Mitochondria in SARS-CoV-2 infection: Immune interactions and molecular approaches in the Post COVID-19 condition, 2026, Barros et al.

[Chandelier]

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

Spoiler: Authors

Barros, Maria Clara; Souza, Felipe Gouvêa de; Costalat, Helenize; Pinho, Catarina Torres; Marques, Karina Carvalho; Epifane-de-Assunção, Matheus; Cavalcante, Giovanna C.; Falcão, Luiz Fábio Magno; Quaresma, Juarez A. S.; Ribeiro-dos-Santos, Ândrea

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.

Web | DOI | PMC | PDF | Genetics and Molecular Biology | Open Access

 

[Chandelier]

Figure 1 -
Mitochondrial genome and the variants already associated with severe COVID.
Protein-coding genes are represented in light blue, while other regions are portrayed in gray. In red, there are the mitochondrial variants associated with an increased risk of developing the severe form of covid and, in green, those associated with a protective effect. Source: Authors (created with Inkscape v.1.4.3).