Human herpesvirus 6 major immediate early promoter has strong activity in T cells and is useful for heterologous gene expression

<p>Abstract</p> <p>Background</p> <p>Human herpesvirus-6 (HHV-6) is a beta-herpesvirus. HHV-6 infects and replicates in T cells. The HHV-6-encoded major immediate early gene (MIE) is expressed at the immediate-early infection phase. Human cytomegalovirus major immediate early promoter (CMV MIEp) is commercially available for the expression of various heterologous genes. Here we identified the HHV-6 MIE promoter (MIEp) and compared its activity with that of CMV MIEp in various cell lines.</p> <p>Methods</p> <p>The HHV-6 MIEp and some HHV-6 MIEp variants were amplified by PCR from HHV-6B strain HST. These fragments and CMV MIEp were subcloned into the pGL-3 luciferase reporter plasmid and subjected to luciferase reporter assay. In addition, to investigate whether the HHV-6 MIEp could be used as the promoter for expression of foreign genes in a recombinant varicella-zoster virus, we inserted HHV-6 MIEp-DsRed expression casette into the varicella-zoster virus genome.</p> <p>Results</p> <p>HHV-6 MIEp showed strong activity in T cells compared with CMV MIEp, and the presence of intron 1 of the MIE gene increased its activity. The NF-κB-binding site, which lies within the R3 repeat, was critical for this activity. Moreover, the HHV-6 MIEp drove heterologous gene expression in recombinant varicella-zoster virus-infected cells.</p> <p>Conclusions</p> <p>These data suggest that HHV-6 MIEp functions more strongly than CMV MIEp in various T-cell lines.</p

Human herpesvirus 6 envelope components enriched in lipid rafts: evidence for virion-associated lipid rafts

In general, enveloped viruses are highly dependent on their lipid envelope for entry into host cells. Here, we demonstrated that during the course of virus maturation, a significant proportion of human herpesvirus 6 (HHV-6) envelope proteins were selectively concentrated in the detergent-resistant glycosphingolipid- and cholesterol-rich membranes (rafts) in HHV-6-infected cells. In addition, the ganglioside GM1, which is known to partition preferentially into lipid rafts, was detected in purified virions, along with viral envelope glycoproteins, gH, gL, gB, gQ1, gQ2 and gO indicating that at least one raft component was included in the viral particle during the assembly process

Effects of varicella zoster virus or herpes simplex virus type I infection in vitro on response of human peripheral blood mononuclear cells to phytohemagglutinin.

Examination was made of the in vitro response of human peripheral blood mononuclear cells (PBNMCs) to phytohemagglutinin (PHA) following treatment with varicella zoster virus (VZV) or herpes simplex virus type 1 (HSV 1). Cell proliferation was determined by colorimetric assay using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide. The response to PHA was depressed in all cases by virus infection of PBMNCs prior to PHA treatment. When the infection with the viruses was after PHA treatment, PHA response differed. For VZV infection, the response increased in four out of six samples, but was reduced in the other two. The response to PHA was depressed in all six samples by HSV 1 infection.</p

Human Herpesvirus 6-Associated Hemophagocytic Syndrome in a Healthy Adult

Virus-associated hemophagocytic syndrome is a fulminant disorder associated with systemic viral infection and characterized pathologically by multiple-organ infiltration of hemophagocytic histiocytes into the lymphoreticular tissues. This is the first report of a previously healthy adult in whom Human herpesvirus 6 reactivation induced this syndrome with severe hemodynamic and respiratory distress

Varicella-zoster virus ORF 58 gene is dispensable for viral replication in cell culture

<p>Abstract</p> <p>Background</p> <p>Open reading frame 58 (ORF58) of varicella-zoster virus (VZV) lies at the 3'end of the Unique long (U_L) region and its functional is unknown. In order to clarify whether ORF58 is essential for the growth of VZV, we constructed a deletion mutant of ORF58 (pOka-BACΔ58) from the Oka parental genome cloned into a bacterial artificial chromosome (pOka-BAC).</p> <p>Results</p> <p>The ORF58-deleted virus (rpOkaΔ58) was reconstituted from the pOka-BACΔ58 genome in MRC-5 cells, indicating that the ORF58 gene is non-essential for virus growth. Comparison of the growth rate of rpOkaΔ58 and recombinant wild-type virus by assessing plaque sizes revealed no significant differences between them both in MRC-5 cells and malignant melanoma cells.</p> <p>Conclusion</p> <p>This study shows that the ORF58 gene is dispensable for viral replication and does not affect the virus' ability to form plaques <it>in vitro</it>.</p