Therefore, these GPCR-fAABs were studied recently on 31 individuals who had recovered from the acute phase of Covid-19 but were still suffering from long-Covid symptoms including neurological and heart problems. The tested people had 2-7 types of GPCR-fAABs acting on their target GPCRs. Some of them caused faster beating of heart cells including α1-adrenoceptor, β2adrenoceptor, nociceptin-like opioid receptor and angiotensin II AT1-receptor while some slower including muscarinic M2-receptor, MAS-receptor, and ETA-receptor. Scientists also think that these autoantibodies might be causing these long Covid symptoms . Furthermore, severe systematic inflammation is a major factor in SARS Cov-2 which occurs due to several pro-resolving lipid mediators i.e. SPMs. These mediators have shown positive results in treatment of various previous viruses including HIV, HSV and Hepatitis C virus which further necessitates further studies on them for their role in SARS Cov-2. According to research, these SPMs lead to inflammation via GPCRs which has been reviewed in a recent study . A recent study has stated the involvement of GPR4 which is a pro-inflammatory GPCR in the pathogenesis of Covid-19. It has highest expression in the endothelial cells and it works as a gatekeeper for endothelium and blood cells interaction regulation and for the infiltration of leukocytes. It is also responsible for the regulation of permeability of blood vessels and edema of tissues in case of inflammation. Therefore, antagonism of GPR4 is required for the mitigation of these hyper-inflammatory conditions etc. .