PMID- 9557667
OWN - NLM
STAT- MEDLINE
DCOM- 19980520
LR  - 20200724
IS  - 0022-538X (Print)
IS  - 1098-5514 (Electronic)
IS  - 0022-538X (Linking)
VI  - 72
IP  - 5
DP  - 1998 May
TI  - Temporal mapping of transcripts in herpesvirus 6 variants.
PG  - 3837-44
AB  - To define the molecular features characteristic of the early stages of infection 
      of lymphocytes with human herpesvirus 6 (HHV-6) variant A or B, we studied the 
      temporal regulation of expression of selected sets of viral genes. Thus, U42, 
      U94, U89-U90, U73, and U39 are alpha genes since their transcripts (i) were made 
      in the presence of inhibitors of protein synthesis and (ii) were detected 3 h 
      after infection of untreated cells. U41, U53, U31, and U19 are beta genes since 
      their expression is inhibited by cycloheximide but not by phosphonoacetate, an 
      inhibitor of DNA synthesis. U100 is a gamma gene since its spliced transcript 
      encoding the structural glycoprotein gp82/105 was first detected 16 h after 
      infection of untreated cells but could not be detected in cells treated with 
      phosphonoacetate. HHV-6 variants differ in the transcription patterns of their 
      genes. U16-U17 originates a splice transcript and is regulated as alpha in HHV-6B 
      and as beta in HHV-6A. U91 generates two transcripts, amplified as 476- and 
      374-bp PCR fragments. The 476-bp fragment is alpha in HHV-6A-infected cells but 
      beta in HHV-6B-infected cells. Conversely, the 374-bp fragment is beta in 
      HHV-6A-infected cells and alpha in HHV-6B-infected cells. Furthermore, the 
      spliced product of U18-U19-U20 (526 bp) is beta in HHV-6A-infected cells, but 
      only a partially spliced form (1.9 kb) was detected at late stages of infection 
      in HHV-6B. HHV-6 transcription was also studied in nonproductive lymphoid cells, 
      and the same transcription pattern detected during lytic infection was observed. 
      Also, HHV-6 variants maintain the differences in U91, U16-17, and U18-U19-U20. We 
      conclude that, as expected from the sequencing data, gene expression is generally 
      similar in HHV-6 variants. However, transcription of selected genes in HHV-6A and 
      HHV-6B differs with respect to temporal regulation and splicing pattern. 
      Furthermore, the identification of viral functions expressed during the different 
      stages of lytic replication suggests that reverse transcription-PCR for HHV-6 
      genes is a useful diagnostic approach to differentiate between latent and 
      productive HHV-6 infection.
FAU - Mirandola, P
AU  - Mirandola P
AD  - Dipartimento di Medicina Sperimentale e Diagnostica, Universita di Ferrara, 
      Italy.
FAU - Menegazzi, P
AU  - Menegazzi P
FAU - Merighi, S
AU  - Merighi S
FAU - Ravaioli, T
AU  - Ravaioli T
FAU - Cassai, E
AU  - Cassai E
FAU - Di Luca, D
AU  - Di Luca D
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Virol
JT  - Journal of virology
JID - 0113724
RN  - 0 (Immediate-Early Proteins)
RN  - 0 (RNA, Viral)
SB  - IM
MH  - Cell Line
MH  - Gene Expression Regulation, Viral
MH  - *Genetic Variation
MH  - Herpesvirus 6, Human/*genetics
MH  - Humans
MH  - Immediate-Early Proteins/genetics
MH  - RNA, Viral/*analysis
MH  - *Transcription, Genetic
MH  - Tumor Cells, Cultured
PMC - PMC109607
EDAT- 1998/04/29 00:00
MHDA- 1998/04/29 00:01
PMCR- 1998/05/01
CRDT- 1998/04/29 00:00
PHST- 1998/04/29 00:00 [pubmed]
PHST- 1998/04/29 00:01 [medline]
PHST- 1998/04/29 00:00 [entrez]
PHST- 1998/05/01 00:00 [pmc-release]
AID - 2180 [pii]
AID - 10.1128/JVI.72.5.3837-3844.1998 [doi]
PST - ppublish
SO  - J Virol. 1998 May;72(5):3837-44. doi: 10.1128/JVI.72.5.3837-3844.1998.