Mitochondria in SARS-CoV-2 infection: Immune interactions and molecular approaches in the Post COVID-19 condition

Abstract

Abstract Mutations in mitochondrial genes can disrupt key cellular functions and contribute to the development of various complex diseases. The pandemic of COVID-19, caused by the SARS-CoV-2 infection, has been associated as the cause of certain mitochondrial dysfunctions, including physiological and genetic due to infection processes as increased release of reactive oxygen species (ROS), formation of the NLR family pyrin domain containing 3 (NLRP3) inflammasome, mitophagy impairment and mitochondrial apoptotic pathway. This review compiled the main interactions between SARS-CoV-2 infection and mitochondria, highlighting mainly the genetic and immunological mechanisms that contribute to the progression of the disease and how the persistence of this inflammatory and dysfunctional state can lead to cardiac, muscular and neurological sequelae, characterizing the post COVID-19 condition.