Abstract

Cellular senescence is defined as a self-imposed, cell cycle proliferation arrest, when cells are subjected to stress encompassing genotoxic, oxidative, replicative damage etc. Senescent cells, secrete plethora of factors including cytokines and chemokines, collectively referred as senescence associated secretory phenotype (SASP). SASP aids in clearing up the damaged cells, by recruiting immune cells, known as senescence surveillance. Several studies have reported enhanced expression of endogenous retrovirus (ERVs) in senescence. Due to their bidirectional transcription, ERVs are capable of eliciting interferon response, assisting in immune clearance. In turn, failure of senescence surveillance leads to accumulation of senescent cells, culminating in functional decline and aging. Though ERVs play an essential role in immune clearance, their role in evading surveillance have not been explored. This study examined the possibility of ERV suppression as an escape mechanism of surveillance. The results indicate that prolonged senescence suppresses ERVs via RNautophagy. Autophagy inhibitor, chloroquine (CQ), activates the ERV expression. In conclusion, this study implicates the role of RNautophagy in ERV suppression as a probable mechanism to escape immune surveillance.