Global bifurcation in a virus, defective genomes, satellite RNAs tripartite system: breakdown of a coexistence quasi-neutral curve

Abstract: The dynamics of wild-type (wt) RNA viruses and their defective viral genomes (DVGs) have been extensively studied both experimentally and theoretically. This research has paid special attention to the interference effects of DVGs on wt accumulation, transmission, disease severity, and induction of immunological responses. This subject is currently a highly active. However, viral infections involving wt, DVGs and other subviral genetic elements, like viral RNA satellites (satRNAs) have received scarce attention. Satellites are molecular parasites genetically different from the wt virus, which exploit the products of the latter for their own replication in as much as DVGs do, and thus they need to coinfect host cells along with the wt virus to complete their replication cycle. Here, we analyze a mathematical model describing the initial replication phase of a wt virus producing DVGs and coinfecting with a satRNA. The model has three different dynamical regimes depending upon the wt replication rate ($\alpha$), the fraction of DVGs produced during replication ($\omega$), and the replication rate of the satRNA ($\beta$): ($i$) full extinction when $\beta > \alpha (1 - \omega)$; ($ii$) a bistable regime with full coexistence governed by a quasi-neutral curve of equilibria and full extinction when $\beta = \alpha (1 - \omega)$; and ($iii$) a scenario of bistability separating full extinction from wt-DVGs coexistence with no satRNA when $\beta < \alpha (1 - \omega)$. The transition from scenarios ($i$) to ($iii$) occurs through the creation and destruction of a quasi-neutral curve of equilibria in a global bifurcation that we name as \textit{quasi-neutral nullcline confluence} (QNC) bifurcation: at the bifurcation value, two nullcline hypersurfaces coincide, giving rise to the curve of equilibria.