Human cancers are known to have elaborate mechanistic strategies to evade apoptosis, promote limitless replication, tissue invasion and insensitivity to anti-growth signals [18].
It may be insufficient to eliminate the viruses but only counteract viral replication to evade immune elimination and establish a persistent infection with a long host survival and a high spread of the virus in the human population, like HBV, HCV, and HIV-1 (Russo and Potenza, 2011).
On the contrary, the RNA virus co-opt host-miRNAs to suppress their own replication to evade immune elimination and establish a strong infection.
Considering the important roles of the ISGs in deterring invading pathogens, one can imagine that PRRSV must have evolved strategies to evade them during its replication.
On the other side, the targets found here may be a reflection of a virus adaptation phenomenon in which they take advantage of the host miRNAs to suppress their own replication to evade immune elimination and establish in this way a persistent infection as has been suggested by Mahajan et al., [ 47].
Thus, the ability of HRBECs to evade apoptosis and continue DNA replication after XE exposure portrays the acquisition of two fundamental phenotypes of cancer.
As suggested many years ago, the suppression of UpA dinucleotides among RNA viruses infecting mammalian, plant and insect cells may therefore represent their specific adaptation to evade RNA degradation during their replication cycle.
Co-option of host miRNAs by viruses reveal their intelligent plan to control their replication in order to evade immune elimination until they undergoes successful transmission and establish a strong infection.
Smaller non-autonomous Helitrons are better able to evade host repression or show greater replication efficiency within the RCR mechanism.
In contrast, some RNA viruses, which do not use nuclear components of the host cell for their replication, develop strategies to evade host immune defenses by interfering with the nuclear cytoplasmic protein transport.
