scholarly journals Human herpesvirus 6

2010 ◽  
Vol 151 (13) ◽  
pp. 523-532 ◽  
Author(s):  
József Ongrádi ◽  
Valéria Kövesdi ◽  
G. Péter Medveczky
Keyword(s):  
Human Herpesvirus ◽  
Human Herpesvirus 6 ◽  
Exanthema Subitum ◽  
Herpesvirus 6

Az 1986-ban felfedezett emberi 6-os herpeszvírus A és B változata molekuláris tulajdonságai alapján a legősibb emberi herpeszvírus. A B változat cseppfertőzéssel terjed a tünetmentes vírusürítő felnőttekről a két év alatti kisgyermekekre, akikben alkalmilag exanthema subitum jöhet létre. A vírus a CD4+ macrophagokat, lymphocytákat fertőzi, utóbbiakban élethossziglan lappangás, időnként a nyálmirigyekben vírustermeléssel járó perzisztencia alakul ki. Felnőttkorban ez a változat csontvelő- és szervátültetések kapcsán, immunszuppresszió talaján reaktiválódik, és akár halálos szövődményeket hoz létre. Sclerosis multiplex, idült fáradtság tünetegyüttes, Hodgkin- és nem Hodgkin-lymphomák kialakulásában kofaktor. A CD+-sejteket fertőző és bennük lappangó A változat közvetlen kórokozó képessége nem ismert. A HIV-fertőzést rendkívül erősen transzaktiváljain vitroés betegekben egyaránt. Papillomavírusok által okozott daganatokban is transzaktivátor. Mindkét vírusváltozat kórokozó képessége a megváltozott citokin- és kemokinegyensúlyon alapszik. A két változat elkülönítése szerológiailag nehézkes, erre a savóból vagy a fehérvérsejtekből végzett változatspecifikus PCR alkalmas. A súlyos komplikációk kezelésére, esetleg kemoprofilaxisára ganciclovir, esetleg foscarnet és cidofovir használható.

scholarly journals In vitro cellular tropism of human B-lymphotropic virus (human herpesvirus-6).

1988 ◽  
Vol 167 (5) ◽  
pp. 1659-1670 ◽  
Author(s):  
P Lusso ◽  
P D Markham ◽  
E Tschachler ◽  
F di Marzo Veronese ◽  
S Z Salahuddin ◽  
...  
Keyword(s):  
T Cell ◽  
T Lymphocytes ◽  
Cell Population ◽  
Mononuclear Cells ◽  
Human Herpesvirus ◽  
Human Herpesvirus 6 ◽  
Infected Cells ◽  
Cellular Tropism ◽  
Herpesvirus 6

We investigated the cellular tropism of human B-lymphotropic virus (HBLV) (also designated Human Herpesvirus-6) in vitro by infecting fresh MN cells from normal human adult peripheral blood, umbilical cord blood, bone marrow, tonsil, and thymus. Cultures from all the sources examined contained infectable cells, as shown by the appearance of characteristic enlarged, round-shaped, short-lived cells expressing HBLV-specific markers. Detailed immunological analysis demonstrated that the vast majority of these cells expressed T cell-associated antigens (i.e., CD7, CD5, CD2, CD4, and to a lesser extent, CD8). The CD3 antigen and the TCR-alpha/beta heterodimer were not detectable on the surface membrane, but were identified within the cytoplasm of HBLV-infected cells, by both immunofluorescence and radioimmunoprecipitation assay. A proportion of the HBLV-infected cell population also expressed the CD15 and class II MHC DR antigens. By means of immunoselection procedures it was possible to show that a consistent proportion of HBLV-infectable cells were contained within the CD3-depleted immature T cell population, while the depletion of CD2+ cells completely abrogated the infectability of the cultures. Northern blot analysis confirmed the T cell origin of HBLV-infected cells, demonstrating the expression of full size TCR-alpha and -beta chain mRNA. In addition to fresh T cells, HBLV was able to infect normal T lymphocytes expanded in vitro with IL-2 for greater than 30 d. These results indicate that HBLV is selectively T cell tropic in the course of the in vitro infection of normal mononuclear cells and may therefore be directly involved in the pathogenesis of T cell related hematological disorders. In particular, in light of the cytopathic effect exerted in vitro on CD4+ T lymphocytes, a possible role of HBLV in immune deficiency conditions should be considered.

In vitro sensitivity of human herpesvirus-6 to antiviral drugs

1989 ◽  
Vol 140 ◽  
pp. 219-228 ◽  
Author(s):  
H. Agut ◽  
H. Collandre ◽  
J.-T. Aubin ◽  
D. Guétard ◽  
V. Favier ◽  
...  
Keyword(s):  
Human Herpesvirus ◽  
Antiviral Drugs ◽  
Human Herpesvirus 6 ◽  
In Vitro Sensitivity ◽  
Herpesvirus 6

scholarly journals Human Herpesvirus 6 Infection Presenting as an Acute Febrile Illness Associated with Thrombocytopenia and Leukopenia

2016 ◽  
Vol 2016 ◽  
pp. 1-3 ◽  
Author(s):  
Maja Arnež ◽  
Tatjana Avšič-Županc ◽  
Tina Uršič ◽  
Miroslav Petrovec
Keyword(s):  
Human Herpesvirus ◽  
Febrile Illness ◽  
Hantavirus Infection ◽  
Human Herpesvirus 6 ◽  
Endemic Region ◽  
Course Of Illness ◽  
Granulocytic Anaplasmosis ◽  
Tick Borne Encephalitis ◽  
Exanthema Subitum ◽  
Herpesvirus 6

We present an infant with acute fever, thrombocytopenia, and leukopenia, coming from an endemic region for tick-borne encephalitis, human granulocytic anaplasmosis, and hantavirus infection. The primary human herpesvirus 6 infection was diagnosed by seroconversion of specific IgM and IgG and by identification of viral DNA in the acute patient’s serum. The patient did not show skin rash suggestive of exanthema subitum during the course of illness.

