Scientists identify interferon beta which act as likely culprit in persistent viral infections like that of HIV,HEPATITIS B & HEPATITIS C INFECTION

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Interferon proteins are normally considered virus-fighters, but scientists have found evidence that one of them, interferon beta, has an immune-suppressing effect that can help some viruses like HIV,Hepatitis b & C in establish persistent infections.
Interferons, discovered nearly 60 years ago, are among the proteins secreted by cells in response to viral invasion. Their known functions include activating T cells, interfering with viral replication and enhancing the presentation of viral proteins to the immune system. They have long been considered essentially antiviral and immune-boosting, and lab-grown IFN type I proteins are used to treat hepatitis C infections and some cancers.
Yet, it is becoming clear that interferons don't simply boost the immune system. In a study reported in Science in 2013, for example, Oldstone and his laboratory found evidence that type I interferon signaling has a strong braking effect on the immune response -- a braking effect that may be co-opted by infecting viruses to enhance their survival. Oldstone notes blockade of type I interferon receptor signaling corrected virus-induced disorganization of secondary lymphoid tissue, allowed migration of T cells in the lymphoid tissue and diminished molecules responsible for aborting virus-specific T cell activity -- all leading to restoration of T cell function and control of the viral infection.
For the new study, Oldstone and his team sought to identify whether IFNα or IFNβ was responsible for that braking effect. IFNβ was the prime suspect. In the mouse model of persistent infection, which uses a variant ("clone 13") of the mouse-infecting LCMV virus, IFNβ is produced in the mice at much higher levels than those seen with a non-persistent LCMV variant (ARM 53b). If IFNb is blocked viral replication diminishes but by blocking IFNα with an antibody that neutralizes six subtypes had none of these beneficial effects. Moreover, blocking IFNα activity led to greater viral spread early in the infection. These results implied that, although IFNα and IFNβ signal through the same cellular receptor, IFNα proteins are important in limiting early virus spread, whereas IFNβ is an immunosuppressive molecule or increase viral spread
By blocking INFb now vaccine fr HIV is also being tried.