{Reference Type}: Journal Article
{Title}: Self-inhibiting percolation and viral spreading in epithelial tissue.
{Author}: Xu X;Nielsen BF;Sneppen K;
{Journal}: Elife
{Volume}: 13
{Issue}: 0
{Year}: 2024 Jun 28
{Factor}: 8.713
{DOI}: 10.7554/eLife.94056
{Abstract}: SARS-CoV-2 induces delayed type-I/III interferon production, allowing it to escape the early innate immune response. The delay has been attributed to a deficiency in the ability of cells to sense viral replication upon infection, which in turn hampers activation of the antiviral state in bystander cells. Here, we introduce a cellular automaton model to investigate the spatiotemporal spreading of viral infection as a function of virus and host-dependent parameters. The model suggests that the considerable person-to-person heterogeneity in SARS-CoV-2 infections is a consequence of high sensitivity to slight variations in biological parameters near a critical threshold. It further suggests that within-host viral proliferation can be curtailed by the presence of remarkably few cells that are primed for IFN production. Thus, the observed heterogeneity in defense readiness of cells reflects a remarkably cost-efficient strategy for protection.