| Literature DB >> 27683235 |
Randall J Cohrs1,2, Hussain Badani3, Nicholas L Baird3, Teresa M White3, Bridget Sanford3, Don Gilden3,4.
Abstract
Varicella zoster virus (VZV), a human neurotropic alphaherpesvirus, becomes latent after primary infection and reactivates to produce zoster. To study VZV latency and reactivation, human trigeminal ganglia removed within 24 h after death were mechanically dissociated, randomly distributed into six-well tissue culture plates and incubated with reagents to inactivate nerve growth factor (NGF) or phosphoinositide 3-kinase (PI3-kinase) pathways. At 5 days, VZV DNA increased in control and PI3-kinase inhibitor-treated cultures to the same extent, but was significantly more abundant in anti-NGF-treated cultures (p = 0.001). Overall, VZV DNA replication is regulated in part by an NGF pathway that is PI3-kinase-independent.Entities:
Keywords: Human; Latency; Nerve growth factor; Phosphoinositide-3-kinase; Trigeminal ganglion; VZV
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Year: 2016 PMID: 27683235 PMCID: PMC5464606 DOI: 10.1007/s13365-016-0480-1
Source DB: PubMed Journal: J Neurovirol ISSN: 1355-0284 Impact factor: 2.643