Journal
INTERNATIONAL IMMUNOPHARMACOLOGY
Volume 100, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.intimp.2021.108150
Keywords
Coronavirus; Purinergic signaling; ATP; Adenosine; Therapy
Categories
Ask authors/readers for more resources
COVID-19 is caused by a new member of the Coronaviridae family, the SARS-CoV-2 virus, which infects the respiratory tract by binding to ACE2 receptors. The infection triggers immune responses and cytokine storm, leading to severe respiratory symptoms and potential organ failure. Modulating purinergic receptors may offer a promising therapeutic approach to mitigate the severity of the disease.
The etiological agent of coronavirus disease (COVID-19) is the new member of the Coronaviridae family, a severe acute respiratory syndrome coronavirus 2 virus (SARS-CoV-2), responsible for the pandemic that is plaguing the world. The single-stranded RNA virus is capable of infecting the respiratory tract, by binding the spike (S) protein on its viral surface to receptors for the angiotensin II-converting enzyme (ACE2), highly expressed in the pulmonary tissue, enabling the interaction of the virus with alveolar epithelial cells promoting endocytosis and replication of viral material. The infection triggers the activation of the immune system, increased purinergic signaling, and the release of cytokines as a defense mechanism, but the response can become exaggerated and prompt the so-called cytokine storm, developing cases such as severe acute respiratory syndrome (SARS). This is characterized by fever, cough, and difficulty breathing, which can progress to pneumonia, failure of different organs and death. Thus, the present review aims to compile and correlate the mechanisms involved between the immune and purinergic systems with COVID-19, since the modulation of purinergic receptors, such as A2A, A2B, and P2X7 expressed by immune cells, seems to be effective as a promising therapy, to reduce the severity of the disease, as well as aid in the treatment of acute lung diseases and other cases of generalized inflammation.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available