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James M. Trauer

Publications and source records attributed to James M. Trauer.

2 recordsLinked to original sources

Quantifying the direct and indirect impact of COVID-19 vaccination: evidence from Victoria, Australia

Vaccines not only directly protect vaccinated individuals but also contribute to protect the entire population via indirect herd-immunity benefits. However, researchers have long struggled to quantify these indirect effects at the population level, hindering assessment of vaccination program effectiveness. We developed a new method to estimate these effects, thereby markedly improving measures of the number of infections, hospitalizations, and deaths averted by vaccination. Our population-based analysis of 6,440,000 residents of Victoria, Australia reveal strong indirect effects during the Delta outbreak (September-November 2021). By modelling a non-vaccination counterfactual, we conservatively estimate 316,000 infections were averted (95\% BCI: 232k-406k), as well as 33,500 hospitalizations (95\% BCI: 22.2k-46.2k), and 4,900 deaths (95\% BCI: 2.9k-7.3k). These are 4.0, 7.5, and 8.0 times higher, respectively, than observed. Half of the averted infections and around one-quarter of hospitalizations and deaths were attributable to indirect protection. Homogeneous vaccination across LGAs could have reduced outcomes by approximately 25\%.

q-bio.PE

Coupled, multi-strain epidemic models of mutating pathogens

We introduce and analyze coupled, multi-strain epidemic models designed to simulate the emergence and dissemination of mutant (e.g. drug-resistant) pathogen strains. In particular, we investigate the mathematical and biological properties of a general class of multi-strain epidemic models in which the infectious compartments of each strain are coupled together in a general manner. We derive explicit expressions for the basic reproduction number of each strain and highlight their importance in regulating the system dynamics (e.g. the potential for an epidemic outbreak) and the existence of nonnegative endemic solutions. Importantly, we find that the basic reproduction number of each strain is independent of the mutation rates between the strains --- even under quite general assumptions for the form of the infectious compartment coupling. Moreover, we verify that the coupling term promotes strain coexistence (as an extension of the competitive exclusion principle) and demonstrate that the strain with the greatest reproductive capacity is not necessarily the most prevalent. Finally, we briefly discuss the implications of our results for public health policy and planning.

q-bio.PE