Abstract:551
552K. YAMANISHI balloon-like cells could be observed. When the cells were fixed and stained with the sera of acute and convalescent phase of ES, positive staining was observed only with the convalescent sera. Next, the cultured cells were observed by electron microscopy (EM) as reported elsewhere (74). The typical herpesvirus particles were found in the nucleus and cytoplasm of the cultured cells. Thus, the diameter of virion was 90-110 nm in the nucleus and 150-170 nm in the cytoplasm (91, 95), suggesting… Show more
“…It has also been established that reactivation of HHV-6 causes various clinical manifestations, including lymphadenitis, pneumonitis, hepatitis, meningoencephalitis, infectious mononucleosis-like disease, hemophagocytic syndrome, and hypersensitivity syndrome (3)(4)(5)(6). HHV-6 isolates are divided into two subgroups, HHV-6A and HHV-6B, on the basis of their tropism for certain cell lines, reactivities with mAbs and HHV-6-specific T lymphocyte clones, and restriction enzyme cleavage patterns (7)(8)(9).…”
We have recently reported that down-regulation of CXC chemokine receptor (CXCR) 4 in CD4+ T lymphocytes is induced by human herpesvirus (HHV) 6 infection. In this study, we further studied the mechanisms of HHV-6-induced CXCR4 down-regulation, focusing on the regulation of CXCR4 transcription. Down-regulation of CXCR4 transcription was detected in HHV-6A-infected JJHAN and HHV-6B-infected MT-4 cell lines, as we had previously reported for HHV-6-infected peripheral blood CD4+ T lymphocytes. Luciferase assays revealed that a YY1-binding site around −320 relative to the transcription start site is important for down-regulation of CXCR4 transcription in HHV-6-infected cells. The binding activity of YY1, which is a repressor of CXCR4 transcription, to the CXCR4 promoter appeared to significantly increase in HHV-6-infected cells compared with the binding activity in mock-infected cells. Immunoprecipitation assays showed that in HHV-6-infected cells association of c-Myc with YY1 was decreased and that of Max with c-Myc was increased, whereas association of Mad with Max appeared to be decreased. The amounts of each of YY1, c-Myc, Max, and Mad proteins synthesized in cells were not altered by HHV-6 infection. These data indicate that the decreased association of YY1 with c-Myc that is caused by impaired interaction in the c-Myc/Max/Mad network results in increased binding activity of YY1 to the CXCR4 promoter, mediating down-regulation of CXCR4 production in HHV-6-infected cells.
“…It has also been established that reactivation of HHV-6 causes various clinical manifestations, including lymphadenitis, pneumonitis, hepatitis, meningoencephalitis, infectious mononucleosis-like disease, hemophagocytic syndrome, and hypersensitivity syndrome (3)(4)(5)(6). HHV-6 isolates are divided into two subgroups, HHV-6A and HHV-6B, on the basis of their tropism for certain cell lines, reactivities with mAbs and HHV-6-specific T lymphocyte clones, and restriction enzyme cleavage patterns (7)(8)(9).…”
We have recently reported that down-regulation of CXC chemokine receptor (CXCR) 4 in CD4+ T lymphocytes is induced by human herpesvirus (HHV) 6 infection. In this study, we further studied the mechanisms of HHV-6-induced CXCR4 down-regulation, focusing on the regulation of CXCR4 transcription. Down-regulation of CXCR4 transcription was detected in HHV-6A-infected JJHAN and HHV-6B-infected MT-4 cell lines, as we had previously reported for HHV-6-infected peripheral blood CD4+ T lymphocytes. Luciferase assays revealed that a YY1-binding site around −320 relative to the transcription start site is important for down-regulation of CXCR4 transcription in HHV-6-infected cells. The binding activity of YY1, which is a repressor of CXCR4 transcription, to the CXCR4 promoter appeared to significantly increase in HHV-6-infected cells compared with the binding activity in mock-infected cells. Immunoprecipitation assays showed that in HHV-6-infected cells association of c-Myc with YY1 was decreased and that of Max with c-Myc was increased, whereas association of Mad with Max appeared to be decreased. The amounts of each of YY1, c-Myc, Max, and Mad proteins synthesized in cells were not altered by HHV-6 infection. These data indicate that the decreased association of YY1 with c-Myc that is caused by impaired interaction in the c-Myc/Max/Mad network results in increased binding activity of YY1 to the CXCR4 promoter, mediating down-regulation of CXCR4 production in HHV-6-infected cells.
