Review Part 3: Human herpesvirus-6 in multiple non-neurological diseases.

HHV-6 Foundation, Santa Barbara, California, USA.
Journal of Medical Virology (Impact Factor: 2.22). 11/2010; 82(11):1903-10. DOI: 10.1002/jmv.21860
Source: PubMed

ABSTRACT J. Med. Virol. 82:1903–1910, 2010. © 2010 Wiley-Liss, Inc.

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    ABSTRACT: Abstract Background. Human herpesvirus-6B (HHV-6B) antigens are commonly found in the intestinal mucosa of patients with immunosuppression. In a series of immunocompetent patients with adenomatous, polyp HHV-6B antigen expression from mucosal biopsies was more intense than in biopsies taken from patients receiving immunosuppressive drugs because of kidney transplantation or inflammatory bowel disease. Methods. HHV-6B and cytomegalovirus (CMV) antigen expression was determined from mucosal biopsy samples by immunohistochemistry. HHV-6-DNA content was studied in adenomatous polyps (seven tubular adenomas and one tubulovillous adenoma) taken from eight immunocompetent patients and in three mucosal biopsy samples taken from immunocompetent patients without adenomas using in situ hybridization (ISH) method. Results. HHV-6B antigen expression on mucosal biopsies was strongly positive in five of eight patients with adenomas and negative in all patients without adenoma. CMV antigen expression on mucosal biopsies was faintly positive in three of adenoma patients. HHV-6 ISH was positive in seven of eight adenomatous polyps, most intense in the tubulovillous adenoma and negative in all three mucosal biopsies of patients without adenomas. Conclusion. Intensive HHV-6-DNA expression was found in adenomatous polyps of the colon. Further studies on involvement of HHV-6 in the development of gastrointestinal polyps are warranted.
    Scandinavian Journal of Gastroenterology 10/2013; · 2.33 Impact Factor
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    ABSTRACT: The tumor suppressor p53 pathway, whose alterations are highly associated with all types of human cancers, plays an essential role in preventing tumor development and progression mostly through its downstream target genes. Over the last decade, a growing list of p53 microRNA (miRNA) targets has been identified as additional downstream players of this pathway. Further studies of these miRNAs have revealed their more complicated regulations and functions in executing and/or regulating p53 activity. Here, we review the p53 miRNA targets identified thus far, and discuss how they fine-tune p53 stress responses, mediate the crosstalk between p53 and other signaling pathways, and expand the role of p53 in other human diseases in addition to cancers.
    Journal of Molecular Cell Biology 04/2014; · 7.31 Impact Factor
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    ABSTRACT: Background The triggering agent of multiple sclerosis is still unknown and many viruses, including human herpesvirus-6 (HHV-6), are under suspicion. In earlier study we found patients who had HHV-6 reactive OCBs in their CSF. We wanted to investigate whether HHV-6 has an active role in diseases with demyelination. Objective To analyze the HHV-6-reactive cases in detail and investigate the possible independent role of HHV-6 in the development of central nervous system involvements with demyelination. Study design We studied serum and CSF samples that were collected over a period of one year, from all patients who had oligoclonal bands (OCB) in cerebrospinal fluid (CSF) and were examined in the Department of Neurology, University Central Hospital of Helsinki, Finland. Clinical evaluation was accomplished blinded of HHV-6 analysis and follow-up time was two years. All patients underwent MRI of the head and clinically indicated CSF analysis. Results The 17 patients with HHV-6-reactive OCBs were significantly younger and had significantly more IgG-OCBs in comparison to patients without HHV-6-reactive OCBs. Initial diagnoses in patients with HHV-6-reactive OCBs remained the same during the follow-up time. Conclusion Patients with HHV-6-positive OCBs appear to form a separable group. In progressive neurological diseases HHV-6 may have a role in long-term infection with demyelination.
    Journal of Clinical Virology 10/2014; · 3.47 Impact Factor