trans-Activation of the HIV Promoter by a cDNA and Its Genomic Clones of Human Herpesvirus-6

Yi, Zili; Chang, Cheow K.; Gao, Qian; Chandran, Bala; Wood, Charles

doi:10.1006/viro.1994.1129

Cited by 32 publications

(22 citation statements)

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“…It is well known that many apoptotic cells are present in affected lymph nodes of patients with Kikuchi's disease, supporting the present finding that HHV-6 induces apoptosis of lymphocytes in vivo. It has been reported that HHV-6 is an important cofactor for the development of AIDS Lusso et al, 1989 ;Zhou et al, 1994). Taken together with these previous reports, the present data demonstrating that HHV-6 itself induces apoptosis of CD4 + T lymphocytes via an innocent bystander mechanism, as reported recently for HIV-1-induced apoptosis (Finkel et al, 1995), provide new insight into the pathogenesis of AIDS.…”

supporting

confidence: 74%

“…ehime-u.ac.jp et al, 1991, 1993, 1995). Secondly, HHV-6 can coinfect CD4 + T lymphocytes with HIV-1, resulting in trans-activation of the HIV-1 long terminal repeat and acceleration of cell death Lusso et al, 1989 ;Zhou et al, 1994). In addition to these findings, it has recently been demonstrated that inoculation with HHV-6 renders CD4 + T lymphocytes susceptible to apoptosis in vitro (Inoue et al, 1997).…”

mentioning

confidence: 93%

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Apoptosis of CD4+ T lymphocytes in human herpesvirus-6 infection.

Yasukawa

Inoue

Ohminami

et al. 1998

Journal of General Virology

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The present authors have recently reported that inoculation with human herpesvirus-6 (HHV-6) renders CD4 M T lymphocytes susceptible to apoptosis in vitro. In order to confirm that apoptosis of CD4 M T lymphocytes also occurs in HHV-6 infection in vivo, apoptosis of lymphocytes isolated from nine patients with exanthem subitum and from an adult patient with severe HHV-6 infection was examined. Peripheral blood mononuclear cells were cultured for 3 days and apoptosis of lymphocytes was then examined by flow cytometry of propidium iodidestained DNA. The percentages of hypodiploid DNA, indicating apoptosis, in lymphocytes from 10 patients with HHV-6 infection were significantly higher than those from five infant patients with noninfectious diseases and five healthy adults (P 0n0002). DNA fragmentation was also detected by agarose gel electrophoresis in lymphocytes from patients with HHV-6 infection. Apoptosis appeared to occur predominantly in CD4 M T lymphocytes and HHV-6 was isolated from the CD4 M T lymphocyte fraction. These data demonstrate that HHV-6 renders CD4 M T lymphocytes susceptible to apoptosis in vivo.

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supporting

confidence: 74%

mentioning

confidence: 93%

Apoptosis of CD4+ T lymphocytes in human herpesvirus-6 infection.

Yasukawa

Inoue

Ohminami

et al. 1998

Journal of General Virology

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“…The DNA polymerase processivity factor, encoded by the HHV-6 U27 gene, was shown to transactivate the HIV-1 LTR in CV-1 cells. The presence of NF-B binding sites was mandatory for the response to pU27 (461).…”

Section: Transactivation By Hhv-6 Proteinsmentioning

confidence: 99%

Update on Human Herpesvirus 6 Biology, Clinical Features, and Therapy

2005

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Human herpesvirus 6 (HHV-6) is a betaherpesvirus that is closely related to human cytomegalovirus. It was discovered in 1986, and HHV-6 literature has expanded considerably in the past 10 years. We here present an up-to-date and complete overview of the recent developments concerning HHV-6 biological features, clinical associations, and therapeutic approaches. HHV-6 gene expression regulation and gene products have been systematically characterized, and the multiple interactions between HHV-6 and the host immune system have been explored. Moreover, the discovery of the cellular receptor for HHV-6, CD46, has shed a new light on HHV-6 cell tropism. Furthermore, the in vitro interactions between HHV-6 and other viruses, particularly human immunodeficiency virus, and their relevance for the in vivo situation are discussed, as well as the transactivating capacities of several HHV-6 proteins. The insight into the clinical spectrum of HHV-6 is still evolving and, apart from being recognized as a major pathogen in transplant recipients (as exemplified by the rising number of prospective clinical studies), its role in central nervous system disease has become increasingly apparent. Finally, we present an overview of therapeutic options for HHV-6 therapy (including modes of action and resistance mechanisms)

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“…The protein binds to viral DNA polymerase, thereby greatly increasing the rate of DNA synthesis (23). An additional role for p41 as a transcription factor is suggested by experiments showing that cotransfection of plasmid constructs expressing p41 enhance transcription of chloramphenicol acetyl transferase from reporter plasmids containing the HIV long terminal repeats (35). Two monoclonal antibodies (MAbs), MAb to p41 (7) and MAb to p41/38 (20), have been described to react with both HHV-6A and HHV-6B.…”

mentioning

confidence: 99%

Definition of a Divergent Epitope That Allows Differential Detection of Early Protein p41 from Human Herpesvirus 6 Variants A and B

Linde

Dahl

et al. 2001

J Clin Microbiol

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The human herpesvirus 6 (HHV-6) early protein, p41, encoded by the U27 gene has been detected in oligodendrocytes of multiple sclerosis (MS) patients by using a monoclonal antibody (MAb to p41/38). We here report the antigenic epitope of HHV-6 p41 recognized by this MAb. First, we established that the MAb to p41/38 recognizes a nuclear antigen in HHV-6A strain GS-infected cells but not in HHV-6B strain Z29-infected cells. Secondly, we compared the reactivity of the MAb to p41/38 to that of another p41-specific MAb (MAb to p41) on immunoblots with purified p41-glutathione S-transferase fusion protein from strains GS and Z29 and GSand Z29-infected-cell lysates. The two MAbs were tested in an enzyme-linked immunosorbent assay against a panel of synthetic peptides covering the amino acid substitutions between the GS-and Z29-derived p41 proteins, as determined by DNA sequencing of our cloned isolates of the U27 gene. The MAb to p41/38 reacted specifically with a peptide comprising p41 residues 321 to 340 from strain GS. The critical residue in this peptide was serine 328, as the substitution S328N in the Z29 strain rendered the corresponding peptide nonreactive. The p41 S328 marker was present in three of three HHV-6A strains, while four of four sequenced p41 genes from HHV-6B strains had N328. Our findings are of value for the interpretation of previous findings of p41 expression in brains of MS patients and may allow a more detailed analysis of the role of HHV-6 variants in other disorders.

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trans-Activation of the HIV Promoter by a cDNA and Its Genomic Clones of Human Herpesvirus-6

Cited by 32 publications

References 0 publications

Apoptosis of CD4+ T lymphocytes in human herpesvirus-6 infection.

Apoptosis of CD4+ T lymphocytes in human herpesvirus-6 infection.

Update on Human Herpesvirus 6 Biology, Clinical Features, and Therapy

Definition of a Divergent Epitope That Allows Differential Detection of Early Protein p41 from Human Herpesvirus 6 Variants A and B

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