A target-cell limited model can reproduce influenza infection dynamics in hosts with differing immune responses.

We consider a hierarchy of ordinary differential equation models that describe the within-host viral kinetics of influenza infections: the IR model explicitly accounts for an immune response to the virus, while the simpler, target-cell limited TEIV and TV models do not. We show that when the IR model is fitted to pooled experimental murine data of the viral load, fraction of dead cells, and immune response levels, its parameters values can be determined. However, if, as is common, only viral load data are available, we can estimate parameters of the TEIV and TV models but not the IR model.

The risk of SARS-CoV-2 outbreaks in low prevalence settings following the removal of travel restrictions.

Background: Countries around the world have introduced travel restrictions to reduce SARS-CoV-2 transmission. As vaccines are gradually rolled out, attention has turned to when travel restrictions and other non-pharmaceutical interventions (NPIs) can be relaxed.

Methods: Using SARS-CoV-2 as a case study, we develop a mathematical branching process model to assess the risk that, following the removal of NPIs, cases arriving in low prevalence settings initiate a local outbreak.

Infection, inflammation and intervention: mechanistic modelling of epithelial cells in COVID-19.

While the pathological mechanisms in COVID-19 illness are still poorly understood, it is increasingly clear that high levels of pro-inflammatory mediators play a major role in clinical deterioration in patients with severe disease. Current evidence points to a hyperinflammatory state as the driver of respiratory compromise in severe COVID-19 disease, with a clinical trajectory resembling acute respiratory distress syndrome, but how this 'runaway train' inflammatory response emerges and is maintained is not known. Here, we present the first mathematical model of lung hyperinflammation due to SARS-CoV-2 infection.

Accounting for cross-immunity can improve forecast accuracy during influenza epidemics.

Previous exposure to influenza viruses confers cross-immunity against future infections with related strains. However, this is not always accounted for explicitly in mathematical models used for forecasting during influenza outbreaks. We show that, if an influenza outbreak is due to a strain that is similar to one that has emerged previously, then accounting for cross-immunity explicitly can improve the accuracy of real-time forecasts.