The Interaction of Viruses with the Cellular Senescence Response

Simple Summary Cellular senescence is considered a stress response that protects cells against malignant transformation, facilitates tissue repair and development, and prevents virus replication. However, excessive accumulation of senescent cells is associated with chronic diseases such as age-related disorders, cancer, inflammatory diseases and virus replication. The relationship between virus and cellular senescence is proving to be very complex. Cellular senescence can be induced in response to virus infection restricting virus propagation. Some viruses are able to exploit the senescence program to improve their replication, while others have developed strategies to subvert senescence. Therapeutic approaches to eliminate senescent cells may be used as a mechanism to ameliorate age-related diseases, but they may have an impact on virus replication. Here we review the available evidence revealing an interplay between cellular senescence and virus replication. We also discuss the consequences that treatment with senolytic agents may have on virus replication. Cellular senescence is viewed as a mechanism to prevent malignant transformation, but when it is chronic, as occurs in age-related diseases, it may have adverse effects on cancer. Therefore, targeting senescent cells is a novel therapeutic strategy against senescence-associated diseases. In addition to its role in cancer protection, cellular senescence is also considered a mechanism to control virus replication. Both interferon treatment and some viral infections can trigger cellular senescence as a way to restrict virus replication. However, activation of the cellular senescence program is linked to the alteration of different pathways, which can be exploited by some viruses to improve their replication. It is, therefore, important to understand the potential impact of senolytic agents on viral propagation. Here we focus on the relationship between virus and cellular senescence and the reported effects of senolytic compounds on virus replication.