Telomeric sequences from human herpesvirus 6 do not mediate nuclear retention of episomal DNA in human cells

1998 ◽  
Vol 143 (3) ◽  
pp. 563-570 ◽  
Author(s):  
G. H. Bulboaca ◽  
H. Deng ◽  
S. Dewhurst ◽  
M. P. Calos
Keyword(s):  
Human Herpesvirus ◽  
Human Cells ◽  
Human Herpesvirus 6 ◽  
Nuclear Retention ◽  
Telomeric Sequences ◽  
Herpesvirus 6 ◽  
Episomal Dna

scholarly journals Human Herpesvirus 6 Variant A but Not Variant B Induces Fusion from Without in a Variety of Human Cells through a Human Herpesvirus 6 Entry Receptor, CD46

2002 ◽  
Vol 76 (13) ◽  
pp. 6750-6761 ◽  
Author(s):  
Yasuko Mori ◽  
Tsukasa Seya ◽  
Hong Lan Huang ◽  
Pilailuk Akkapaiboon ◽  
Panadda Dhepakson ◽  
...  
Keyword(s):  
Human Herpesvirus ◽  
Syncytium Formation ◽  
Human Cells ◽  
Target Cells ◽  
Functional Difference ◽  
Human Herpesvirus 6 ◽  
Fusion Event ◽  
Target Cell Membrane ◽  
Herpesvirus 6 ◽  
Entry Receptor

ABSTRACT Human herpesvirus 6 (HHV-6) is a lymphotropic betaherpesvirus that productively infects T cells and monocytes. HHV-6 isolates can be differentiated into two groups, variants A and B (HHV-6A and HHV-6B). Here, we show a functional difference between HHV-6A and -6B in that HHV-6A induced syncytium formation of diverse human cells but HHV-6B did not. The syncytium formation induced by HHV-6A was observed 2 h after infection; moreover, it was found in the presence of cycloheximide, indicating that HHV-6A induced fusion from without (FFWO) in the target cells. Furthermore, the fusion event was dependent on the expression of the HHV-6 entry receptor, CD46, on the target cell membrane. In addition, we determined that short consensus repeat 2 (SCR2), -3, and -4 of the CD46 ectodomain were essential for the formation of the virus-induced syncytia. Monoclonal antibodies against glycoproteins B and H of HHV-6A inhibited the fusion event, indicating that the syncytium formation induced by HHV-6A required glycoproteins H and B. These findings suggest that FFWO, which HHV-6A induced in a variety of cell lines, may play an important role in the pathogenesis of HHV-6A, not only in lymphocytes but also in various tissues, because CD46 is expressed ubiquitously in human tissues.

Cytomegalovirus, human herpesvirus-6, and human herpesvirus-7 in hematological patients

2003 ◽  
Vol 40 (2) ◽  
pp. 154-162 ◽  
Author(s):  
A. A. Clark ◽  
C. C. Emery ◽  
D. D. Griffiths
Keyword(s):  
Human Herpesvirus ◽  
Human Herpesvirus 6 ◽  
Hematological Patients ◽  
Herpesvirus 6

Leukocytoclastic Vasculitis Associated with HHV6-A/ciHHV6-A and HHV6-B Coinfection in an Immunocompetent Woman

2019 ◽  
Vol 19 (2) ◽  
pp. 221-225 ◽  
Author(s):  
Agata Calvario ◽  
Caterina Foti ◽  
Maria Scarasciulli ◽  
Paolo Romita ◽  
Eva Eliassen ◽  
...  
Keyword(s):  
Transcriptional Activity ◽  
Skin Infection ◽  
Leukocytoclastic Vasculitis ◽  
Human Herpesvirus ◽  
Small Vessel Vasculitis ◽  
Case Description ◽  
Human Herpesvirus 6 ◽  
Late Antigen ◽  
Herpesvirus 6 ◽  
Systemic Symptoms

Background and Objective: Leukocytoclastic vasculitis (LCV) is a small vessel vasculitis that can be limited to the skin but may also affect other organs. Often, its cause is unknown. LCV has previously been reported to occur with the reactivation of human herpesvirus 6 (HHV-6). Here, we report a second instance of HHV-6 reactivation in a 43-year-old woman with idiopathic cutaneous LCV. </P><P> Case Description: In this case, the patient was immunocompetent, and testing revealed that she had inherited chromosomally integrated human herpesvirus 6 variant A (iciHHV6-A) with a parallel skin infection of HHV-6B. The integrated ciHHV-6A strain was found to be transcriptionally active in the blood, while HHV-6B late antigen was detected in a skin biopsy. The patient’s rash was not accompanied by fever nor systemic symptoms and resolved over four weeks without any therapeutic intervention.Conclusion:In light of the transcriptional activity documented in our case, further examination of a possible role for HHV-6 in the etiology of LCV is warranted.

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