Susceptibility of Human Herpesvirus 6 to Antivirals In Vitro

1990 ◽  
Vol 162 (3) ◽  
pp. 634-637 ◽  
Author(s):  
William H. Burns ◽  
Gordon R. Sandford
Keyword(s):  
Human Herpesvirus ◽  
Human Herpesvirus 6 ◽  
Herpesvirus 6

Inhibition of Cord Blood Cell Expansion by Human Herpesvirus 6 In Vitro

2004 ◽  
Vol 13 (2) ◽  
pp. 197-203 ◽  
Author(s):  
Andreas Nitsche ◽  
Jessika Fleischmann ◽  
Kai-Michael Klima ◽  
Aleksandar Radonić ◽  
Stefanie Thulke ◽  
...  
Keyword(s):  
Blood Cell ◽  
Cord Blood ◽  
Cell Expansion ◽  
Human Herpesvirus ◽  
Human Herpesvirus 6 ◽  
Cord Blood Cell ◽  
Herpesvirus 6

scholarly journals Functional Interaction between Human Herpesvirus 6 Immediate-Early 2 Protein and Ubiquitin-Conjugating Enzyme 9 in the Absence of Sumoylation

2006 ◽  
Vol 80 (20) ◽  
pp. 10218-10228 ◽  
Author(s):  
Andru Tomoiu ◽  
Annie Gravel ◽  
Robert M. Tanguay ◽  
Louis Flamand
Keyword(s):  
Human Herpesvirus ◽  
Immediate Early ◽  
Human Herpesvirus 6 ◽  
Interacting Protein ◽  
Ubiquitin Conjugating Enzyme ◽  
Herpesvirus 6 ◽  
Transcriptional Complex ◽  
Conjugating Enzyme

ABSTRACT The immediate-early 2 (IE2) protein of human herpesvirus 6 is a potent transactivator of cellular and viral promoters. To better understand the biology of IE2, we generated a LexA-IE2 fusion protein and screened, using the yeast two-hybrid system, a Jurkat T-cell cDNA library for proteins that could interact with IE2. The most frequently isolated IE2-interacting protein was the human ubiquitin-conjugating enzyme 9 (Ubc9), a protein involved in the small ubiquitin-like modifier (SUMO) conjugation pathway. Using deletion mutants of IE2, we mapped the IE2-Ubc9-interacting region to residues 989 to 1037 of IE2. The interaction was found to be of functional significance to IE2, as Ubc9 overexpression significantly repressed promoter activation by IE2. The C93S Ubc9 mutant exhibited a similar effect on IE2, indicating that the E2 SUMO-conjugating function of Ubc9 is not required for its repressive action on IE2. No consensus sumoylation sites or evidence of IE2 conjugation to SUMO could be demonstrated under in vivo or in vitro conditions. Moreover, expression levels and nuclear localization of IE2 were not altered by Ubc9 overexpression, suggesting that Ubc9's repressive function likely occurs at the transcriptional complex level. Overall, our results indicate that Ubc9 influences IE2's function and provide new information on the complex interactions that occur between herpesviruses and the sumoylation pathway.

scholarly journals Human Herpesvirus 6 Open Reading Frame U12 Encodes a Functional β-Chemokine Receptor

1998 ◽  
Vol 72 (7) ◽  
pp. 6104-6112 ◽  
Author(s):  
Yuji Isegawa ◽  
Zou Ping ◽  
Kazushi Nakano ◽  
Nakaba Sugimoto ◽  
Koichi Yamanishi
Keyword(s):  
Chemokine Receptors ◽  
Human Herpesvirus ◽  
Murine Cytomegalovirus ◽  
Human Herpesvirus 6 ◽  
Monocyte Chemoattractant Protein 1 ◽  
Reading Frame ◽  
Homologous Genes ◽  
Inflammatory Proteins ◽  
Herpesvirus 6

ABSTRACT Human herpesvirus 6 (HHV- 6), which belongs to the betaherpesvirus subfamily and infects mainly T cells in vitro, causes acute and latent infections. HHV- 6 contains two genes (U12 and U51) that encode putative homologs of cellular G-protein-coupled receptors (GCR), while three other betaherpesviruses, human cytomegalovirus, murine cytomegalovirus, and human herpesvirus 7, have three, one, and two GCR-homologous genes, respectively. The U12 gene is expressed late in infection from a spliced mRNA. The U12 gene was cloned, and the protein was expressed in cells and analyzed for its biological characteristics. U12 functionally encoded a calcium-mobilizing receptor for β-chemokines such as regulated upon activation, normal T expressed and secreted (RANTES), macrophage inflammatory proteins 1α and 1β (MIP-1α and MIP-1β) and monocyte chemoattractant protein 1 but not for the α-chemokine interleukin-8, suggesting that the chemokine selectivity of the U12 product was distinct from that of the known mammalian chemokine receptors. These findings suggested that the product of U12 may play an important role in the pathogenesis of HHV- 6 through transmembrane signaling by binding with β-chemokines.

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