The Impact of SARS-Cov-2 Virus Infection on the Endocrine System

Noel Pratheepan Somasundaram, Ishara Ranathunga, Vithiya Ratnasamy, Piyumi Sachindra Alwis Wijewickrama, Harsha Anuruddhika Dissanayake, Nilukshana Yogendranathan, Kavinga Kalhari Kobawaka Gamage, Nipun Lakshitha de Silva, Manilka Sumanatilleke, Prasad Katulanda, Ashley Barry Grossman, Noel Pratheepan Somasundaram, Ishara Ranathunga, Vithiya Ratnasamy, Piyumi Sachindra Alwis Wijewickrama, Harsha Anuruddhika Dissanayake, Nilukshana Yogendranathan, Kavinga Kalhari Kobawaka Gamage, Nipun Lakshitha de Silva, Manilka Sumanatilleke, Prasad Katulanda, Ashley Barry Grossman

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus has spread across the globe rapidly causing an unprecedented pandemic. Because of the novelty of the disease, the possible impact on the endocrine system is not clear. To compile a mini-review describing possible endocrine consequences of SARS-CoV-2 infection, we performed a literature survey using the key words Covid-19, Coronavirus, SARS CoV-1, SARS Cov-2, Endocrine, and related terms in medical databases including PubMed, Google Scholar, and MedARXiv from the year 2000. Additional references were identified through manual screening of bibliographies and via citations in the selected articles. The literature review is current until April 28, 2020. In light of the literature, we discuss SARS-CoV-2 and explore the endocrine consequences based on the experience with structurally-similar SARS-CoV-1. Studies from the SARS -CoV-1 epidemic have reported variable changes in the endocrine organs. SARS-CoV-2 attaches to the ACE2 system in the pancreas causing perturbation of insulin production resulting in hyperglycemic emergencies. In patients with preexisting endocrine disorders who develop COVID-19, several factors warrant management decisions. Hydrocortisone dose adjustments are required in patients with adrenal insufficiency. Identification and management of critical illness-related corticosteroid insufficiency is crucial. Patients with Cushing syndrome may have poorer outcomes because of the associated immunodeficiency and coagulopathy. Vitamin D deficiency appears to be associated with increased susceptibility or severity to SARS-CoV-2 infection, and replacement may improve outcomes. Robust strategies required for the optimal management of endocrinopathies in COVID-19 are discussed extensively in this mini-review.

Keywords: COVID-19; Endocrine; SARS-CoV2.

© Endocrine Society 2020.

Figures

Figure 1.
Figure 1.
Viral entry and cellular pathogenesis. The SARS-CoV-2 virus enters the respiratory tract via the epithelial cells in the nasal cavity (1). The virus binds via its membrane spike protein S, to the cell membrane protein ACE2 in lungs (2). TMPRSS2, another cell membrane protein, triggers cleavage of the S protein into 2 subunits (3). The S1 subunit promotes fusion of the viral envelope with the host cell membrane culminating endocytosis of the virus (4). The virus then releases its genomic RNA into the host cell (5). The viral RNA is translated into polyproteins pp1a and 1ab, both of which in turn undergo proteolysis by vital proteinases into small particles. In parallel, more genomic RNA are produced via the enzyme replicase (6). The genomic RNA gets transcribed into mRNA (7) and results in viral protein synthesis via translation (8). The replicated genomic RNA and the synthesized viral proteins are incorporated into virions in the RER and Golgi apparatus (9). The virions are ultimately released from the host cell as vesicles via exocytosis (10). pp1a and 1ab, viral replicase polyproteins; RER, rough endoplasmic reticulum; S, Spike protein; TMPRSS2, transmembrane protease serine 2.
Figure 2.
Figure 2.
Postulated mechanisms of vitamin D in prevention of COVID-19 infection. Vitamin D treatment inhibits the T-helper-1 cell (Th1) response, which reduces serum levels of pro-inflammatory cytokines and induces the production of anti-inflammatory Th2 cytokines. Vitamin D treatment downregulates the expression of DPP4/CD26, which may play a role in the virulence of the SARS-CoV-2. SARS-CoV-2 uses angiotensin-converting enzyme-2 (ACE2) for cellular entry. However, upregulation of ACE 2, protects against lipopolysaccharide induced acute lung injury. Vitamin D is found to be a negative endocrine regulator of RAAS. Vitamin D inhibited renin, ACE, and Ang II expression, and induced ACE2 levels. ACE2, converts angiotensin II to angiotensin 1-7. Upon binding AT1R, angiotensin II causes inflammation, fibrosis, and apoptosis. AT-(1-7) opposes the effects of angiotensin II by interacting with its own receptor. Red arrows indicates inhibitory action and green arrows, stimulatory action. ACE1, angiotensin-converting enzyme 1; ACE2, angiotensin-converting enzyme 2; AT1R, type 1 angiotensin 2 receptor; AT1-7, heptapeptide angiotensin (1-7); DPP4/CD26, dipeptidyl peptidase 4/cluster of differentiation 26; Th1, T helper 1 cells; Th2, T helper 2 cells.

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