Different mechanisms regulate productive herpes simplex virus 1 (HSV-1) and HSV-2 infections in adult trigeminal neurons

Andrea S. Bertke, Aye Aye Ma, Mathew S. Margolis, Todd P. Margolis

Research output: Contribution to journalArticlepeer-review

25 Scopus citations

Abstract

Herpes simplex virus 1 (HSV-1) and HSV-2 establish latency in different neuronal subtypes (A5+and KH10+) in murine trigeminal ganglia, results which correlate with restricted productive infection in these neurons in vitro. HSV-2 latency-associated transcript (LAT) contains a cis-acting regulatory element near the transcription start site that promotes productive infection in A5+ neurons and a second element in exon 1 that inhibits productive infection in KH10+ neurons. HSV-1 contains no such regulatory sequences, demonstrating different mechanisms for regulating productive HSV infection in neurons.

Original languageEnglish
Pages (from-to)6512-6516
Number of pages5
JournalJournal of virology
Volume87
Issue number11
DOIs
StatePublished - Jun 2013

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