This review investigates links between post-acute sequelae of SARS-CoV-2 infection (PASC), post-infection viral persistence, mitochondrial involvement and aberrant innate immune response and cellular metabolism during SARS-CoV-2 infection. Advancement of proteomic and metabolomic studies now allows deeper investigation of alterations to cellular metabolism, autophagic processes and mitochondrial dysfunction caused by SARS-CoV-2 infection, while computational biology and machine learning have advanced methodologies of predicting virus–host gene and protein interactions. Particular focus is given to the interaction between viral genes and proteins with mitochondrial function and that of the innate immune system. Finally, the authors hypothesise that viral persistence may be a function of mitochondrial involvement in the sequestration of viral genetic material. While further work is necessary to understand the mechanisms definitively, a number of studies now point to the resolution of questions regarding the pathogenesis of PASC.

Quantitative assessment of mitochondrial DNA copy number is an emerging field of study in the diagnosis and evaluation of age-related pathology and frailty in the elderly, along with the assessment of other acute and chronic diseases that are often necessary within this patient cohort. Aim: to analyze current advances in the quantitative assessment of mitochondrial DNA copy number as a tool for diagnosing and evaluating age-related pathology, frailty, and comorbid conditions in the elderly. Material and methods. The author independently conducted a thorough review of literature available from the NIH, PubMed database, providing a detailed narrative of updates in the field. As clinical trials seek to further develop practical techniques, the author then undertook a search of relevant trials at ClinicalTrials.gov, including this as a table in the body text. Results. The review provides a thorough examination of the theoretical foundation of mitochondrial biogenesis, fusion-fission processes, and control and repair of mitochondrial genetic material, and how advances in these topics may be applied to better understand the processes being measured in quantitative mitochondrial DNA analysis. Conclusions. Detailed examination of the crosstalk between mitochondrial control proteins and nuclear factors, and the fundamental role of energy homeostasis apparatus within ageing processes underpins the advances in translational aspects of mitochondrial medicine and allows more effective exploitation of this emerging field.

Idiopathic pulmonary fibrosis (IPF) is characterised by a variable and unpredictable clinical course. While GAP (gender, age, physiology) score remains the

The state of mitochondrial homeostasis, comprising the processes of mitochondrial biogenesis, selective removal of damaged or dysfunctional mitochondria, mitochondrial dynamics (fusion and fission), as well as signaling systems of mitochondrial metabolism regulation are analyzed in this review. Particular attention is paid to how the bioenergetic demands of tissues are modulated in viral SARS-CoV, hepatitis B, C infections and asthma. Keywords: fusion and fission, hepatitis, metabolism, mitochondrial homeostasis, mitogenesis, mitophagy, SARS‑CoV-2