Scientists identify interferon beta as likely culprit in persistent viral infections

[Bob]

Discussion about interferon beta acting as an immune suppressant rather than an immune stimulant, and the potential to inhibit it to treat persistent viral infections. In relation to ME, I guess it raises the question of whether we have an over active immune system or a suppressed immune system or both.


Scientists identify interferon beta as likely culprit in persistent viral infections

May 13, 2015
Scripps Research Institute

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 establish persistent infections.

Read more:
http://www.sciencedaily.com/releases/2015/05/150513124930.htm


Research paper:
Blockade of Interferon Beta, but Not Interferon Alpha, Signaling Controls Persistent Viral Infection.
Ng CT et al.
Cell Host & Microbe
May 2015
DOI: 10.1016/j.chom.2015.04.005

Highlights

• •IFNα controls early viral dissemination, but does not affect long-term viral control
• •IFNβ contributes to disruption of splenic architecture
• •Blocking IFNβ improves T cell responses and accelerates clearance of persistent virus
• •IFNβ blockade decreases rates of CD8α−DC infection, suggesting a mechanism of action

Summary
Although type I interferon (IFN-I) is thought to be beneficial against microbial infections, persistent viral infections are characterized by high interferon signatures suggesting that IFN-I signaling may promote disease pathogenesis. During persistent lymphocytic choriomeningitis virus (LCMV) infection, IFNα and IFNβ are highly induced early after infection, and blocking IFN-I receptor (IFNAR) signaling promotes virus clearance. We assessed the specific roles of IFNβ versus IFNα in controlling LCMV infection. While blockade of IFNβ alone does not alter early viral dissemination, it is important in determining lymphoid structure, lymphocyte migration, and anti-viral T cell responses that lead to accelerated virus clearance, approximating what occurs during attenuation of IFNAR signaling. Comparatively, blockade of IFNα was not associated with improved viral control, but with early dissemination of virus. Thus, despite their use of the same receptor, IFNβ and IFNα have unique and distinguishable biologic functions, with IFNβ being mainly responsible for promoting viral persistence.

 

[halcyon]

Did they only test this theory on the one type of viral infection? I would be very surprised if this applied widely to other viruses. There seems to be a lot of evidence that IFN-β is protective in enterovirus infections and can clear persistent infection.

 

[Seven7]

Mine have been low in every test (extremely low ) was the official result.