TY - JOUR
T1 - The HSV-1 latency associated transcript (LAT) variants 1704 and 1705 are glycoprotein C negative
AU - Wroblewska, Zofia
AU - Spivack, Jordan G.
AU - Otte, Jessica
AU - Steiner, Israel
AU - Brown, Moira
AU - MacLean, Alasdair
AU - Fraser, Nigel W.
N1 - Funding Information:
We thank Dr. R. Eisenberga nd Dr. G. Cohen for helpful discussiona nd the gift of monospecifics era againstH SV-1 glycoproteins,D r. M. Trousdale for rabbit serum againstv ariant 1704,D r. E. Gonczol and Therese Nash for critical reading of the manuscript,S hirley Peterson for editorial work, and Cheryl McFadden for preparationo f this manuscript.T his work was supportedb y Public Health Service grant No. AI23968 from NIH.
PY - 1991/7
Y1 - 1991/7
N2 - The latency associated transcripts (LAT) of herpes simplex virus type 1 (HSV-1) are encoded by diploid genes that are expressed during latent infections. Two LAT variant viruses, 1704 and 1705, were compared with the parental strain 17+. Variant 1705 has a deletion affecting one copy of the LAT genes, expresses LATs during latent infection and reactivates normally. Variant 1704 has deletions affecting both LAT gene copies, does not express LATs during latent infection, and its reactivation is impaired (Steiner et al., 1989). Comparison of infected cell proteins by immunoprecipitation and Western blot analysis revealed one significant difference between HSV-1 strain 17+, 1704 and 1705; glycoprotein C (gC) was not synthesized by 1704 or 1705. Since both 1704 and 1705 are gC minus, the reactivation defect of 1704 is most likely related to the absence of the LATs, and not to the absence of gC.
AB - The latency associated transcripts (LAT) of herpes simplex virus type 1 (HSV-1) are encoded by diploid genes that are expressed during latent infections. Two LAT variant viruses, 1704 and 1705, were compared with the parental strain 17+. Variant 1705 has a deletion affecting one copy of the LAT genes, expresses LATs during latent infection and reactivates normally. Variant 1704 has deletions affecting both LAT gene copies, does not express LATs during latent infection, and its reactivation is impaired (Steiner et al., 1989). Comparison of infected cell proteins by immunoprecipitation and Western blot analysis revealed one significant difference between HSV-1 strain 17+, 1704 and 1705; glycoprotein C (gC) was not synthesized by 1704 or 1705. Since both 1704 and 1705 are gC minus, the reactivation defect of 1704 is most likely related to the absence of the LATs, and not to the absence of gC.
KW - Herpes simplex virus type 1
KW - Latency associated transcript
KW - Latent infection
UR - http://www.scopus.com/inward/record.url?scp=0025741506&partnerID=8YFLogxK
U2 - 10.1016/0168-1702(91)90109-9
DO - 10.1016/0168-1702(91)90109-9
M3 - ???researchoutput.researchoutputtypes.contributiontojournal.article???
C2 - 1659061
AN - SCOPUS:0025741506
SN - 0168-1702
VL - 20
SP - 193
EP - 200
JO - Virus Research
JF - Virus Research
IS - 2
ER -