1887

Abstract

Explantation into culture of dorsal root ganglia (DRG) latently infected with herpes simplex virus type 1 (HSV-1) causes reactivation of the virus. Previous studies have suggested that either latency-associated transcripts (LATs) were removed as an early consequence of reactivation or, alternatively, there was a population of latently infected cells which did not contain LATs. We have now attempted to detect this population of neurons by inserting a reporter gene ( gene), under the control of promoters other than LAT, into the HSV-1 strain 17 mutant 1814, which was used in the earlier studies. One of these promoters, the human cytomegalovirus enhancer, resulted in weak expression of β-galactosidase in DRG neurons for at least 5 months. The pattern of staining was predominantly homogeneous in neurons at 3 or 5 days post-infection or at 3 days post-explantation, and was predominantly speckled in latently infected neurons (1 to 5 months post-infection). About 30% of the β-galactosidase-positive neurons did not contain LATs by hybridization. However, the detergents used to enable penetration of the substrate for β-galactosidase had also reduced the levels of the LATs; in neurons which originally had only small numbers of LATs this may have reduced levels to below those detectable by the methods used. There was, therefore, no unequivocal evidence for a population of latently HSV-1-infected cells which did not express LATs.

Loading

Article metrics loading...

/content/journal/jgv/10.1099/0022-1317-76-6-1527
1995-06-01
2019-11-21
Loading full text...

Full text loading...

http://instance.metastore.ingenta.com/content/journal/jgv/10.1099/0022-1317-76-6-1527
Loading

Most Cited This Month

This is a required field
Please enter a valid email address
Approval was a Success
Invalid data
An Error Occurred
Approval was partially successful, following selected items could not be processed due to error