Differential tropism of human herpesvirus 6 (HHV-6) variants and induction of latency by HHV-6A in oligodendrocytes
Autor: | Karen Yao, Jenny Ahlqvist, Nahid Akhyani, Anna Fogdell-Hahn, Julie Fotheringham, Steven Jacobson |
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Rok vydání: | 2005 |
Předmět: |
Gene Expression Regulation
Viral Multiple Sclerosis Viral protein MO3.13 Herpesvirus 6 Human T-Lymphocytes viruses oligodendrocytes Biology medicine.disease_cause Article Cell Line Cellular and Molecular Neuroscience Virology Virus latency Exanthema Subitum medicine Humans Encephalitis Viral RNA Messenger Antigens Viral latency Tropism Cytopathic effect virus diseases biochemical phenomena metabolism and nutrition biology.organism_classification medicine.disease Virus Latency Oligodendroglia Neurology Cell culture human herpesvirus 6 Human herpesvirus 6 Neurology (clinical) Viral disease Viral load |
Zdroj: | Journal of Neurovirology |
ISSN: | 1538-2443 1355-0284 |
DOI: | 10.1080/13550280591002379 |
Popis: | 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. |
Databáze: | OpenAIRE |
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