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Biology subjects

Fryer, H.

Publications and source records attributed to Fryer, H..

2 recordsLinked to original sources

Viral burdens are associated with age and viral variant in a population-representative study of SARS-CoV-2 that accounts for time-since-infection related sampling bias.

In this study, we evaluated the impact of viral variant, in addition to other variables, on within-host viral burdens, by analysing cycle threshold (Ct) values derived from nose and throat swabs, collected as part of the UK COVID-19 Infection Survey. Because viral burden distributions determined from community survey data can be biased due to the impact of variant epidemiology on the time-since-infection of samples, we developed a method to explicitly adjust observed Ct value distributions to account for the expected bias. Analysing the adjusted Ct values using partial least squares regression, we found that among unvaccinated individuals with no known prior infection, the average Ct value was 0.94 lower among Alpha variant infections, compared those with the predecessor strain, B.1.177. However, among vaccinated individuals, it was 0.34 lower among Delta variant infections, compared to those with the Alpha variant. In addition, the average Ct value decreased by 0.20 for every 10 year age increment of the infected individual. In summary, within-host viral burdens are associated with age, in addition to the interplay of vaccination status and viral variant.

genetics↗

A mathematical model of antibiotic resistance gene flow from livestock and spread amongst humans

The evolution and spread of antibiotic resistance poses a major threat to human health. The high level of antibiotic use in the rearing of livestock is contributing to the origin and persistence of antibiotic resistance amongst humans. Understanding how resistance genes spread from livestock to humans and investigating the impact of managing antibiotic use in livestock will be important for guiding strategies to reduce the risk to humans. We have developed a mathematical model of the transmission of resistance genes from livestock to humans and their spread amongst the human population. Using this framework we demonstrate that although resistant zoonotic foodborne infections do not contribute significantly to the annual burden of death, they could be a source of resistance amongst other pathogens, including those that exclusively spread between humans. Amongst these pathogens, only livestock-derived resistant strains that are associated with a net fitness cost would be expected to decline in prevalence following control strategies aimed at reducing the impact on humans of antibiotic use in livestock. Author SummaryAntibiotics are an essential component of human health care. They are also used in the rearing of livestock for human consumption, which contributes to the development of antibiotic resistant pathogens. Although humans are known to be at risk from antibiotic resistance that evolves amongst livestock, the number of human lives that are at stake remains unclear. Furthermore, the number of lives that could be saved through interventions to reduce antibiotic use in livestock has not been evaluated. Here, we have developed a mathematical framework to explore these questions. Using this framework we explicitly demonstrate that there are too many uncertainties to calculate the number of preventable human deaths. Nevertheless, the importance of reserving new and currently effective antibiotics for human use is clear. Once resistance genes that do not have a fitness disadvantage have spread from livestock to humans, it is too late for interventions targeted at livestock to affect their prevalence in humans in the long term.

zoology↗