| First Author | Allen SJ | Year | 2011 |
| Journal | J Virol | Volume | 85 |
| Issue | 21 | Pages | 11448-56 |
| PubMed ID | 21880769 | Mgi Jnum | J:177047 |
| Mgi Id | MGI:5293549 | Doi | 10.1128/JVI.00678-11 |
| Citation | Allen SJ, et al. (2011) Adaptive and Innate Transforming Growth Factor {beta} Signaling Impact Herpes Simplex Virus 1 Latency and Reactivation. J Virol 85(21):11448-56 |
| abstractText | Innate and adaptive immunity play important protective roles by combating herpes simplex virus 1 (HSV-1) infection. Transforming growth factor beta (TGF-beta) is a key negative cytokine regulator of both innate and adaptive immune responses. Yet, it is unknown whether TGF-beta signaling in either immune compartment impacts HSV-1 replication and latency. We undertook genetic approaches to address these issues by infecting two different dominant negative TGF-beta receptor type II transgenic mouse lines. These mice have specific TGF-beta signaling blockades in either T cells or innate cells. Mice were ocularly infected with HSV-1 to evaluate the effects of restricted innate or adaptive TGF-beta signaling during acute and latent infections. Limiting innate cell but not T cell TGF-beta signaling reduced virus replication in the eyes of infected mice. On the other hand, blocking TGF-beta signaling in either innate cells or T cells resulted in decreased latency in the trigeminal ganglia of infected mice. Furthermore, inhibiting TGF-beta signaling in T cells reduced cell lysis and leukocyte infiltration in corneas and trigeminal ganglia during primary HSV-1 infection of mice. These findings strongly suggest that TGF-beta signaling, which generally functions to dampen immune responses, results in increased HSV-1 latency. |
