS2, primarily due to pro-inflammatory conditions, in patients with variables related to lung cancer risk, could lead to titers. virals and the development of severe COVID-19.

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

Lung cancer (a burning cancer) has an active but weakened and / or fatigued lung tumor microenvironment (TME), resulting in a weakened innate immune response to SARS-CoV-2 infection. MTCT in lung cancer, which is infiltrated by immune cells and chronically inflamed, has an immunologically activated profile that may promote the disruption of innate immune responses against SARS-CoV-2 in the lungs.

Additionally, tumor cells can experience cytokine storms due to many underlying causes, which could affect the innate immune responses generated against SARS-CoV-2 infection and the severity of COVID-19. On the other hand, the disruption of the innate immune response following infection with SARS-CoV-2 can promote the growth of lung cancer and / or other cancers.


The current COVID-19 pandemic is affecting people who have a pre-existing immunocompromised profile (eg, cancer patients). Because cancer populations are so diverse (in terms of tumor type and treatment), inconsistent reports of negative results from SARS-CoV-2 infection have been recorded. The development of treatments that can prevent negative outcomes and promote healthy recovery will be facilitated by mechanical knowledge of the progression of infections in homogeneous cancer populations.


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