It has long been known that many classical immune-surveillance networks, such as NF-kappa B signaling, IL6/STAT3 signaling, autophagy, cytokines, cellular membranes, heat shock proteins (HSPs), and cytoskeletons [1–3], which are supposed to protect the host from viral infections, could be exploited by viruses to ensure their survival. This evidence concerns the gene IL6 and viral infectious disease.