The COVID-19 pandemic, caused by the SARS-CoV-2 virus, has introduced the medical community to the phenomenon of long COVID, a condition characterized by persistent symptoms following the resolution of the acute phase of infection. Among the myriad of symptoms reported by long COVID sufferers, chronic fatigue, cognitive disturbances, and exercise intolerance are predominant, suggesting systemic alterations beyond the initial viral pathology. Emerging evidence has pointed to mitochondrial dysfunction as a potential underpinning mechanism contributing to the persistence and diversity of long COVID symptoms. This review aims to synthesize current findings related to mitochondrial dysfunction in long COVID, exploring its implications for cellular energy deficits, oxidative stress, immune dysregulation, metabolic disturbances, and endothelial dysfunction. Through a comprehensive analysis of the literature, we highlight the significance of mitochondrial health in the pathophysiology of long COVID, drawing parallels with similar clinical syndromes linked to post-infectious states in other diseases where mitochondrial impairment has been implicated. We discuss potential therapeutic strategies targeting mitochondrial function, including pharmacological interventions, lifestyle modifications, exercise, and dietary approaches, and emphasize the need for further research and collaborative efforts to advance our understanding and management of long COVID. This review underscores the critical role of mitochondrial dysfunction in long COVID and calls for a multidisciplinary approach to address the gaps in our knowledge and treatment options for those affected by this condition.

Background: Post-COVID manifestation is defined as persistent symptoms or long-term complications beyond 4 weeks from disease onset. Fatigue and memory impairment are common post-COVID symptoms. We aimed to explore associations between the timeline and severity of post-COVID fatigue and anti-SARS-CoV-2 antibodies. Methods: Fatigue and memory impairment were assessed in a total of 101 post-COVID subjects using the Chalder fatigue scale (CFQ-11) and a visual analogue scale. Using the bimodal scoring system generated from CFQ-11, a score ≥4 was defined as severe fatigue. Serum anti-SARS-CoV-2 spike (anti-S-Ig) and nucleocapsid (anti-NC-Ig) antibodies were examined at two time points: 4–12 weeks after onset of symptoms, and beyond 12 weeks. Results: The serum level of anti-S-Ig was significantly higher in patients with non-severe fatigue compared to those with severe fatigue at 4–12 weeks (p = 0.006) and beyond 12 weeks (p = 0.016). The serum level of anti-NC-Ig remained high in patients with non-severe fatigue at both time points. In contrast, anti-NC-Ig decreased significantly in severe fatigue cases regardless of the elapsed time (4–12 weeks: p = 0.024; beyond 12 weeks: p = 0.005). The incidence of memory impairment was significantly correlated with lower anti-S-Ig levels (−0.359, p < 0.001). Conclusion: The systemic immune response reflected by antibodies to SARS-CoV-2 is strongly correlated with the severity of post-COVID fatigue.

Background: The effect of post-vaccination adverse events on immunogenicity is unknown. We aimed to explore relationship between post-vaccination adverse reactions and antibody levels during 6-month follow-up. Methods: Blood was serially drawn from healthcare workers after the second dose of BNT162b2 mRNA vaccine (Day 12, 30, 60, 90, 120, 150, and 180) and anti-SARS-CoV-2 spike IgG (S-IgG) levels were measured. Following each vaccine dose, volunteers completed a questionnaire regarding adverse reactions (symptomatic vs. asymptomatic groups). Results: A total of 395 subjects received the second dose of the vaccine. The main results were as follows: (i) fever after the 2nd dose was independently associated with the median S-IgG level at all follow-up time points; (ii) significantly higher S-IgG levels were observed in the symptomatic group of patients without prior COVID-19 infection throughout the entire follow-up period; (iii) prior COVID-19 positivity resulted in higher S-IgG levels only in the asymptomatic group from Day 90 of the follow-up period; (iv) both prior COVID-19 disease with asymptomatic status and symptomatic status without prior COVID-19 infection resulted in similar S-IgG antibody levels; (v) significantly lower serum S-IgG levels were observed in smokers. Conclusion: Fever may play an important role in the post-vaccination immune response in the long term.

