Review SARS-CoV-2 Infection: A Possible Risk Factor for Incidence and Recurrence of Cancers
-
Abdollah Jafarzadeh
,
Rohit Gosain
,
Seyed Mohammad Javad Mortazavi
,
Maryam Nemati
,
Sara Jafarzadeh
,
Abbas Ghaderi
Abstract
COVID-19 and malignancy can affect the susceptibility of one another. Clinically recovered COVID-19 individuals display immune abnormalities that persist several months after discharge. The lymphopenia-related immunosuppression, functional exhaustion of cytotoxic lymphocytes (such as CD8+ cytotoxic T-cells and natural killer cells), hyperinflammatory responses, oxidative stress, downregulation of interferon response, development of the myeloid-derived suppressor cells, downregulation of tumor suppressor proteins and perhaps reactivation of the latent oncogenic viruses may directly and/or indirectly play a role in the cancer development and recurrence in severe COVID-19 patients. SARS-CoV-2-infected malignant patients may be at higher risk of death of their cancer than SARS-CoV-2-uninfected patients with the same cancers. On the other side, the patients with some types of cancers may be more vulnerable to SARS-CoV-2 infection compared with the non-cancerous individuals, due to their immunocompromised state resulted from malignancy, chemotherapy, and other concomitant abnormalities as well as perhaps greater expression of angiotensin-converting enzyme 2. SARS-CoV-2-infected cancerous patients are unable to produce an effective anti-virus immune response and may exhibit more severe forms of COVID-19. This review described the possible impacts of SARS-CoV-2 infection on cancer development and recurrence, and the potential cancer impacts on COVID-19 development, while the possible interventions are highlighted.
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6. Greenhalgh T, Knight M, A'Court C, et al. Management of post-acute covid-19 in primary care. BMJ. 2020;370:m3026.
7. Honigsbaum M, Krishnan L. Taking pandemic sequelae seriously: from the Russian influenza to COVID-19 long-haulers. Lancet. 2020;396(10260):1389-1391.
8. Saini G, Aneja R. Cancer as a prospective sequela of long COVID-19. BioEssays. 2021;43(6):e2000331.
9. Marshall M. The lasting misery of coronavirus long-haulers. Nature. 2020;585(7825):339-341.
10. Desai A, Sachdeva S, Parekh T, et al. COVID-19 and Cancer: Lessons From a Pooled Meta-Analysis. JCO Global Oncol. 2020;6:557-559.
11. Hu Y, Sun J, Dai Z, et al. Prevalence and severity of corona virus disease 2019 (COVID-19): A systematic review and meta-analysis. J Clin Virol. 2020;127:104371.
12. Richardson S, Hirsch JS, Narasimhan M, et al. Presenting Characteristics, Comorbidities, and Outcomes Among 5700 Patients Hospitalized With COVID-19 in the New York City Area. 2020;323(20):2052-2059.
13. Grasselli G, Zangrillo A, Zanella A, et al. Baseline Characteristics and Outcomes of 1591 Patients Infected With SARS-CoV-2 Admitted to ICUs of the Lombardy Region, Italy. JAMA. 2020;323(16):1574-1581.
14. Onder G, Rezza G, Brusaferro S. Case-Fatality Rate and Characteristics of Patients Dying in Relation to COVID-19 in Italy. JAMA. 2020;323(18):1775-1776.
15. Casey SC, Li Y, Felsher DW. An essential role for the immune system in the mechanism of tumor regression following targeted oncogene inactivation. Immunol Res. 2014;58(2-3):282-291.
16. Monzavi-Karbassi B, Pashov A, Kieber-Emmons T. Tumor-Associated Glycans and Immune Surveillance. Vaccines. 2013;1(2):174-203.
17. Sheikhi A, Jafarzadeh A, Kokhaei P, et al. Whole Tumor Cell Vaccine Adjuvants: Comparing IL-12 to IL-2 and IL-15. Iran J Immunol. 2016;13(3):148-166.
18. Jafarzadeh A, Minaee K, Farsinejad AR, et al. Evaluation of the circulating levels of IL-12 and IL-33 in patients with breast cancer: influences of the tumor stages and cytokine gene polymorphisms. Iran J Basic Med Sci. 2015;18(12):1189-1198.
19. Golubovskaya V, Wu L. Different Subsets of T Cells, Memory, Effector Functions, and CAR-T Immunotherapy. Cancers (Basel). 2016;8(3):36.
20. Spranger S. Mechanisms of tumor escape in the context of the T-cell-inflamed and the non-T-cell-inflamed tumor microenvironment. Int Immunol. 2016;28(8):383-91.
21.Yang J, Zhong M, Zhang E, et al. Broad phenotypic alterations and potential dysfunction of lymphocytes in individuals clinically recovered from COVID-19. J Mol Cell Biol. 2021;13(3):197-209.
22. Shuwa HA, Shaw TN, Knight SB, et al. Alterations in T and B cell function persist in convalescent COVID-19 patients. Med (N Y) . 2021;2(6):720-735.e4.
23. Kostopoulos IV, Orologas-Stavrou N, Rousakis P, et al. Recovery of Innate Immune Cells and Persisting Alterations in Adaptive Immunity in the Peripheral Blood of Convalescent Plasma Donors at Eight Months Post SARS-CoV-2 Infection. Microorganisms. 2021;9(3):546.
24. Palka-Kotlowska M, Custodio-Cabello S, Oliveros-Acebes E, et al. Review of risk of COVID-19 in cancer patients and their cohabitants. Int J Infect Dis. 2021;105:15-20.
