Articles: biological-models.
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Mathematical biosciences · Nov 2020
Could masks curtail the post-lockdown resurgence of COVID-19 in the US?
The community lockdown measures implemented in the United States from late March to late May of 2020 resulted in a significant reduction in the community transmission of the COVID-19 pandemic throughout the country. However, a number of US states are currently experiencing an alarming post-lockdown resurgence of the pandemic, triggering fears for a devastating second pandemic wave. We designed a mathematical model for addressing the key question of whether or not the universal use of face masks can halt such resurgence (and possibly avert a second wave, without having to undergo another cycle of major community lockdown) in the states of Arizona, Florida, New York and the entire US. ⋯ In particular, for this high lockdown lifting scenario, none of the four jurisdictions will experience a second wave if half of their residents wear face masks consistently after their respective lockdown period. A diagnostic testing strategy that increases the maximum detection rate of asymptomatic infected individuals (followed by contact tracing and self-isolation of the detected cases) greatly reduces the burden of the pandemic in all four jurisdictions, particularly if also combined with a universal face mask use strategy. Finally, it is shown that the universal use of face masks in public, with at least moderate level of compliance, could halt the post-lockdown resurgence of COVID-19, in addition to averting the potential for (and severity of) a second wave of the pandemic in each of the four jurisdictions.
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Mathematical biosciences · Nov 2020
Modeling COVID-19 pandemic using Bayesian analysis with application to Slovene data.
In the paper, we propose a semiparametric framework for modeling the COVID-19 pandemic. The stochastic part of the framework is based on Bayesian inference. The model is informed by the actual COVID-19 data and the current epidemiological findings about the disease. ⋯ It is estimated that the proportion of infected people in Slovenia was among the lowest in Europe (0.350%, 90% CI [0.245-0.573]%), that infection fatality rate in Slovenia until the end of first wave was 1.56% (90% CI [0.94-2.21]%) and the proportion of unidentified cases was 88% (90% CI [83-93]%). The proposed framework can be extended to more countries/regions, thus allowing for comparison between them. One such modification is exhibited on data for Slovene hospitals.
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The health impact of COVID-19 may differ in African settings as compared to countries in Europe or China due to demographic, epidemiological, environmental and socio-economic factors. We evaluated strategies to reduce SARS-CoV-2 burden in African countries, so as to support decisions that balance minimising mortality, protecting health services and safeguarding livelihoods. ⋯ In African settings, as elsewhere, current evidence suggests large COVID-19 epidemics are expected. However, African countries have fewer means to suppress transmission and manage cases. We found that self-isolation of symptomatic persons and general physical distancing are unlikely to avert very large epidemics, unless distancing takes the form of stringent lockdown measures. However, both interventions help to mitigate the epidemic. Shielding of high-risk individuals can reduce health service demand and, even more markedly, mortality if it features high uptake and low contact of shielded and unshielded people, with no increase in contact among shielded people. Strategies combining self-isolation, moderate physical distancing and shielding could achieve substantial reductions in mortality in African countries. Temporary lockdowns, where socioeconomically acceptable, can help gain crucial time for planning and expanding health service capacity.
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Animal models of COVID-19 have been rapidly reported after the start of the pandemic. We aimed to assess whether the newly created models reproduce the full spectrum of human COVID-19. ⋯ Most of the animal models of COVID-19 recapitulated mild pattern of human COVID-19 with full recovery phenotype. No severe illness associated with mortality was observed, suggesting a wide gap between COVID-19 in humans and animal models.
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Coronavirus disease 2019 (COVID-19) is an infectious disease with fast spreading all over the world caused by the SARS-CoV-2 virus which can culminate in a severe acute respiratory syndrome by the injury caused in the lungs. However, other organs can be also damaged. SARS-CoV-2 enter into the host cells using the angiotensin-converting enzyme 2 (ACE2) as receptor, like its ancestor SARS-CoV. ⋯ In this opinion article, we conjecture a dialogue by the figure of Sérgio Ferreira which brought together basic science of classical pharmacology and clinical repercussions in COVID-19, then we propose that in the course of SARS-CoV-2 infection: i) downregulation of ACE2 impairs the angiotensin II and DABK inactivation; ii) BK and its metabolite DABK seems to be in elevated levels in tissues by interferences in kallikrein/kinin system; iii) BK1 receptor contributes to the outbreak and maintenance of the inflammatory response; iv) kallikrein/kinin system crosstalks to RAS and coagulation system, linking inflammation to thrombosis and organ injury. We hypothesize that targeting the kallikrein/kinin system and BKB1R pathway may be beneficial in SARS-CoV-2 infection, especially on early stages. This route of inference should be experimentally verified by SARS-CoV-2 infected mice.