During the early stages, human papillomavirus type 16 (HPV16) replication promotes protein synthesis and inhibits autophagy to facilitate viral infection via the interaction of the HPV16 PsV with epidermal growth factor receptor (EGFR) and epidermal growth factor receptor (KGFR) in HaCaT cells (human keratinocytes), which leads to the rapid activation of the PI3K/Akt/mTOR pathway and the impairment of autophagy (Surviladze et al., 2013). Here, MTOR is linked to viral infectious disease.