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Background: Previous evidence showed that persons experiencing post‐COVID‐19 with "brain fog" were characterized by abnormal resting‐state electroencephalographic (rsEEG) rhythms reflecting vigilance dysfunctions. In the present exploratory study, we tested the hypothesis that in post‐COVID persons with normal cognitive status, abnormalities in those rhythms (and vigilance function) may be related to fatigue. Method: We enrolled post‐COVID participants about one year after their infection, which claimed "brain fog." They underwent clinical/neuropsychological assessment and 61‐channel‐EEG recordings. Matched controls (never COVID‐19 affected) were included. Using eLORETA freeware, regional neural current densities were estimated in the rsEEG cortical sources at individual delta, theta, and alpha bands and at beta and gamma fixed bands. Clinical and instrumental data were evaluated in the long COVID‐19 patients as a function of fatigue symptoms over the controls. Result: The post‐COVID patients had no cognitive deficits at the group level. Those patients showed lower posterior rsEEG alpha source activities than the controls. Notably, this effect was more significant with the long COVID‐19 patients experiencing fatigue symptoms than those without (Fig. 1). Conclusion: In post‐COVID patients with normal cognition, abnormal rsEEG alpha source activation may indicate a significant relationship between vigilance dysfunction and fatigue. [ABSTRACT FROM AUTHOR]

Given human immunodeficiency virus‐1 (HIV‐1)‐infected patients have alterations in the type I interferon (IFN‐I) pathway and are also at elevated risk of atherosclerosis, we evaluated IFN‐I response and subclinical cardiovascular disease (CVD) association in HIV‐1‐infected patients. Transcript levels of IFN‐α/β and IFN‐stimulated gene 56 (ISG56) were evaluated by RT/real‐time PCR in peripheral blood mononuclear cells collected from asymptomatic HIV‐1‐positive male patients at high risk of developing CVD (n = 34) and healthy subjects (n = 21). Stenosis degree (≥ or <50%), calcium volume score, calcium Agatston score, and myocardial extracellular volume were examined by coronary computerized tomography scan. Carotid intima‐media thickness (cIMT), Framingham risk score, atherosclerotic cardiovascular disease (ASCVD) score, and risk score developed by data collection on adverse effects of anti‐HIV drugs (D:A:D) were also measured. Increased IFN‐α, IFN‐β, and ISG56 levels were observed in all HIV‐1‐infected males compared to healthy controls (p <.001 for all genes analyzed). HIV‐1‐infected patients with a stenosis degree ≥50% showed a higher Framingham risk score (p =.019), which was correlated with IFN‐β and ISG56 levels. HIV‐1‐infected males with enhanced IFN‐I levels and stenosis displayed a higher ASCVD calculated risk (p =.011) and D:A:D score (p =.004). Also, there was a trend toward higher IFN‐α and ISG56 mRNA levels in HIV‐1‐positive patients with an increased cIMT (p >.05). Dysregulation of IFN‐I response might participate in the pathogenesis of HIV‐1‐associated CVD. [ABSTRACT FROM AUTHOR]