Since overexpression of optn or p62 mRNAs resulted in decreased Mm infection burden, we postulated that elevation of the Optn or p62 protein levels would result in increased targeting of Mm to autophagy by these ubiquitin receptors, in a manner dependent on the functions of the Lc3 interaction (LIR) and ubiquitin binding domains (UBAN/UBA). The gene discussed is CD300C; the disease is infection.