Epstein-Barr virus and human herpesvirus type 6 infection in patients with psoriasis.

The association of psoriasis with latent human herpesvirus infection has not been well described. To better understand the relationship between severe psoriasis and its treatment with latent human herpesvirus infection, we performed a cross-sectional study to determine if patients with severe psoriasis and psoriasis patients treated with immunosuppressive therapies have higher rates of Epstein-Barr virus and human herpesvirus 6 replication compared to healthy controls. The prevalence of Epstein-Barr virus and human herpesvirus 6 replication was measured in white blood cells by quantitative polymerase chain reaction. We found no evidence of active viral replication in white blood cells of healthy controls (0/10; 95% confidence interval 0-0.26), patients with severe psoriasis (0/25; 95% confidence interval 0-0.11) or severe psoriasis patients on immunosuppressive treatment (0/26; 95% confidence interval 0-0.11). The results of this study suggest that neither severe psoriasis alone, nor in combination with immunosuppressive therapy, is associated with an increase in Epstein-Barr virus or human herpesvirus 6 replication in white blood cells.

Langerhans cell histiocytosis and human herpes virus 6 (HHV-6), an analysis by real-time polymerase chain reaction.

Patients with Langerhans cell histiocytosis (LCH) usually present to orthopedic surgeons because this disease most commonly affects bone. The pathogenesis of LCH is unknown, although roles for environmental, infectious, immunologic, and genetic causes have been postulated. More specifically, there is limited data suggesting that human herpes virus 6 (HHV-6) may be a potential etiologic agent. Frozen biopsy material was obtained from 13 patients with LCH and 20 patients without the disease. After ensuring histologic adequacy of the material, the tissue was tested for HHV-6 by qualitative and quantitative real-time TaqMan PCR. Four of 13 patients with LCH had evidence of HHV-6 DNA in their tissue while 7 of 20 control patients tested positive for HHV-6 genome. Viral loads are reported for the positive patients; no statistical difference was observed in the presence or quantity of HHV-6 DNA found in either population, suggesting that the prevalence of HHV-6 in the tissue of LCH patients is the same as that found in tissue from individuals without disease.

Impact of human immunodeficiency virus type 1 (HIV-1) genetic diversity on performance of four commercial viral load assays: LCx HIV RNA Quantitative, AMPLICOR HIV-1 MONITOR v1.5, VERSANT HIV-1 RNA 3.0, and NucliSens HIV-1 QT.

Human immunodeficiency virus type 1 (HIV-1) evolution and changing strain distribution present a challenge to nucleic acid-based assays. Reliable patient monitoring of viral loads requires the detection and accurate quantification of genetically diverse HIV-1. A panel of 97 HIV-1-seropositive plasma samples collected from Cameroon, Brazil, and South Africa was used to compare the performance of four commercially available HIV RNA quantitative tests: Abbott LCx HIV RNA Quantitative assay (LCx), Bayer Versant HIV-1 RNA 3.0 (bDNA), Roche AMPLICOR HIV-1 MONITOR v1.5 (Monitor v1.5), and bioMérieux NucliSens HIV-1 QT (NucliSens). The panel included group M, group O, and recombinant viruses based on sequence analysis of gag p24, pol integrase, and env gp41. The LCx HIV assay quantified viral RNA in 97 (100%) of the samples. In comparison, bDNA, Monitor v1.5, and NucliSens quantified viral RNA in 96.9%, 94.8%, and 88.6% of the samples, respectively. The two group O specimens were quantified only by the LCx HIV assay. Analysis of nucleotide mismatches at the primer/probe binding sites for Monitor v1.5, NucliSens, and LCx assays revealed that performance characteristics reflected differences in the level of genetic conservation within the target regions.