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Understanding and monitoring the epidemiological time delay dynamics of SARS-CoV-2 infection provides insights that are key to discerning changes in the phenotype of the virus, the demographics impacted, the efficacy of treatment, and the ability of the health service to manage large volumes of patients. This paper analyses how the pandemic has evolved in the United Kingdom through the temporal changes to the epidemiological time delay distributions for clinical outcomes. Using the most complete clinical data presently available, we have analysed, through a doubly interval censored Bayesian modelling approach, the time from infection to a clinical outcome. Across the pandemic, for the periods that were defined as epidemiologically distinct, the modelled mean ranges from 8.0 to 9.7 days for infection to hospitalisation, 10.3 to 15.0 days for hospitalisation to death, and 17.4 to 24.7 days for infection to death. The time delay from infection to hospitalisation has increased since the first wave of the pandemic. A marked decrease was observed in the time from hospitalisation to death and infection to death at times of high incidence when hospitals and ICUs were under the most pressure. There is a clear relationship between age groups that is indicative of the youngest and oldest demographics having the shortest time delay distributions before a clinical outcome. A statistically significant difference was found between genders for the time delay from infection to hospitalisation, which was not found for hospitalisation to death. The results by age group indicate that younger demographics that require clinical intervention for SARS-CoV-2 infection are more likely to require earlier hospitalisation that leads to a shorter time to death, which is suggestive of the largely more vulnerable nature of these individuals that succumb to infection. The distinction found between genders for exposure to hospitalisation is revealing of gender healthcare seeking behaviours., Competing Interests: The authors have declared that no competing interests exist. The authors were employed by the Department of Health and Social Care but received no specific funding for this study.

The objective of this paper is to model lost Quality Adjusted Life Years (QALYs) from symptoms arising from COVID-19 disease in the UK population, including symptoms of 'long-COVID'. The scope includes QALYs lost to symptoms, but not deaths, due to acute COVID-19 and long-COVID. The prevalence of symptomatic COVID-19, encompassing acute symptoms and long-COVID symptoms, was modelled using a decay function. Permanent injury as a result of COVID-19 infection, was modelled as a fixed prevalence. Both parts were combined to calculate QALY loss due to COVID-19 symptoms. Assuming a 60% final attack rate for SARS-CoV-2 infection in the population, we modelled 299,730 QALYs lost within 1 year of infection (90% due to symptomatic COVID-19 and 10% permanent injury) and 557,764 QALYs lost within 10 years of infection (49% due to symptomatic COVID-19 and 51% due to permanent injury). The UK Government willingness-to-pay to avoid these QALY losses would be £17.9 billion and £32.2 billion, respectively. Additionally, 90,143 people were subject to permanent injury from COVID-19 (0.14% of the population). Given the ongoing development in information in this area, we present a model framework for calculating the health economic impacts of symptoms following SARS-CoV-2 infection. This model framework can aid in quantifying the adverse health impact of COVID-19, long-COVID and permanent injury following COVID-19 in society and assist the proactive management of risk posed to health. Further research is needed using standardised measures of patient reported outcomes relevant to long-COVID and applied at a population level. [ABSTRACT FROM AUTHOR]

Notable cross-country differences exist in the diffusion of the Covid-19 and in its lethality. Contact patterns in populations, and in particular intergenerational contacts, have been argued to be responsible for the most vulnerable, the elderly, getting infected more often and thus driving up mortality in some context, like in the southern European one. This paper asks a simple question: is it between whom contacts occur that matters or is it simply how many contacts people have? Due to the high number of confounding factors, it is extremely difficult to empirically assess the impact of single network features separately. This is why we rely on a simulation exercise in which we counterfactually manipulate single aspects of countries' age distribution and network structures. We disentangle the contributions of the kind and of the number of contacts while holding constant the age structure. More precisely, we isolate the respective effects of inter-age contact patterns, degree distribution and clustering on the virus propagation across age groups. We use survey data on face-to-face contacts for Great Britain, Italy, and Germany, to reconstruct networks that mirror empirical contact patterns in these three countries. It turns out that the number of social contacts (degree distribution) largely accounts for the higher infection rates of the elderly in the Italian context, while differences in inter-age contacts patterns are only responsible for minor differences. This suggests that policies specifically targeting inter-age contacts would be little effective. [ABSTRACT FROM AUTHOR]

