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Table of Contents
LETTER TO THE EDITOR
Year : 2020  |  Volume : 11  |  Issue : 2  |  Page : 113-114

Systemic effects of SARS-CoV: A brief insight


1 Department of Pathology, King George's Medical University, Lucknow, Uttar Pradesh, India
2 Department of Microbiology, King George's Medical University, Lucknow, Uttar Pradesh, India

Date of Submission30-Mar-2020
Date of Decision02-Apr-2020
Date of Acceptance03-May-2020
Date of Web Publication10-Jun-2020

Correspondence Address:
Dr. Atin Singhai
Department of Pathology, King George's Medical University, Lucknow, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/INJMS.INJMS_18_20

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How to cite this article:
Singhai A, Jain P. Systemic effects of SARS-CoV: A brief insight. Indian J Med Spec 2020;11:113-4

How to cite this URL:
Singhai A, Jain P. Systemic effects of SARS-CoV: A brief insight. Indian J Med Spec [serial online] 2020 [cited 2020 Aug 13];11:113-4. Available from: http://www.ijms.in/text.asp?2020/11/2/113/286346



Dear Editor,

SARS-CoV2 was first reported in China where several cases of pneumonia were reported in December 2019. The virus causes a disease called COVID-19 that has already been declared a pandemic by the WHO, and truly living to declaration, it has engulfed almost all the countries across the globe. In trending situation, it becomes imperative to know immunopathogenesis and systemic effects of SARS-CoV infection. Primarily, it presents with fever and respiratory symptoms; however, in few cases, it rapidly progresses to multisystemic disease with widespread extrapulmonary dissemination, resulting in viral shedding in respiratory secretions, stools, urine, cerebrospinal fluid (CSF), and even sweat.[1]

Coronaviruses, in general, exercise their pathogenicity by an innate immune response that involves moderate (TNF-α/IL-6) to significant (MIP-1α/RANTES/IP-10/MCP-1) upregulation of proinflammatory cytokines. They escape inhibition by IFN-β by interfering with its activation by IFN regulatory factor 3.[2]

Infected patients demonstrate lymphopenia and thrombocytopenia, which is attributed to SARS-CoV-induced apoptosis of uninfected-related blood cells, thereby also causing prolongation of coagulation profiles. These changes are manifested in the spleen as white pulp atrophy and in the liver as mildly elevated serum hepatic enzymes.[2]

Pulmonary involvement by SARS-CoV proceeds through stages of viral replication, immune hyperactivity, and ultimately pulmonary destruction manifested by diffuse alveolar damage, epithelial cells proliferation, and increase of macrophages. This results in the formation of multinucleated giant cells that lead to characteristic syncytium formation which entraps respiratory secretions, leading to severe respiratory distress.[1]

Cardiovascular involvement by SARS-CoV proceeds through viral binding to angiotensin-converting enzyme 2 (ACE2) that downregulates its related protective pathways and leads to myocardial inflammation causing arrhythmias. In addition, it also increases likelihood of coronary plaque rupture and stent thrombosis in under-treatment cardiac patients, due to surge in proinflammatory cytokines activity.[3]

Acute renal impairment in SARS-CoV infection is rare but fatal, associated with significant mortality rates. It occurs as a part of spectrum of multiorgan failure, and renal biopsy findings typically show marked tubular necrosis without any significant glomerular changes. Viral shedding in urine has been reported in such cases.[4],[5]

SARS-CoV also replicates in enterocytes, but the upregulation of TGF-β and an antiapoptotic host cellular response ensures minimal disruption of intestinal mucosa, thereby clinically manifesting as only mild gastric upset and diarrhea. However, viral shedding in stools is also reported.[4]

SARS-CoV has been isolated in the CSF of those infected patients presenting with convulsions. It has been shown to infect human astrocytes and microglia in primary cultures as well as immortalized glial cells.[4]

There is no consensus literature of musculoskeletal involvement by SARS-CoV, but it renders patients of myasthenia gravis and alike diseases at fatal risk of severe respiratory distress.[4]

There are preliminary reports of SARS-CoV affecting male gonadal function through viral binding to ACE2 receptors, resulting in the increase of serum luteinizing hormone (LH) but decreased testosterone to LH and follicle-stimulating hormone-to-LH ratios. SARS-CoV is not found to have any deleterious effects on pregnancy.[4],[6]

The above-presented brief commentary of systemic manifestations of COVID is an attempt to guide and alert treating physicians for impending multiorgan involvement in SARS-CoV infection.

Financial support and sponsorship

None.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Xu Z, Shi L, Wang Y, Zhang J, Huang L, Zhang C, et al. Pathological findings of COVID-19 associated with acute respiratory distress syndrome. Lancet Respir Med 2020;8:420-2.  Back to cited text no. 1
    
2.
Perlman S, Dandekar AA. Immunopathogenesis of coronavirus infections: Implications for SARS. Nat Rev Immunol 2005;5:917-27.  Back to cited text no. 2
    
3.
Xiong TY, Redwood S, Prendergast B, Chen M. Coronaviruses and the cardiovascular system: Acute and long-term complications. Eur Heart J 2020;41:1798-800.  Back to cited text no. 3
    
4.
Gu J, Korteweg C. Pathology and pathogenesis of severe acute respiratory syndrome. Am J Pathol 2007;170:1136-47.  Back to cited text no. 4
    
5.
Huang C, Wang Y, Li X, Ren L, Zhao J, Hu Y, et al. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet 2020;395:497-506.  Back to cited text no. 5
    
6.
Ling MA, Xie W, Li D, Shi L, Mao Y, Xiong Y, et al. Effect of SARS-CoV-2 infection upon male gonadal function: A single center-based study. medRxiv; 2020.  Back to cited text no. 6
    




 

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