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Complete replication cycle and acquisition of tegument in nucleus of human herpesvirus 6A in astrocytes and in T‐cells
Author(s) -
Ahlqvist Jenny,
Donati Donatella,
Martinelli Elena,
Akhyani Nahid,
Hou Jean,
Major Eugene O.,
Jacobson Steven,
FogdellHahn Anna
Publication year - 2006
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.20737
Subject(s) - viral tegument , virology , nucleus , human herpesvirus , biology , replication (statistics) , viral replication , human herpesvirus 6 , microbiology and biotechnology , virus , herpesviridae , viral disease
The ultrastructural replication cycle of human herpesvirus 6A and 6B, both T‐lymphotropic viruses, with tropism for the central nervous system, was compared by electron microscopy in the same cells, that is, in the T‐lymphoblastoid cell line SupT‐1 and in human astrocytes. Both HHV‐6A and HHV‐6B replicated efficiently in SupT‐1 and formed viral particles. The tegument is the least characterized structure of the herpesviral particle and both variants were able to form intranuclear membrane compartments called tegusomes in SupT‐1 where tegumentation occurred. Also, tegumentation occurred in HHV‐6A infected cells in the nucleoplasm without the presence of a tegusome. This suggests that there is more than one possible route of tegumentation. Differences in the replication cycles between HHV‐6A and HHV‐6B were also observed in the cytoplasm. One such difference was that prominent annulate lamellae were only found in the cytoplasm of HHV‐6A infected cells. In astrocytes a successful formation of viral particles was only seen with the HHV‐6A variant. The HHV‐6A virus life cycle in astrocytes resembled the life cycle in the T‐cell line SupT‐1, except that no annulate lamellae were found. Complete viral particles were found extracellularly around the astrocytes and the supernatant of infected astrocytes were able to re‐infect SupT‐1 cells. This suggests that HHV‐6A infection in astrocytes can generate complete, viable, and infectious viral particles. The HHV‐6 variants behave differently in the same type of cells and have different tropisms for astrocytes, supporting the notion that the variants might induce different diseases. J. Med. Virol. 78:1542–1553, 2006. © 2006 Wiley‐Liss, Inc.