COVID-19 and central nervous system interplay: A big picture beyond clinical manifestation.

The coronavirus disease (COVID-19) caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV2) has been declared a pandemic. Global research updates confirm that the infected patients manifest a range of clinical symptoms and sometimes remain entirely asymptomatic, posing a greater threat to the people coming in contact. Despite several case reports coming up every day, our knowledge about the neurotropic mechanism of the SARS-CoV-2, immunological responses, and the mode of disease progression and mechanism of crosstalk between the central nervous system (CNS), heart, lungs, and other major organs is not complete. Report of anosmia, ataxia, dysgeusia, and altered psychological status of the infected COVID-19 patients offers some clue to the possible route of viral entry and multiplication. In this review, we have critically assessed the involvement of CNS dysregulation in COVID-19 patients. The probable mechanism of immunological responses, the impairment of the coagulation pathway, the onset of cytokine storm, its interplay with the HPA axis, and hypoxia are discussed in detail here. Based on the latest research findings and some case reports of hospitalized COVID-19 patients, it is evident that the CNS involvement in disease progression is alarming. Accurate and timely detection of viral load in CNS is necessary to allow prompt and effective treatment modalities.