Abstract:
Pain is one of the clinical manifestations that can vary from mild to severe symptoms in COVID-19 patients. Pain symptoms
can be initiated by direct viral damage to the tissue or by indirect tissue injury followed by nociceptor sensitization. The
most common types of pain that are reported to occur in COVID-19 patients are headache, myalgia, and chest pain. With
more and more cases coming in the hospitals, many new and unique symptoms of pain are being reported. Testicular and
abdominal pain are rare cases of pain that are also being reported and are associated with COVID-19. The SARS-CoV-2 virus
has a high afnity for angiotensin-converting enzyme-2 receptor (ACE-2) which acts as an entry point for the virus. ACE-2/
Ang II/AT 1 receptor also participates directly in the transmission of pain signals from the dorsal horn of the spinal cord.
It induces a series of complicated responses in the human body. Among which the cytokinetic storm and hypercoagulation
are the most prominent pathways that mediate the sensitization of sensory neurons facilitating pain. The elevated immune
response is also responsible for the activation of infammatory lipid mediators such as COX-1 and COX-2 enzymes for the
synthesis of prostaglandins (PGs). PG molecules especially PGE2 and PGD2 are involved in the pain transmission and are
found to be elevated in COVID-19 patients. Though arachidonic acid pathway is one of the lesser discussed topics in COVID19 pathophysiology, still it can be useful for explaining the unique and rarer symptoms of pain seen in COVID-19 patients.
Understanding diferent pain pathways is very crucial for the management of pain and can help healthcare systems to end the
current pandemic situation. We herein review the role of various molecules involved in the pain pathology of COVID-19.
