Fig 7. A model of TCV p28-mediated SIE.

Step 1: the concentration of p28 translated from the genome of primary invader (top right, black dots) is relatively low. They interact with each other relatively slowly, allowing the incorporation of p88, and enclosure of the complex by mitochondrion outer membrane to form VRCs. Step 2: genomic RNA of the primary invader enters VRCs to initiate replication. We hypothesize that some VRCs stay vacant and await the entry of newly synthesized viral RNA. However, the majority of progeny RNA will probably not have the chance to repeat the replication cycle in the same cell. Also beginning with this step, large amounts of progeny RNA become template for p28 translation, drastically increasing the intracellular concentration of p28. Step 3: higher p28 concentration propels faster p28 polymerization, leading to quick formation of oversized p28 polymers that escape the membrane enclosure. Note that the forms of polymeric p28 complexes are hypothetical as we do not yet know the specific mode of p28-p28 interactions. Step 4: since the p28 polymers are by definition capable of nucleating homologous monomers, they are expected to capture the p28 monomers (blue dots) translated from superinfector genomes, preventing them from forming new VRCs.