Understanding novel COVID-19: Its impact on organ failure and risk assessment for diabetic and cancer patients

Abstract

The current pandemic outbreak of COVID-19 originated from Wuhan, China. It is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) with significant mortality and morbidity rate. The severe risk factors are commonly detected in patients of older age and with medical comorbidities like cancer and diabetes. Scientists and doctors have scrambled to gain knowledge about the novel virus and its pathophysiology in order to discover possible therapeutic regimens and vaccines for COVID-19. The therapeutic strategies like targeting the viral genome emphasize the promising approach to target COVID-19. Additionally, blocking the receptor, ACE2 via the neutralizing antibodies for viral escape that prevents it from entering into the cells provides another therapeutic regimen. In this review article, we have presented the effect of SARS-CoV-2 infection in comorbid patients and discussed organ failure caused by this virus. Based on the data available from the scientific literature and ongoing clinical trials, we have focused on therapeutic strategies. We hope that we would fill the gaps that puzzled the researchers and clinicians with the best of our knowledge collected for the betterment of the patients for the coming future.

Keywords: COVID-19; Clinical trials; Pandemic; SARS; SARS-CoV-2.

Graphical abstract

Fig. 1

Inhibition of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) entry, replication, and endocytosis. Angiotensin type I receptor (AT₁R) upregulates ADAM metallopeptidase domain 17 (ADAM17), that potentiates the shredding of angiotensin, converting enzyme 2 (ACE2) through ADAM17. Soluble ACE2 prevents the binding of SARS-CoV-2 with transmembrane bound ACE2. This could reduce the viral spread. Lopinavir and remdesivir inhibit RNA-dependent RNA polymerase (RdRp) and coronavirus main proteinase (3CL^pro). Arbidol inhibits the interaction between ACE2 of host and S protein membrane of SARS-CoV-2. Chloroquine and hydroxychloroquine inhibit entry, replication, and endocytosis of SARS-CoV-2. Camostat inhibits transmembrane serine protease 2 (TMPRSS2), which is important for the SARS-CoV-2 infection. TMPRSS2 is the host protein, and activates the spike proteins (S-protein) of SARS-CoV-2 by priming.

Fig. 2

Angiotensin converting enzyme (ACE) catalyzes the conversion of angiotensin I to angiotensin II. ACE2 catalyses the formation of angiotensin (1-9) and angiotensin (1-7) from angiotensin I and angiotensin II respectively.