Background: Long COVID is a condition characterized by long-term sequelae persisting after the typical convalescence period of COVID-19. Previous reports have suggested the role of an unsatisfactory immune response and impaired viral clearance in the pathogenesis of long COVID syndrome. We focused on potential associations between post-vaccination changes of antibody titers and the severity of long COVID symptoms and factors influencing the state of remission observed in patients with long COVID after vaccination. Methods: The severity of long COVID symptoms and serum anti-SARS-CoV-2 spike (S-Ig) and nucleocapsid (NC-Ig) levels were assessed in 107 post-COVID subjects at two time points: at baseline, and 17–24 weeks later. Besides, vaccination status was also assessed. Symptoms were evaluated based on the Chalder fatigue scale (CFQ-11) and visual analogue scale (VAS). Results: Serum level of S-Ig and NC-Ig at baseline were significantly higher in the patients with non-severe fatigue than those with severe fatigue, and this difference remained significant at follow-up in the case of NC-Ig. NC-Ig level above median was as an independent predictor for complete remission at follow-up. The difference in NC-Ig levels in subgroup analyses (severe fatigue vs. non-severe fatigue; complete remission vs. incomplete remission or progression) was found to be significant only in patients who received vaccination. Conclusions: The immune response against the SARS-CoV-2 nucleocapsid may play a more important role than the spike in the course of long-term COVID syndrome.

Small scale observational evidence suggested that Vitamin E (VE) might play beneficial role in human and animal respiratory conditions of various origin by stabilizing surfactant functions. The intra-aleveolar VE level is directly proportionate to the lung’s response to inflammation. Electronic cigarette or vaping associated lung injury was a dominantly respiratory syndrome in the United States with seemingly strong association between potential Vitamin E acetate inhalation exposure and the onset of symptoms. This systematic review intended to assess if there was previous evidence of any potential respiratory/gastrointestinal toxicity associated with Vitamin E acetate or any of its derivatives. A systematic review was constructed and prospectively registered at PROSPERO to search important clinical databases between 2000 and 2020 for full text human articles investigating the effect of VEA or any of its derivatives administered via any route (oral/parenteral/aerosolised) in adults with any respiratory conditions. Out of 363 records investigating the effect of VEA and/or its derivatives/isomers in (any) lung injury (inflammatory, oxidative, infective, asthma/COPD) seven articles qualified. The papers reported various surrogate outcomes (APACHEII score, spirometry, etc) with equivocal results. There was one case report of harmful exposure to both Vitamin E (intramuscular) and Vitamin E acetate (topical). The present review found evidence of neither harm nor any significant clinical improvement associated with the administration of VEA or any derivatives via any route in adult inflammatory lung conditions however, the articles were of low-level evidence. Further studies are needed to correct flaws in research to explore the role of Vitamin E in pulmonology.

The pooled worldwide prevalence of low-back pain-related presentations in primary care varies between 6.8% and 28.4% in the high-income countries rendering it a major healthcare/economy problem. To best manage this complex bio-psycho-social condition a 360-degree approach is needed, as the psycho-social components are often more important than the scant pathophysiology. Pattern analysis of cannabis users suggested that attempts to alleviate musculo-skeletal pain is often seen as a major drive to use cannabinoids. Unlike NSAIDs/opioids, cannabidiol might directly affect more than one modality of pain signaling/perception. The 2019 guideline of the National Institute for Clinical Excellence recommended further studies with cannabidiol in pain medicine because of its excellent safety profile and presumed therapeutic potential. Therefore, we have researched relevant databases for pharmaco-physiological papers published between 2000 and 2021 to collate evidence in a narrative fashion to determine the clinical rationale for this cannabinoid in low-back pain. Observational research reported good results with CBD in pain and fear reduction, which are both key factors in low-back pain. Given the paucity of high-quality evidence, further research is needed to determine the efficacy/non-inferiority of CBD in primary/emergency care setting, using multimodal assessment of various patient-reported outcomes.