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Background Natural disasters and infectious diseases result in widespread disruption to human health and livelihood. At the scale of a global pandemic, the co-occurrence of natural disasters is inevitable. However, the impact of natural disasters on the spread of COVID-19 has not been extensively evaluated through epidemiological modelling. Methods We create an agent-based epidemiology model based on COVID-19 clinical, epidemiological, and geographic data. We first model 35 scenarios with varying natural disaster timing and duration for a COVID-19 outbreak in a theoretical region. We then evaluate the potential effect of an eruption of Vesuvius volcano on the spread of COVID-19 in Campania, Italy. Results In a majority of cases, the occurrence of a natural disaster increases the number of disease related fatalities. For a natural disaster fifty days after infection onset, the median increase in fatalities is 2, 59, and 180% for a 2, 14, and 31-day long natural disaster respectively, when compared to the no natural disaster scenario. For the Campania case, the median increase in fatalities is 1.1 and 2.4 additional fatalities per 100,000 for eruptions on day 1 and 100 respectively, and 60.0 additional fatalities per 100,000 for an eruption close to the peak in infections (day 50). Conclusion Our results show that the occurrence of a natural disaster in most cases leads to an increase in infection related fatalities, with wide variance in possible outcomes depending on the timing of the natural disaster relative to the peak in infections and the duration of the natural disaster.
BACKGROUND:The COVID-19 pandemic poses a serious threat to global health, and pathogenic mutations are a major challenge to disease control. We developed a statistical framework to explore the association between molecular-level mutation activity of SARS-CoV-2 and population-level disease transmissibility of COVID-19.METHODS:We estimated the instantaneous transmissibility of COVID-19 by using the time-varying reproduction number (Rt). The mutation activity in SARS-CoV-2 is quantified empirically depending on (i) the prevalence of emerged amino acid substitutions and (ii) the frequency of these substitutions in the whole sequence. Using the likelihood-based approach, a statistical framework is developed to examine the association between mutation activity and Rt. We adopted the COVID-19 surveillance data in California as an example for demonstration.RESULTS:We found a significant positive association between population-level COVID-19 transmissibility and the D614G substitution on the SARS-CoV-2 spike protein. We estimate that a per 0.01 increase in the prevalence of glycine (G) on codon 614 is positively associated with a 0.49% (95% CI: 0.39 to 0.59) increase in Rt, which explains 61% of the Rt variation after accounting for the control measures. We remark that the modeling framework can be extended to study other infectious pathogens.CONCLUSIONS:Our findings show a link between the molecular-level mutation activity of SARS-CoV-2 and population-level transmission of COVID-19 to provide further evidence for a positive association between the D614G substitution and Rt. Future studies exploring the mechanism between SARS-CoV-2 mutations and COVID-19 infectivity are warranted.
Successful clinical drug development requires rational design of combination treatments based on preclinical data. Anti-hepatitis C virus (HCV) drugs exhibit significant diversity in antiviral effect. Dose-response assessments can be used to determine parameters profiling the diverse antiviral effect during combination treatment. In the current study, a combined experimental and mathematical approaches were used to compare and score different combinations of anti-HCV treatments. A “required concentration index” was generated and used to rank the antiviral profile of possible double- and triple-drug combinations against HCV genotype 1b and 2a. Rankings varied based on target HCV genotype. Interestingly, multidrug (double and triple) treatment not only augmented antiviral activity, but also reduced genotype-specific efficacy, suggesting another advantage of multidrug treatment. The current study provides a quantitative method for profiling drug combinations against viral genotypes, to better inform clinical drug development.
BACKGROUND:A hepatitis A epidemic occurred among men who have sex with men (MSM) in Japan in 2017-2018. In this study, we employ a parsimonious mathematical model to epidemiologically investigate the dynamics of infection, aiming to evaluate the effectiveness of campaign-based interventions among MSM to raise awareness of the situation.METHODS:A mathematical model describing a mixture of human-to-human transmission and environmental transmission was fitted to surveillance data. Taking seasonally varying environmental transmission into account, we estimated the reproduction number of hepatitis A virus during the course of epidemic, and, especially, the abrupt decline in this reproduction number following campaign-based interventions.RESULTS:The reproduction number prior to the countermeasures ranged from 2.6 to 3.1 and then began to decrease following campaign-based interventions. After the first countermeasure, the reproduction number decreased, but the epidemic remained supercritical (i.e., Rt > 1). The value of Rt dropped well below one following the second countermeasure, which used web articles to widely disseminate information about the epidemic risk.CONCLUSIONS:Although the effective reproduction number, Rt, changes because of both intrinsic and extrinsic factors, the timing of the examined countermeasures against hepatitis A in the MSM population was consistent with the abrupt declines observed in Rt. Even without vaccination, the epidemic was brought under control, and risky behaviors may have been changed by the increase in situation awareness reached through web articles.