“…ES is a common disease of infants or young children characterized by 3-4 days of high fever, followed by skin rash (11,20,21). Restriction enzyme analyses of DNAs of isolates obtained from peripheral blood of ES patients showed that these viruses were HHV-6B variants, similar to the Z29 prototype strain (6).…”
mentioning
confidence: 99%
“…Restriction enzyme analyses of DNAs of isolates obtained from peripheral blood of ES patients showed that these viruses were HHV-6B variants, similar to the Z29 prototype strain (6). In some cases ES is accompanied by a wide range of clinical complications from meningoencephalitis to fatal fulminant hepatitis (11,20,22,23). It was suggested that HHV-7 also causes ES, although in many of these cases the observed ES was associated with a large increase of HHV-6 antibody titers (16,19,24,25).…”
Human herpesviruses 6 and 7 (HHV-6 and HHV-7) are prevalent lymphotropic viruses that infect more than 80% of children at infancy or during early childhood.Infection ranges from asymptomatic to severe disease. HHV-6B causes exanthem subitum. The virus can be recovered from peripheral blood mononuclear cells during the acute phase of exanthem subitum, but the host remains latently infected throughout life. In immunocompromised patients undergoing kidney, liver, or bone marrow transplantation latent HH`V-6B is reactivated, at times causing severe or fatal disease. Here, we describe the establishment of an in vitro system for reactivation of HHV-6B and HHV-7 from latency. HHV-7 is reactivated from latently infected peripheral blood mononuclear cells by T-cell activation. HHV-6B could not be reactivated under similar conditions; however, the latent HHV-6B could be recovered after the cells were infected with HHV-7. Once reactivated, the HHV-6B genomes became prominent and the HHV-7 disappeared. We conclude that HHV-7 can provide a transacting function(s) mediating HHV-6 reactivating from latency. Understanding the activation process is critical for the development of treatments to control the activation of latent viruses so as to avoid these sometimes life threatening infections in transplant recipients.
“…Subsequent studies have revealed that HHV-6 is a causative agent of exanthem subitum in infants at primary infection (45). Reactivation of HHV-6 occurs frequently in patients who are immune deficient, such as organ transplant recipients and those with AIDS (24), and causes various disorders, including lymphadenitis, pneumonitis, hepatitis, meningoencephalitis, retinitis, infectious mononucleosis-like disease, hemophagocytic syndrome, and hypersensitivity syndrome (2,6,41,42,44). HHV-6 isolates are divided into two subgroups, HHV-6A and HHV-6B, on the basis of their tropism for certain cell lines, their reactivities with monoclonal antibodies (MAbs) and HHV-6-specific T-lymphocyte clones, and their restriction enzyme cleavage patterns (11,38,50).…”
Human herpesvirus 6 (HHV-6) has a tropism for T lymphocytes and monocytes/macrophages, suggesting that HHV-6 infection affects the immunosurveillance system. In the present study, we investigated the HHV-6-induced phenotypic and functional alterations of dendritic cells (DCs), which are professional antigenpresenting cells. HHV-6 infection of monocyte-derived immature DCs appeared to induce the up-regulation of CD80, CD83, CD86, and HLA class I and class II molecules, suggesting that HHV-6 infection induces the maturation of DCs. In addition, the antigen capture capacity of DCs was found to decrease following infection with HHV-6. In contrast to up-regulation of mature-DC-associated surface molecules on HHV-6-infected DCs, their capacity for presentation of alloantigens and exogenous virus antigens to T lymphocytes decreased significantly from that of uninfected DCs. In contrast, there appeared to be no reduction in the capacity for presentation of an HLA class II-binding peptide to the peptide-specific CD4 ؉ T lymphocytes. These data indicate that HHV-6 infection induces phenotypic alterations and impairs the antigen presentation capacity of DCs. The present data also suggest that the dysfunction of HHV-6-infected DCs is attributable mainly to impairment of the antigen capture and intracellular antigen-processing pathways.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.