:
Viral interference, originally, referred to a state of temporary immunity, is a state
whereby infection with a virus limits replication or production of a second infecting virus. However,
replication of a second virus could also be dominant over the first virus. In fact, dominance
can alternate between the two viruses. Expression of type I interferon genes is many times upregulated
in infected epithelial cells. Since the interferon system can control most, if not all, virus infections
in the absence of adaptive immunity, it was proposed that viral induction of a nonspecific
localized temporary state of immunity may provide a strategy to control viral infections. Clinical
observations also support such a theory, which gave credence to the development of superinfection
therapy (SIT). SIT is an innovative therapeutic approach where a non-pathogenic virus is used
to infect patients harboring a pathogenic virus.
:
For the functional cure of persistent viral infections and for the development of broad- spectrum
antivirals against emerging viruses a paradigm shift was recently proposed. Instead of the virus,
the therapy should be directed at the host. Such a host-directed-therapy (HDT) strategy could be
the activation of endogenous innate immune response via toll-like receptors (TLRs). Superinfection
therapy is such a host-directed-therapy, which has been validated in patients infected with two
completely different viruses, the hepatitis B (DNA), and hepatitis C (RNA) viruses. SIT exerts
post-infection interference via the constant presence of an attenuated non-pathogenic avian double-
stranded (ds) RNA viral vector which boosts the endogenous innate (IFN) response. SIT
could, therefore, be developed into a biological platform for a new “one drug, multiple bugs”
broad-spectrum antiviral treatment approach.