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PMID:21880769
| Citation |
Allen, SJ, Mott, KR, Wechsler, SL, Flavell, RA, Town, T and Ghiasi, H (2011) Adaptive and innate transforming growth factor beta signaling impact herpes simplex virus 1 latency and reactivation. J. Virol. 85:11448-56 |
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| Abstract |
Innate and adaptive immunity play important protective roles by combating herpes simplex virus 1 (HSV-1) infection. Transforming growth factor β (TGF-β) is a key negative cytokine regulator of both innate and adaptive immune responses. Yet, it is unknown whether TGF-β 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-β receptor type II transgenic mouse lines. These mice have specific TGF-β 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-β signaling during acute and latent infections. Limiting innate cell but not T cell TGF-β signaling reduced virus replication in the eyes of infected mice. On the other hand, blocking TGF-β signaling in either innate cells or T cells resulted in decreased latency in the trigeminal ganglia of infected mice. Furthermore, inhibiting TGF-β 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-β signaling, which generally functions to dampen immune responses, results in increased HSV-1 latency. |
| Links |
PubMed PMC3194985 Online version:10.1128/JVI.00678-11 |
| Keywords |
Animals; Disease Models, Animal; Eye/virology; Gene Expression Regulation, Viral; Herpesvirus 1, Human/physiology; Keratitis, Herpetic/immunology; Keratitis, Herpetic/virology; Mice; Mice, Transgenic; Rodent Diseases/immunology; Rodent Diseases/virology; Signal Transduction; Transforming Growth Factor beta/metabolism; Trigeminal Ganglion/immunology; Trigeminal Ganglion/virology; Virus Activation; Virus Latency; Virus Replication |
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