A mutant deleted for most of the herpes simplex virus type 1 (HSV-1) UOL gene does not affect the spontaneous reactivation phenotype in rabbits.
The mechanisms involved in the herpes simplex virus type 1 (HSV-1) latency-reactivation cycle are not fully understood. The latency-associated transcript (LAT) is the only HSV-1 RNA abundantly detected during neuronal latency. LAT plays a significant role in latency because LAT(-) mutants have a reduced reactivation phenotype. Several novel viral transcripts have been identified within the LAT locus, including UOL, which is located just upstream of LAT. The authors report here on a mutant, DeltaUOL, which has a 437-nucleotide deletion that deletes most of UOL. DeltaUOL replicated similarly to its wild-type parental McKrae HSV-1 strain in infected cells, the eyes, trigeminal ganglia, and brains of mice and rabbits. It was indistinguishable from wild-type virus as regards explant-induced reactivation in mice, and spontaneous reactivation in rabbits. In contrast, DeltaUOL was significantly less virulent in mice. Thus, UOL appears to be dispensable for the wild-type reactivation phenotype while appearing to play a role in neurovirulence in ocularly infected animals.
Chan
David
D
Department of Ophthalmology, University of California at Irvine, School of Medicine, Irvine, California, USA.
Cohen
Jacob
J
Naito
Julie
J
Mott
Kevin R
KR
Osorio
Nelson
N
Jin
Ling
L
Fraser
Nigel W
NW
Jones
Clinton
C
Wechsler
Steven L
SL
Perng
Guey Chuen
GC
D000818:Animals; D004279:DNA, Viral / Q000235:genetics; D004195:Disease Models, Animal; D017353:Gene Deletion; D005814:Genes, Viral; D006561:Herpes Simplex / Q000503:physiopathology*; D018259:Herpesvirus 1, Human / Q000235:genetics*; D009154:Mutation; D011817:Rabbits; D015183:Restriction Mapping; D014775:Virus Activation / Q000502:physiology*
D004279:DNA, Viral