Table 1.

The multifactorial etiology of the pathophysiology of LC.

Host Conditions	Viral Agents	Downstream Effects
Age Sex Ethnicity Genetic factors Metabolic/endocrine diseases Chronic inflammation Immunological imbalances/autoimmune diseases	Occult persistence of the SARS-CoV-2 virus Persistence of SARS-CoV-2 viral components Reactivation of latent viruses [(Epstein–Barr virus (EBV), Cytomegalovirus (CMV), human immunodeficiency virus (HIV), herpes simplex virus 1, human herpesvirus 6 (HHV-6), and human herpesvirus 7 (HHV-7)]	Grade of lesions from primary acute SARS-CoV-2 infection Vascular endothelial abnormalities Microclots Thromboses Dysfunctional neurological signaling Reduction in tissue oxygen/hypoxia Disruption of the intestinal microbiome