The process is tightly regulated by the evolutionarily conserved Atg genes, of which Atg5 is one such crucial mediator.

This suggests that Epg5 and other Atg genes function in macrophages to limit innate immune inflammation in the lung.

Thus Atg genes in myeloid cells dampen virus-induced systemic inflammation, creating an environment that fosters efficient MHV68 reactivation from latency.