Musculoskeletal and neuromuscular dysfunction due to covid-19 infection: A review

Abstract

The emergence of the novel coronavirus-based illness, COVID-19, in late 2019 marked a watershed moment in modern history. Initially identified in Wuhan, China, this viral epidemic swiftly transformed into a global pandemic, affecting worldwide. The World Health Organization (WHO) officially labeled the virus as “Severe Acute Respiratory Syndrome Coronavirus 2” (SARS-CoV-2) and the ensuing disease as Coronavirus Disease 2019 (COVID-19) on February 11, 2020. The spectrum of effects induced by COVID-19 encompasses a diverse array of conditions, ranging from sensory disturbances like anosmia and ageusia to more intricate manifestations, including headaches and, alarmingly, multiorgan failure and neuromuscular dysfunction, and even deaths were reported. COVID-19 triggers a vigorous inflammatory response characterized by the overproduction of pro-inflammatory cytokines. “Cytokine storm” significantly underwrites the worsening of the condition of patients, resulting in abnormalities such as ARDS. The major reason behind mortality from COVID-19 is respiratory failure instigated by ARDS. Throughout the early respiratory contamination, SARS-CoV-2 was hypothesized to target type-II pneumocytes lining the respiratory passage that specifically expressed TMPRSS2 and ACE2 receptors. The extra-pulmonary consequences of COVID-19 have been linked to the occurrence of these receptors in the skeletomuscular and brain tissues. As a result, it is condemning to comprehend the unique pathophysiological mechanisms behind the virus's manner of invasion in the tissues and also the disease's consequences. In this article, we focus on the complications caused by COVID-19 on musculoskeletal and neural tissues, the route of invasion, and the future perspective of dealing with the receptors whose expression leads to COVID-19 infection.