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• W2607193810 abstract "ABSTRACT A defining characteristic of alphaherpesviruses is the establishment of lifelong latency in host sensory ganglia with occasional reactivation causing recurrent lytic infections. As an alternative to rodent models, we explored the use of an immortalized cell line derived from human dorsal root ganglia. HD10.6 cells proliferate by virtue of a transduced tetracycline-regulated v- myc oncogene. In the presence of doxycycline, HD10.6 cells mature to exhibit neuronal morphology and express sensory neuron-associated markers such as neurotrophin receptors TrkA, TrkB, TrkC, and RET and the sensory neurofilament peripherin. Infection of mature HD10.6 neurons by herpes simplex virus 1 (HSV-1) results in a delayed but productive infection. However, infection at a low multiplicity of infection (MOI) in the presence of acyclovir results in a quiescent infection resembling latency in which viral genomes are retained in a low number of neurons, viral gene expression is minimal, and infectious virus is not released. At least some of the quiescent viral genomes retain the capacity to reactivate, resulting in viral DNA replication and release of infectious virus. Reactivation can be induced by depletion of nerve growth factor; other commonly used reactivation stimuli have no significant effect. IMPORTANCE Infections by herpes simplex viruses (HSV) cause painful cold sores or genital lesions in many people; less often, they affect the eye or even the brain. After the initial infection, the virus remains inactive or latent in nerve cells that sense the region where that infection occurred. To learn how virus maintains and reactivates from latency, studies are done in neurons taken from rodents or in whole animals to preserve the full context of infection. However, some cellular mechanisms involved in HSV infection in rodents are different from those in humans. We describe the use of a human cell line that has the properties of a sensory neuron. HSV infection in these cultured cells shows the properties expected for a latent infection, including reactivation to produce newly infectious virus. Thus, we now have a cell culture model for latency that is derived from the normal host for this virus." @default.
• W2607193810 created "2017-04-28" @default.
• W2607193810 creator A5026553060 @default.
• W2607193810 creator A5087578365 @default.
• W2607193810 creator A5088746880 @default.
• W2607193810 creator A5090610293 @default.
• W2607193810 date "2017-06-15" @default.
• W2607193810 modified "2023-09-23" @default.
• W2607193810 title "An Immortalized Human Dorsal Root Ganglion Cell Line Provides a Novel Context To Study Herpes Simplex Virus 1 Latency and Reactivation" @default.
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• W2607193810 doi "https://doi.org/10.1128/jvi.00080-17" @default.
• W2607193810 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5446634" @default.
• W2607193810 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/28404842" @default.
• W2607193810 hasPublicationYear "2017" @default.
• W2607193810 type Work @default.
• W2607193810 sameAs 2607193810 @default.

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