Eroded telomeres, mitogenic oncogenes, anticancer therapeutics, virus infection and pro-senescent cytokines as triggers, PTEN loss, CDK inhibition, cooperation of upstream damage signaling (replication stress, DNA damage), elevated cell-cycle inhibitor expression and heterochromatinization of growth-promoting gene loci; SASP-mediated paracrine senescence as a reinforcing mechanism (Acosta et al., 2013; Alimonti et al., 2010; Bartkova et al., 2006; Braumüller et al., 2013; Coppé et al., 2008; Di Micco et al., 2006; Narita et al., 2003; Perez et al., 2015; Reimann et al., 2010). This evidence concerns the gene PTEN and viral infectious disease.