**2. Impact of diabetes on COVID-19 virus**

#### **2.1 Pathogenesis of COVID-19 virus**

SARS- CoV – 2 is an RNA virus that is the zoonotic source in origin. The transmission of the coronavirus is possible from person to person by respiratory droplets. The symptoms of COVID -19 are range from no signs to mild to moderate. The transmission of coronavirus is possible by specific procedures such as bronchoscopy, endotracheal intubation, and tracheostomy [6].

It enters the human body with S- glycoprotein receptors and binds with the host's ACE2 (Angiotensin-converting enzyme2) receptors, located on the cell membrane. S- Glycoprotein consisting of subunits of S1 and S2 that are found on spikes of the virus [7].

The volume of Furin is more in diabetic patients, which is believed to enhance the viral entry into the human body. The enrichment of the viral entry occurs by the S1 and S2 subunits of spike proteins. Other factors include an acidic environment, and the presence of proteases in diabetic patients increases the replication of the virus [8].

The entry of coronavirus in the body occurs via the pulmonary system. However, it spreads to the other organs comprised of lungs, kidneys, heart, and intestines [9]. Severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV) cause dangerous respiratory symptoms while other coronaviruses cause the common cold (**Figure 1**) [10].

After entry of the coronavirus into the human body, inflammation begins with the development of cytokines and chemokines. The presence of leukocytosis and

*Impact of Cardiovascular Diseases on the Outcome of Patients with COVID-19 DOI: http://dx.doi.org/10.5772/intechopen.101121*

**Figure 1.**

*The role of ACE2 in the regulation of angiotensin system and SARS-CoV-2 infection.*

elevated ESR, C- reactive protein levels is commonly observed in laboratory investigation, indicating coronavirus progression in the body [11].

## **2.2 Pathogenesis of diabetes mellitus**

A lack of insulin causes type 1 diabetes, and type 2 diabetes is caused by insulin resistance. The long-term rise of blood glucose levels causes glucotoxicity in body tissues. This mechanism causes chronic complications to include diabetic ketoacidosis (DKA). The treatment of insulin and sulfonylurea cause hypoglycemia [12].

The infection is the primary responsible factor in causing diabetic ketoacidosis and hyperglycemia; thus, it increases the requirement of insulin, leading to cause uncontrolled hyperglycemia. The presence of C-reactive proteins, plasminogen activator inhibitor-1 in laboratory investigations indicate the association of inflammation and diabetes [13].
