| Interferon alpha (IFNα) was one of the first FDA-approved biotherapeutic treatments.
Since its approval, it has proved to be a powerful cytokine with potent therapeutic
activity but, unfortunately, strong side effects. The overall use of IFNα increased
dramatically when it was approved as the treatment of choice for hepatitis C.
However, nearly half of the individuals infected with genotype 1 of the virus still
fail to respond to therapy (1). Consequently, several pharmaceutical companies
are now trying to turn on the body’s own interferon alpha family of proteins using
immunomodulatory molecules in the hope that this will elicit a more complete
antiviral response. Both therapeutic approaches are not without risk, due to the side
effects associated with IFNα. Additionally, there is a growing amount of published
scientific articles suggesting that IFNα may be involved in certain autoimmune
diseases, including systemic lupus erythematosus (SLE) (2).
Combined, these observations clearly
suggest an increased need to monitor
IFNα levels in both normal and diseased
individuals along with patients undergoing
therapy. How much IFNα produced
by the body in response to new
immunomodulatory therapies will be
functionally equivalent to the current
IFNα exogenous treatment regimen? How
much ‘basal’ IFNα is beneficial to prevent
or limit viral infection and how much
is too much, thereby predisposing an
individual to autoimmune disorders? |
.jpg)
