Widespread neurological and psychiatric sequalae of COVID-19 have been reported affecting all age groups [1] with presence of low-grade chronic inflammation and down-regulated ACE-2 levels making the individual more vulnerable for severe neurological effects of COVID-19 [2] as there will be greater disruption of the blood-brain barrier and hyper inflammation. Systemic immune inflammation index (SII) including neutrophil, platelet and lymphocyte counts serve as potential biomarkers to find an individual's risk of neurological effects of . SARS-CoV2 has been shown to affect the immune pathways associated with the central nervous system (CNS) and the peripheral nervous system (PNS) leading to long-term neurological sequelae [3]. Intracranial hemorrhage, ischemic stroke, parkinsonism, dementia, anxiety disorders and psychotic disorders have been reported as sequalae of . A recently published retrospective cohort study on the neurological and psychiatric sequalae of COVID-19 in 236,379 patients [5] has shown that the incidence of ischemic stroke in about 10% of patients, majority with COVID-19 associated encephalopathy which is alarming and necessitates steps to prevent or manage in those already affected. Werner et al. [6] have reported yet another neurological sequala, incidence of transient global amnesia during the COVID-19 hypothesizing the mechanism to be an encephalitic autoimmune pathology by the SARS CoV2 virus. Neurological manifestations of COVID-19 are thus postulated to be due to the binding of SARS-CoV-2 to ACE-2 activating intracellular pattern recognition receptors (PRRs) which sense the pathogen associated molecular patterns (PAMPs) setting off maladapted immune responses leading to inflammatory and immune activities disrupting the coagulation-embolism pathways in the CNS and PNS [7]. The different types of cells in the CNS and PNS including the glial cells, neurons, endothelial and arterial smooth muscle cells are all affected leading to the neurological manifestations of . However, the effects of SARS-CoV2 on human astrocytes, especially the microglia being the key-players in neural inflammation [6] makes us specifically focus on microglia in the context of conditions that involve neural-inflammation such as stroke, Parkinson's disease, Alzheimer's etc. For recovery, optimal functioning of the neuroglia is essential for synaptic organization, neurotrophic support, phagocytosis of apoptotic cells, debris removal, myelin turnover, control of neuronal Contents lists available at ScienceDirect