Canadian Journal of Medicine

Myocarditis, or inflammation of the muscle layer in the heart wall, is caused by several factors including viral infection. Although the literature briefly alludes to a method of viral entry into cardiomyocytes, this work provides further detail into subsequent novel mechanisms leading to the development of myocarditis following infection by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The keywords "COVID-19”, “SARS-CoV-2”, “Myocarditis”, “viruses”, and “human” were used to run searches on OVID Medline, as well as Google Scholar. Resulting papers were subject to further analysis. SARS-CoV-2 binds to the angiotensin-converting enzyme 2 (ACE2) receptor which is found on type 2 pneumocytes and cardiomyocytes. Infection of cardiomyocytes can overregulate the immune response resulting in a cytokine storm: an uncontrolled increase of proinflammatory cytokines, as is commonly seen in respiratory infections. Cytokines can enter established biological pathways, creating positive feedback, which causes increased inflammation leading to myocarditis. SARS-CoV-2 viral envelope (E) proteins present an alternate association with myocarditis. Less severe myocarditis manifests common symptoms, and detecting it before it worsens may be difficult. Understanding the pathogenesis of myocarditis in COVID-19 could help find and implement preventative measures during future treatment.

Coronavirus disease (COVID-19) is an ongoing global pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Many systematic reviews and meta-analyses discussed the correlation of COVID-19 with a different disease. Given the urgent need for data, some meta-analyses containing datasets included many manuscripts, but their providence was not clearly reported. The possible overlap between some of the studies included in the analyses is a significant issue for conducting systematic reviews during the COVID-19 pandemic.

The current pandemic of COVID-19 is considered a worldwide threat to public health caused
by a novel type of coronaviridae family called SARS-CoV-2. Owing to the urge of finding a
treatment for this virulent virus, many aspects of drug development are swept aside. This
review aimed to clarify the double-edged sword of drug repurposing in COVID-19 via
summarizing the available treatment options and promising candidates for COVID-19 based
on drug repurposing preclinical studies and in-silico approach. Different drugs target SARS
CoV-2 main structures under clinical investigation; some showed limited efficacy and severe
side effects, while others can be promising solutions. Some drugs suppress the cytokine storm
and modulate immune response during viral infection, including anti-interleukin and
glucocorticoids. Antiparasitic agents are repurposed for SARS-CoV-2 infection management.
Various vaccines and monoclonal antibodies are designed against SARS-CoV-2 and are being
evaluated in different preclinical and clinical stages. However, none of them is approved yet.
Convalescent Plasma Transfusion is a promising strategy against SARS-CoV-2 infection,
where impressive results are reported in clinical trials, requiring more validation. Furthermore,
anticoagulant therapy exhibited better disease outcomes in patients admitted to the ICU.
Finally, in-silico studies suggested several potential compounds or FDA-approved drugs
targeting various viral structure subunits. In conclusion, although many clinical trials were
launched to examine potential therapies based on drug repurposing for COVID-19, there is no
definitive treatment till now. Moreover, computational approaches identified several
compounds and FDA-approved drugs with potential inhibitory effects.