Sentence examples for hsv latency from inspiring English sources

We tested this approach in an in vitro HSV latency model using the engineered homing endonuclease (HE) HSV1m5, which recognizes a sequence in the HSV-1 gene UL19, encoding the virion protein VP5.

Not only the trigeminal ganglion is generally accepted to be a site of HSV latency [28],[29], but also the ciliary ganglion has been found to host HSV DNA in asymptomatic humans, offering possible explanations for anterior chamber or retinal herpetic diseases, tissues not directly innervated by trigeminal nerves [30].

HSV latency is static; no virus is produced; and is controlled by a number of viral genes, including latency-associated transcript.

Some of the other in vitro models of HSV latency are based on the use of replication-defective, attenuated virus strains [32].

For example, the HSV latency associated promoter has been shown to drive expression of β-galactosidase long term in sensory neurons, but the promoter is down-regulated in the CNS [10], [11].

In other herpesviruses, the miRNAs expressed by the Large Latency Transcript (LAT) down-regulate the expression of key viral immediate-early or early regulatory proteins [42] and it has been hypothesized that LAT-encoded miRNAs function as a molecular switch between HSV latency and reactivation in infected human ganglia [4], [43].

The HSV latency-associated transcripts (LATs) have been discussed for their potential to repress ICP0 gene expression [62], [63].

Subsequently, a number of key findings from studies designed to decipher LAT function have focused on potential epigenetic mechanisms involved in the establishment and maintenance of HSV-1 latency [18] [23].

CTCF has been implicated as a major determinant controlling HSV-1 latency.

There are reasons to hypothesize that the status of TH and its interaction with TRs modulate chromatin and exert functions in HSV-1 latency and reactivation.

An activity for CTCF at the UI and URI domains expands the repertoire of this transcription factor as a regulator of HSV-1 latency [21].