Vaccination after developing long COVID: Impact on clinical presentation, viral persistence, and immune responses.

BACKGROUND: Vaccination protects against severe COVID-19 manifestations. For those with post-COVID-19 conditions (PCC) or long COVID, the impact of COVID-19 vaccination on the evolution of symptoms, immune responses, and viral persistence is unclear. METHODS: In this prospective observational cohort study, we evaluated the number of PCC symptoms, affected organ systems, and psychological well-being scores before and after patients with PCC received COVID-19 vaccination. We simultaneously evaluated biomarkers of systemic inflammation and levels of plasma cytokines/chemokines. We measured plasma and intracellular levels of SARS-CoV-2 antigens, and immunoreactivity to SARS-CoV-2 antigens in blood. RESULTS: COVID-19 vaccination was associated with decreases in number of PCC symptoms (pre-vaccination: 6.56 ± 3.1 vs post-vaccination: 3.92 ± 4.02; P <0.001) and affected organ systems (pre-vaccination: 3.19 ± 1.04 vs post-vaccination: 1.89 ± 1.12; P <0.001), and increases in World Health Organization (WHO)-5 Well-Being Index Scores (pre-vaccination: 42.67 ± 22.76 vs post-vaccination: 56.15 ± 22.83; P <0.001). Patients with PCC also had significantly decreased levels of several pro-inflammatory plasma cytokines/chemokines after COVID-19 vaccination including sCD40L, GRO-⍺, macrophage inflammatory protein (MIP)-1⍺, interleukin (IL)-12p40, G-colony stimulating factor (CSF), M-CSF, IL-1ß, and stem cell factor (SCF). PCC participants presented a certain level of immunoreactivity toward SARS-CoV-2, that was boosted with vaccination. SARS-CoV-2 S1 antigen persisted in the blood of PCC participants, mostly in non-classical monocytes, regardless of participants receiving vaccination. CONCLUSIONS: Our study shows higher pro-inflammatory responses associated with PCC symptoms and brings forward a possible role for vaccination in mitigating PCC symptoms by decreasing systemic inflammation. We also observed persistence of viral products independent of vaccination that could be involved in perpetuating inflammation through non-classical monocytes.

From early birds to night owls: a longitudinal study of actigraphy-assessed sleep trajectories during the transition from pre- to early adolescence.

STUDY OBJECTIVES: Pre- and early adolescence are believed to constitute periods of important age-related changes in sleep. However, much of the research on these presumed developmental changes has used cross-sectional data or subjective measures of sleep, limiting the quality of the evidence. In addition, little is known about the development of certain features of the sleep-wake cycle pertaining to regularity (e.g. weekend-weekday differences and intra-individual variability) or circadian rhythms (e.g. sleep midpoint). METHODS: This study examined the sleep trajectories of 128 typically developing youth (69 girls) from ages 8 to 12 years on four sleep characteristics: sleep onset, sleep offset, total sleep time (TST), and sleep midpoint. For each of these characteristics, actigraphy-derived estimates of typical (i.e. mean) sleep and sleep regularity were obtained at each time point. Multilevel growth curves were modeled. RESULTS: Overall, the sleep-wake cycle significantly changed between 8 and 12 years. Mean sleep onset, offset and midpoint exhibited an ascending curvilinear growth pattern that shifted later with age, while mean TST decreased linearly. Weekend-weekday differences (social jetlag) for sleep offset and midpoint became more pronounced each year. Weekday TST was longer than weekend TST, though this difference became smaller over time. Finally, intra-individual variability increased over time for all sleep characteristics, with variability in TST ascending curvilinearly. Important between-person and sex differences were also observed. CONCLUSION: This study reveals the marked changes that occur in the sleep of typically developing pre- and early adolescents. We discuss the potential implications of these trajectories.

From Negative Emotionality to Aggressive Behavior: Maternal and Paternal Parenting Stress as Intervening Factors.

Child temperament plays a key role in the development of psychopathology, notably through transactions with the family environment. In particular, temperamental negative emotionality is a documented antecedent of child aggressive behavior, with parenting stress sometimes proposed to play a mediating role in this association. However, research has mostly addressed bivariate associations and seldom considered the full chain linking child negative emotionality to aggression through parenting stress. In addition, most relevant studies have focused on mothers; therefore, possible combined contributions of maternal and paternal stress, such as interactive effects, are under-investigated. Addressing these gaps, this longitudinal multi-informant study aimed to examine the mediating role of maternal parenting stress, paternal parenting stress, and their interaction in the association between infant negative emotionality and child aggression. Among 186 mostly White middle-class families (98 boys), infant negative emotionality was reported by mothers and fathers at 15 months, both parents reported on their own parenting stress at 3 years, and child aggression was assessed by teachers in the first grade of elementary school. The results revealed a moderated mediated pathway, such that there was a significant indirect effect of child negative emotionality on aggression through paternal stress, however only when maternal stress was also high. These findings suggest that the risk of negative emotionality translating to aggressive behavior is magnified when both parents experience high levels of stress in their parenting role. The results also underscore that both parents play significant yet different roles in the process linking early negative emotionality to subsequent aggression.