Network models to evaluate vaccine strategies towards herd immunity in COVID-19.

Vaccination remains a critical element in the eventual solution to the COVID-19 public health crisis. Many vaccines are already being mass produced and supplied in many countries. However, the COVID-19 vaccination programme will be the biggest in history. Reaching herd immunity will require an unprecedented mass immunisation campaign that will take several months and millions of dollars. Using different network models, COVID-19 pandemic dynamics of different countries can be recapitulated such as in Italy. Stochastic computational simulations highlight that peak epidemic sizes in a population strongly depend on the network structure. Assuming a vaccine efficacy of at least 80% in a mass vaccination program, at least 70% of a given population should be vaccinated to obtain herd immunity, independently of the network structure. If the vaccine efficacy reports lower levels of efficacy in practice, then the coverage of vaccination would be needed to be even higher. Simulations suggest that the "Ring of Vaccination" strategy, vaccinating susceptible contact and contact of contacts, would prevent new waves of COVID -19 meanwhile a high percent of the population is vaccinated.

Assessing the impacts of vaccination and viral evolution in contact networks.

A key lesson learned with COVID-19 is that public health measures were very different from country to country. In this study, we provide an analysis of epidemic dynamics using three well-known stochastic network models-small-world networks (Watts-Strogatz), random networks (Erdös-Rényi), and scale-free networks (Barabási-Albert)-to assess the impact of different viral strains, lockdown strategies, and vaccination campaigns. We highlight the significant role of highly connected nodes in the spread of infections, particularly within Barabási-Albert networks. These networks experienced earlier and higher peaks in infection rates, but ultimately had the lowest total number of infections, indicating their rapid transmission dynamics. We also found that intermittent lockdown strategies, particularly those with 7-day intervals, effectively reduce the total number of infections, serving as viable alternatives to prolonged continuous lockdowns. When simulating vaccination campaigns, we observed a bimodal distribution leading to two distinct outcomes: pandemic contraction and pandemic expansion. For WS and ER networks, rapid mass vaccination campaigns significantly reduced infection rates compared to slower campaigns; however, for BA networks, differences between vaccination strategies were minimal. To account for the evolution of a virus into a more transmissible strain, we modeled vaccination scenarios that varied vaccine efficacy against the wild-type virus and noted a decline in this efficacy over time against a second variant. Our results showed that vaccination coverage above 40% significantly flattened infection peaks for the wild-type virus, while at least 80% coverage was required to similarly reduce peaks for variant 2. Furthermore, the effect of vaccine efficacy on reducing the peak of variant 2 infection was minimal. Although vaccination strategies targeting hub nodes in scale-free networks did not substantially reduce the total number of infections, they were effective in increasing the probability of preventing pandemic outbreaks. These findings underscore the need to consider the network structure for effective pandemic control.

A survey of within-host and between-hosts modelling for antibiotic resistance.

Antibiotic resistance is a global public health problem which has the attention of many stakeholders including clinicians, the pharmaceutical industry, researchers and policy makers. Despite the existence of many studies, control of resistance transmission has become a rather daunting task as the mechanisms underlying resistance evolution and development are not fully known. Here, we discuss the mechanisms underlying antibiotic resistance development, explore some treatment strategies used in the fight against antibiotic resistance and consider recent findings on collateral susceptibilities amongst antibiotic classes. Mathematical models have proved valuable for unravelling complex mechanisms in biology and such models have been used in the quest of understanding the development and spread of antibiotic resistance. While assessing the importance of such mathematical models, previous systematic reviews were interested in investigating whether these models follow good modelling practice. We focus on theoretical approaches used for resistance modelling considering both within and between host models as well as some pharmacodynamic and pharmakokinetic approaches and further examine the interaction between drugs and host immune response during treatment with antibiotics. Finally, we provide an outlook for future research aimed at modelling approaches for combating antibiotic resistance.