Background: One of the few studies to estimate infection risk with SARS-CoV-2 in the general population was the UK Office of National Statistics Infection Survey. This survey provided data that allowed us to describe and interpret apparent risk factors for testing positive for SARS-CoV-2 in a period when variants and COVID-19 controls experienced large changes. Method: The ONS published estimates of likelihood of individuals testing positive in two week monitoring periods between 21st November 2021 and 7th May 2022, relating this positivity to social and behavioural factors. We applied meta-regression to these estimates of likelihood of testing positive to determine whether the monitored potential risk factors remained constant during the pandemic. Results: Some risk factors had consistent relationship with risk of infection (always protective or always linked to higher risk, throughout monitoring period). Other risk factors had variable relationship with risk of infection, with changes seeming to especially correlate with the emergence of Omicron BA.2 dominance. These variable factors were mask-wearing habits, history of foreign travel, household size, working status (retired or not) and contact with children or persons age over 70. Conclusion: Relevance of some risk factors to likelihood of testing positive for SARS-CoV-2 may relate to reinfection risk, variant infectiousness and status of social distancing regulations. [ABSTRACT FROM AUTHOR]

We apply Bayesian inference methods to a suite of distinct compartmental models of generalised SEIR type, in which diagnosis and quarantine are included via extra compartments. We investigate the evidence for a change in lethality of COVID-19 in late autumn 2020 in the UK, using age-structured, weekly national aggregate data for cases and mortalities. Models that allow a (step-like or graded) change in infection fatality rate (IFR) have consistently higher model evidence than those without. Moreover, they all infer a close to two-fold increase in IFR. This value lies well above most previously available estimates. However, the same models consistently infer that, most probably, the increase in IFR preceded the time window during which variant B.1.1.7 (alpha) became the dominant strain in the UK. Therefore, according to our models, the caseload and mortality data do not offer unequivocal evidence for higher lethality of a new variant. We compare these results for the UK with similar models for Germany and France, which also show increases in inferred IFR during the same period, despite the even later arrival of new variants in those countries. We argue that while the new variant(s) may be one contributing cause of a large increase in IFR in the UK in autumn 2020, other factors, such as seasonality, or pressure on health services, are likely to also have contributed. [ABSTRACT FROM AUTHOR]

The entire world has suffered a lot since the outbreak of the novel coronavirus (COVID-19) in 2019, so simulation models of COVID-19 dynamics are urgently needed to understand and control the pandemic better. Meanwhile, emotional contagion, the spread of vigilance or panic, serves as a negative feedback to the epidemic, but few existing models take it into consideration. In this study, we proposed an innovative multi-layer hybrid modelling and simulation approach to simulate disease transmission and emotional contagion together. In each layer, we used a hybrid simulation method combining agent-based modelling (ABM) with system dynamics modelling (SDM), keeping spatial heterogeneity while reducing computation costs. We designed a new emotion dynamics model IWAN (indifferent, worried, afraid and numb) to simulate emotional contagion inside a community during an epidemic. Our model was well fit to the data of China, the UK and the US during the COVID-19 pandemic. If there weren't emotional contagion, our experiments showed that the confirmed cases would increase rapidly, for instance, the total confirmed cases during simulation in Guangzhou, China would grow from 334 to 2096, which increased by 528%. We compared the calibrated emotional contagion parameters of different countries and found that the suppression effect of emotional contagion in China is relatively more visible than that in the US and the UK. Due to the experiment results, the proposed multi-layer network model with hybrid simulation is valid and can be applied to the quantitative analysis of the epidemic trends and the suppression effect of emotional contagion in different countries. Our model can be modified for further research to study other social factors and intervention policies in the COVID-19 pandemic or future epidemics. [ABSTRACT FROM AUTHOR]