We formulate and systematically study the global dynamics of a simple model of hepatitis B virus in terms of delay differential equations. This model has two important and novel features compared to the well-known basic virus model in the literature. Specifically, it makes use of the more realistic standard incidence function and explicitly incorporates a time delay in virus production. As a result, the infection reproduction number is no longer dependent on the patient liver size (number of initial healthy liver cells). For this model, the existence and the component values of the endemic steady state are explicitly dependent on the time delay. In certain biologically interesting limiting scenarios, a globally attractive endemic equilibrium can exist regardless of the time delay length.

The growth rate hypothesis (GRH) posits that variation in organismal stoichiometry (C:P and N:P ratios) is driven by growth‐dependent allocation of P to ribosomal RNA. The GRH has found broad but not uniform support in studies across diverse biota and habitats. We synthesise information on how and why the tripartite growth‐RNA‐P relationship predicted by the GRH may be uncoupled and outline paths for both theoretical and empirical work needed to broaden the working domain of the GRH. We found strong support for growth to RNA (r² = 0.59) and RNA‐P to P (r² = 0.63) relationships across taxa, but growth to P relationships were relatively weaker (r² = 0.09). Together, the GRH was supported in ~50% of studies. Mechanisms behind GRH uncoupling were diverse but could generally be attributed to physiological (P accumulation in non‐RNA pools, inactive ribosomes, translation elongation rates and protein turnover rates), ecological (limitation by resources other than P), and evolutionary (adaptation to different nutrient supply regimes) causes. These factors should be accounted for in empirical tests of the GRH and formalised mathematically to facilitate a predictive understanding of growth.