HPV11 exerts dual effects on nasal mucosal cells: promoting proliferation and migration via E6/E7, while concurrently inducing an inhibitory effect through PPARA-mediated autophagy activation. The suppression of autophagy reversed the PPARA-driven inhibition, indicating a key role for the autophagy pathway. These findings suggest that PPARA targeting may be crucial in the pathogenesis of NIP, highlighting a complex interaction between HPV11 integration and host autophagy regulation.
Zhu et al. (Wed,) studied this question.