| First Author | Ng CT | Year | 2015 |
| Journal | Cell Host Microbe | Volume | 17 |
| Issue | 5 | Pages | 653-61 |
| PubMed ID | 25974304 | Mgi Jnum | J:345200 |
| Mgi Id | MGI:6834175 | Doi | 10.1016/j.chom.2015.04.005 |
| Citation | Ng CT, et al. (2015) Blockade of interferon Beta, but not interferon alpha, signaling controls persistent viral infection. Cell Host Microbe 17(5):653-61 |
| abstractText | 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, IFNalpha and IFNbeta are highly induced early after infection, and blocking IFN-I receptor (IFNAR) signaling promotes virus clearance. We assessed the specific roles of IFNbeta versus IFNalpha in controlling LCMV infection. While blockade of IFNbeta 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 IFNalpha was not associated with improved viral control, but with early dissemination of virus. Thus, despite their use of the same receptor, IFNbeta and IFNalpha have unique and distinguishable biologic functions, with IFNbeta being mainly responsible for promoting viral persistence. |
