Different Mechanisms Regulate Productive Herpes Simplex Virus 1 (HSV-1) and HSV-2 Infections in Adult Trigeminal Neurons
Different Mechanisms Regulate Productive Herpes Simplex Virus 1 (HSV-1) and HSV-2 Infections in Adult Trigeminal Neurons
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DOI：
10.1128/jvi.00383-13
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发表时间：
2013-06-01
影响因子：
5.4
通讯作者：
Margolis, Todd P.
中科院分区：
文献类型：
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作者：
Bertke, Andrea S.;Ma, AyeAye;Margolis, Todd P.
单纯疱疹病毒1（HSV-1）和HSV-2在小鼠三叉神经节中的不同神经元亚型（A5+和KH 10+）中建立潜伏期，结果与这些神经元中的体外限制性生产性感染相关。HSV-2潜伏相关转录物（LAT）在转录起始位点附近含有一个顺式作用调节元件，可促进A5+神经元的生产性感染，在外显子1中含有第二个元件，可抑制KH 10+神经元的生产性感染。HSV-1不包含这样的调控序列，表明了在神经元中调控生产性HSV感染的不同机制。
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.