SARS-CoV-2 (COVID-19) Morbidity and Chronic Disease (Type II Diabetes –T2D) and Pancreatic Carcinoma: Clinco-epidemiologic Perspective

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Laurens Holmes, Jr Kerti Deepika Janille Williams Benjamin Ogundele Glen Philipcien Michael Enwere Shikha Jain Naresh Dasari Ram Sanjiv Alur Ramesh Adhikari Gbadebo Ogungbade


Purpose: Viral infections had been historically observed in chronic disease development and complications including although not limited to hepatitis C, influenza A, cytomegalovirus (CMV), Epstein bar virus (EBV), HIV and herpes simplex. Epidemiologic data had implicated CMV, herpes simplex and hepatitis C in type II diabetes (T2D). With the observed increased incidence T2D in COVID-19 among children and adults, this review aimed to examine scientific literature on immune and endocrine systems dysregulation in T2D and pancreatic neoplasm. 

Materials & Method: A qualitative systematic review (QSR) was utilized in assessing the immune system deregulation and endocrine system involvement in chronic disease development such as T2D. The PubMed was the main search engine in studies identification with several search terms such as “SARS-CoV-2 and T2D”, “COVID-19 and T2D”, SARS-CoV-2 and insulin resistant”, etc.  

Results: Viral pathogens such as CMV, influenza A, and herpes simplex and hepatitis C infections have been implicated in decreased insulin sensitivity (IS) and increased insulin resistant (IR). Similarly, these pathogenic microbes increased the T2D incidence and complications. SARS-CoV-2 a COVID-19 causative pathogen had been observed in increased risk and incidence of T2D among children and adults. While data are not currently available on the precise mechanistic process, SARS-CoV-2 viral infection in T2D incidence may be explained by excess pro-inflammatory cytokines elaboration (cytokine storm) resulting in increased IR and decreased IS, leading to glucose intolerance and T2D. Further COVID-19 may increase pancreatic neoplasm in populations with increased incidence of COVID-19, due to pancreatic beta cells and insulin receptors dysregulation and cellular dysfunctionality as abnormal cellular proliferation.

Conclusions/Recommendation: SARS-CoV-2 a causative pathogen in COVID-19 morbidity is associated with increased incidence of T2D, which is explained in part by immune and endocrine system integration dysregulation, resulting in cytokine storm, decreased IS and increased IR, implying glucose intolerance and T2D. Additionally this pathogenic microbe may result in increasing incidence of pancreatic neoplasm, a malignant neoplasm with the worst prognosis and excess mortality due to late stage at diagnosis and marginalized biomarkers of susceptibility and morbidity.  

Keywords: COVID-19, SARS-CoV-2, Type II Diabetes, Increased Insulin resistance, Decreased Insulin Sensitivity

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HOLMES, JR, Laurens et al. SARS-CoV-2 (COVID-19) Morbidity and Chronic Disease (Type II Diabetes –T2D) and Pancreatic Carcinoma: Clinco-epidemiologic Perspective. Medical Research Archives, [S.l.], v. 10, n. 6, june 2022. ISSN 2375-1924. Available at: <>. Date accessed: 20 apr. 2024. doi:
Research Articles


1. O’Connor SM, Taylor CE, Hughes JM. Emerging Infectious Determinants of Chronic Diseases. Emerging Infectious Diseases. 2006;12(7):1051-1057. doi:10.3201/eid1207.060037
2. Rasa S, Nora-Krukle Z, Henning N, et al. Chronic viral infections in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). Journal of Translational Medicine. 2018;16(1). doi:10.1186/s12967-018-1644-y
3. Valaiyapathi B, Gower B, Ashraf AP. Pathophysiology of Type 2 Diabetes in Children and Adolescents. Current Diabetes Reviews. 2018;14. doi:10.2174/1573399814666180608074510
4. Remedi MS, Emfinger C. Pancreatic β-cell identity in diabetes. Diabetes, Obesity and Metabolism. 2016;18:110-116. doi:10.1111/dom.12727
5. Bensellam M, Jonas JC, Laybutt DR. Mechanisms of β-cell dedifferentiation in diabetes: recent findings and future research directions. The Journal of endocrinology. 2018;236(2):R109-R143. doi:10.1530/JOE-17-0516
6. Smatti MK, Cyprian FS, Nasrallah GK, Al Thani AA, Almishal RO, Yassine HM. Viruses and Autoimmunity: A Review on the Potential Interaction and Molecular Mechanisms. Viruses. 2019;11(8):762. doi:10.3390/v11080762
7. Burrell CJ, Howard CR, Murphy FA. Viral Syndromes. Fenner and White’s Medical Virology. Published online 2017:537-556. doi:10.1016/B978-0-12-375156-0.00039-4
8. Houen G, Trier NH. Epstein-Barr Virus and Systemic Autoimmune Diseases. Frontiers in Immunology. 2021;11. doi:10.3389/fimmu.2020.587380
9. Parikh HM, Elgzyri T, Alibegovic A, et al. Relationship between insulin sensitivity and gene expression in human skeletal muscle. BMC Endocrine Disorders. 2021;21(1). doi:10.1186/s12902-021-00687-9
10. Kälsch J, Bechmann LP, Heider D, et al. Normal liver enzymes are correlated with severity of metabolic syndrome in a large population-based cohort. Scientific Reports. 2015;5(1).

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