PMID- 16162481
OWN - NLM
STAT- MEDLINE
DCOM- 20051025
LR  - 20200327
IS  - 1355-0284 (Print)
IS  - 1538-2443 (Electronic)
IS  - 1355-0284 (Linking)
VI  - 11
IP  - 4
DP  - 2005 Aug
TI  - Differential tropism of human herpesvirus 6 (HHV-6) variants and induction of 
      latency by HHV-6A in oligodendrocytes.
PG  - 384-94
AB  - Human herpesvirus 6 (HHV-6) is a ubiquitous beta -herpesvirus associated with a 
      number of clinical disorders. Two closely but biologically distinct variants have 
      been described. HHV-6 variant B causes the common childhood disease exhanthem 
      subitum, and although the pathologic characteristics for HHV-6 variant A are less 
      well defined, HHV-6A has been suggested to be more neurotropic. We studied the 
      effect of both HHV-6 variants in an oligodendrocyte cell line (MO3.13). Infection 
      of M03.13 was monitored by cytopathic effect (CPE), quantitative TaqMan PCR for 
      viral DNA in cells and supernatant, reverse transcriptase-polymerase chain 
      reaction (RT-PCR) to detect viral RNA, and indirect immunofluorescence (IFA) to 
      detect viral protein expression. HHV-6A infection induced significantly more CPE 
      than infection with HHV-6B. HHV-6B induced an abortive infection associated with 
      a decrease of the initial viral DNA load over time, early RNA expression, and no 
      expression of viral antigen. In contrast, infection with HHV-6A DNA persisted in 
      cells for at least 62 days. During the acute phase of infection with HHV-6A, 
      intracellular and extracellular viral load increased and cells expressed the 
      viral protein IE-2 and gp116/54/64. No HHV-6A RNA or protein was expressed after 
      30 days post infection, suggesting that HHV-6A formed a latent infection. These 
      studies provide in vitro support to the hypothesis that HHV-6 can actively infect 
      oligodendrocytes. Our results suggest that HHV-6A and HHV-6B have different 
      tropism in MO3.13 cells and that an initially active HHV-6A infection can develop 
      latency. Differences between HHV-6A and -6B infection in different neural cell 
      types may be associated with different neurological diseases.
FAU - Ahlqvist, Jenny
AU  - Ahlqvist J
AD  - Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, 
      National Institutes of Health, Bethesda, Maryland 20892, USA.
FAU - Fotheringham, Julie
AU  - Fotheringham J
FAU - Akhyani, Nahid
AU  - Akhyani N
FAU - Yao, Karen
AU  - Yao K
FAU - Fogdell-Hahn, Anna
AU  - Fogdell-Hahn A
FAU - Jacobson, Steven
AU  - Jacobson S
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Neurovirol
JT  - Journal of neurovirology
JID - 9508123
RN  - 0 (Antigens, Viral)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Antigens, Viral/genetics
MH  - Cell Line
MH  - Encephalitis, Viral/pathology/virology
MH  - Exanthema Subitum/pathology/*virology
MH  - Gene Expression Regulation, Viral
MH  - Herpesvirus 6, Human/*genetics/*growth & development
MH  - Humans
MH  - Multiple Sclerosis/pathology/virology
MH  - Oligodendroglia/pathology/*virology
MH  - RNA, Messenger/analysis
MH  - T-Lymphocytes/cytology
MH  - *Virus Latency
PMC - PMC7095087
EDAT- 2005/09/16 09:00
MHDA- 2005/10/26 09:00
PMCR- 2020/03/25
CRDT- 2005/09/16 09:00
PHST- 2005/09/16 09:00 [pubmed]
PHST- 2005/10/26 09:00 [medline]
PHST- 2005/09/16 09:00 [entrez]
PHST- 2020/03/25 00:00 [pmc-release]
AID - V713421185866L42 [pii]
AID - 110400384 [pii]
AID - 10.1080/13550280591002379 [doi]
PST - ppublish
SO  - J Neurovirol. 2005 Aug;11(4):384-94. doi: 10.1080/13550280591002379.