25. Abdihamid O, Cai C, Kapesa L, et al. The Landscape of COVID-19 in Cancer Patients: Prevalence, Impacts, and Recommendations. Cancer Manag Res. 2020;12:8923-8933.
26. Xu H, Zhong L, Deng J, et al. High expression of ACE2 receptor of 2019-nCoV on the epithelial cells of oral mucosa. Int J Oral Sci. 2020;12(1):8.
27. Jafarzadeh A, Nemati M, Saha B, et al. Protective Potentials of Type III Interferons in COVID-19 Patients: Lessons from Differential Properties of Type I- and III Interferons. Viral Immunol. 2021;34(5):307-320.
28. Vabret N, Britton GJ, Gruber C, et al. Immunology of COVID-19: current state of the science. Immunity. 2020;52(6):910-941.
29. Zou X, Chen K, Zou J, et al. Single-cell RNA-seq data analysis on the receptor ACE2 expression reveals the potential risk of different human organs vulnerable to 2019-nCoV infection. Front Med. 2020;14(2):185-192.
30. Baig AM, Khaleeq A, Ali U, et al. Evidence of the COVID-19 Virus Targeting the CNS: Tissue Distribution, Host-Virus Interaction, and Proposed Neurotropic Mechanisms. A ACS Chem Neurosci. 2020;11(7):995-998.
31. Vellingiri B, Jayaramayya K, Iyer M, et al. COVID-19: A promising cure for the global panic. Sci Total Environ. 2020;725:138277.
32. Fu Y, Cheng Y, Wu Y. Understanding SARS-CoV-2-Mediated Inflammatory Responses: From Mechanisms to Potential Therapeutic Tools. Virol Sin. 2020;35(3):266-271.
33. Jafarzadeh A, Nemati M, Jafarzadeh S. Contribution of STAT3 to the pathogenesis of COVID-19. Microb Pathog. 2021;154:104836.
34. Chen K, Xiao F, Hu D, et al. SARS-CoV-2 Nucleocapsid Protein Interacts with RIG-I and Represses RIG-Mediated IFN-β Production. Viruses. 2020;13(1):47.
35. Zheng Y, Zhuang MW, Han L, et al. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) membrane (M) protein inhibits type I and III interferon production by targeting RIG-I/MDA-5 signaling. Signal Transduct Target Ther. 2020;5(1):299.
36. van den Berg DF, te Velde AA. Severe COVID-19: NLRP3 Inflammasome Dysregulated. Front Immunol 2020;11:1580.
37. Page EM, Ariëns RAS. Mechanisms of thrombosis and cardiovascular complications in COVID-19. Thromb Res. 2021;200:1-8.
38. Ojo AS, Balogun SA, Williams OT, et al. Pulmonary Fibrosis in COVID-19 Survivors: Predictive Factors and Risk Reduction Strategies. Pulm Med. 2020;2020:6175964.
39. Jafarzadeh A, Jafarzadeh S, Nozari P, et al. Lymphopenia an important immunological abnormality in patients with COVID-19: Possible mechanisms. Scand J Immunol. 2021;93(2):e12967.
40. Yao Z, Zheng Z, Wu K, et al. Immune environment modulation in pneumonia patients caused by coronavirus: SARS-CoV, MERS-CoV and SARS-CoV-2. Aging (Albany NY). 2020;12(9):7639-7651.
41. Jeffers SA, Tusell SM, Gillim-Ross L, et al. CD209L (L-SIGN) is a receptor for severe acute respiratory syndrome coronavirus. Proc Natl Acad Sci U S A. 2004;101(44):15748-15753.
42. Yang ZY, Huang Y, Ganesh L, et al. pH-dependent entry of severe acute respiratory syndrome coronavirus is mediated by the spike glycoprotein and enhanced by dendritic cell transfer through DC-SIGN. J Virol. 2004;78(11):5642-5650.
43. Koch C, Staffler G, Huttinger R, et al. T cell activation-associated epitopes of CD147 in regulation of the T cell response, and their definition by antibody affinity and antigen density. Int Immunol. 1999;11(5):777-786.
44. Wang K, Chen W, Zhou YS, et al. SARS-CoV-2 invades host cells via a novel route: CD147-spike protein. BioRxiv. 2020. 988345.
45. Park A, Iwasaki A. Type I and Type III Interferons - Induction, Signaling, Evasion, and Application to Combat COVID-19. Cell Host Microbe. 2020;27(6):870-878.
46. Zhao Y, Hu J, Li R, et al. Enhanced NK cell adoptive antitumor effects against breast cancer in vitro via blockade of the transforming growth factor-beta signaling pathway. Onco Targets Ther. 2015;8:1553-9.
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| Files | ||
| Issue | Vol 16, No 2 (2022) | |
| Section | Review Article(s) | |
| DOI | https://doi.org/10.18502/ijhoscr.v16i2.9205 | |
| Keywords | ||
| COVID-19; Cancer; SARS-CoV-2; Immunosuppression; Inflammation; Oncology; Malignancy | ||
| Rights and permissions | |
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This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License. |
How to Cite
1.
Jafarzadeh A, Gosain R, Mortazavi SMJ, Nemati M, Jafarzadeh S, Ghaderi A. Review SARS-CoV-2 Infection: A Possible Risk Factor for Incidence and Recurrence of Cancers. Int J Hematol Oncol Stem Cell Res. 2022;16(2):117-127.
