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Int J Environ Res Public Health ; 19(11)2022 05 27.
Article in English | MEDLINE | ID: covidwho-1869596


Public health responses to COVID-19 in long-term residential care facilities (LTRCFs) have restricted family engagement with residents. These restrictions impact on quality of care and the psychosocial and emotional well-being of family caregivers. Following a national cross-sectional web-based survey, respondents were invited to provide personal reflections on visitor restrictions. This study aims to describe the consequences of these restrictions for individuals living in LTRCF and their families during the first wave of the COVID-19 pandemic. Data from open-ended questions contained within the survey were analyzed using Braun and Clarke's (2006) method of thematic analysis. Four themes were identified: 1. Altered Communication and Connection; 2. Emotional and Psychological Impact; 3. Protecting and Caring Role of Staff; 4. Family Role. Throughout the narrative accounts, it is evident that the visitor restrictions impacted on the emotional and mental well-being of families. Some respondents expressed frustration that they could not assist staff in essential care provision, reducing meaning and purpose in their own lives. COVID-19 LTRCF visitor restrictions made little distinction between those providing essential personal care and those who visit for social reasons. A partnership approach to care provision is important and should encompass strategies to maintain the psychosocial and emotional well-being of families and their relatives during times of self-isolating or restrictive measures.

COVID-19 , Pandemics , COVID-19/epidemiology , Cross-Sectional Studies , Humans , Ireland/epidemiology , Nursing Homes
medrxiv; 2022.
Preprint in English | medRxiv | ID: ppzbmed-10.1101.2022.05.31.22275746


Background People with Long Covid (Post-Acute Sequelae of Covid-19) describe multiple symptoms which vary between and within individuals over relatively short time intervals. We aimed to describe the real-time associations between different symptoms and between symptoms and physical activity at the individual patient level. Methods and Findings Intensive longitudinal study of 82 adults with self-reported Long Covid (median duration 12-18 months). Data collection involved a smartphone app with 5 daily entries over 14 days and continuous wearing of a wrist accelerometer. Data items included 7 symptoms (Visual Analog Scales) and perceived demands in the preceding period (Likert scales). Activity was measured using mean acceleration in the 3-hour periods preceding and following app data entry. Analysis used within-person correlations of symptoms pairs and both pooled and individual symptom networks derived from graphical vector autoregression. App data was suitable for analysis from 74 participants (90%) comprising 4022 entries representing 77.6% of possible entries. Symptoms varied substantially within individuals and were only weakly auto-correlated. The strongest between-subject symptom correlations were of fatigue with pain (partial coefficient 0.5) and cognitive difficulty with light-headedness (0.41). Pooled within-subject correlations showed fatigue correlated with cognitive difficulty (partial coefficient 0.2) pain (0.19) breathlessness (0.15) and light-headedness (0.12) but not anxiety. Cognitive difficulty was correlated with anxiety and light-headedness (partial coefficients 0.16 and 0.17). Individual participant correlation heatmaps and symptom networks showed no clear patterns indicative of distinct phenotypes. Symptoms, including fatigue, were inconsistently correlated with prior or subsequent physical activity: this may reflect adjustment of activity in response to symptoms. Delayed worsening of symptoms after the highest activity peak was observed in 7 participants. Conclusion: Symptoms of Long Covid vary within individuals over short time scales, with heterogenous patterns of symptom correlation. The findings are compatible with altered central symptom processing as an additional factor in Long Covid.

59585 , 10333 , 1014 , 5325
medrxiv; 2020.
Preprint in English | medRxiv | ID: ppzbmed-10.1101.2020.11.18.20230599


While changes in SARS-CoV-2 viral load over time have been documented, detailed information on the impact of remdesivir and how it might alter intra-host viral evolution is limited. Sequential viral loads and deep sequencing of SARS-CoV-2 recovered from the upper respiratory tract of hospitalised children revealed that remdesivir treatment suppressed viral RNA levels in one patient but not in a second infected with an identical strain. Evidence of drug resistance to explain this difference was not found. Reduced levels of subgenomic (sg) RNA during treatment of the second patient, suggest an additional effect of remdesivir on viral replication that is independent of viral RNA levels. Haplotype reconstruction uncovered persistent SARS-CoV-2 variant genotypes in four patients. We conclude that these are likely to have arisen from within-host evolution, and not co-transmission, although superinfection cannot be excluded in one case. Sample-to-sample heterogeneity in the abundances of variant genotypes is best explained by the presence of discrete viral populations in the lung with incomplete population sampling in diagnostic swabs. Such compartmentalisation is well described in serious lung infections caused by influenza and Mycobacterium tuberculosis and has been associated with poor drug penetration, suboptimal treatment and drug resistance. Our data provide evidence that remdesivir is able to suppress SARS-CoV-2 replication in vivo but that its efficacy may be compromised by factors reducing penetration into the lung. Based on data from influenza and Mycobacterium tuberculosis lung infections we conclude that early use of remdesivir combined with other agents should now be evaluated. Summary SentenceDeep sequencing of longitudinal samples from SARS-CoV-2 infected paediatric patients identifies evidence of remdesivir-associated inhibition of viral replication in vivo and uncovers evidence of within host evolution of distinct viral genotypes.

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