SARS-CoV-2 modulates inflammatory responses of alveolar epithelial type II cells PI3K/AKT pathway.

Background: SARS-CoV-2 infects through the respiratory route and triggers inflammatory response by affecting multiple cell types including type II alveolar epithelial cells. SARS-CoV-2 triggers signals its Spike (S) protein, which have been shown to participate in the pathogenesis of COVID19.

Aim: Aim of the present study was to investigate the effect of SARS-CoV2 on type II alveolar epithelial cells, focusing on signals initiated by its S protein and their impact on the expression of inflammatory mediators.

SARS-CoV-2/ACE2 Interaction Suppresses IRAK-M Expression and Promotes Pro-Inflammatory Cytokine Production in Macrophages.

The major cause of death in SARS-CoV-2 infected patients is due to de-regulation of the innate immune system and development of cytokine storm. SARS-CoV-2 infects multiple cell types in the lung, including macrophages, by engagement of its spike (S) protein on angiotensin converting enzyme 2 (ACE2) receptor. ACE2 receptor initiates signals in macrophages that modulate their activation, including production of cytokines and chemokines.

EEG theta/beta ratio as a potential biomarker for attentional control and resilience against deleterious effects of stress on attention.

Anxious stress compromises cognitive executive performance. This occurs, for instance, in cognitive performance anxiety (CPA), in which anxiety about one's cognitive performance causes that performance to actually deteriorate (e.g.

Emotional Stroop interference for threatening words is related to reduced EEG δ-β coupling and low attentional control.

Previously, electroencephalographic (EEG) delta-beta coupling (positive correlation between power in the fast beta and slow delta frequency bands) has been related to affective processing. For instance, differences in delta-beta coupling have been observed between people in a psychological stress condition and controls. We previously reported relationships between attentional threat processing and delta-beta coupling and individual differences in attentional control.