HHV-6 Foundation

New papers on HHV-6:

Reactivation of HHV-6 Infection in Patients with Connective Tissue Diseases. Francesco Broccolo and colleagues found that HHV-6 viremia (but not HHV-7) occurred in a significantly higher percentage of patients with autoimmune connective tissue diseases (ACTD) compared to healthy controls (44.8% versus 2.6%) with the highest reactivation frequency (70%) observed in patients with scleroderma. The data suggest that either HHV-6 acts as a pathogenic factor that predisposes patients to ACTD development or ACTD predisposes patients to HHV-6 reactivation. See Abstract from the Journal of Clinical Virology.

HHV-6A infection induces expression of HERV-K18 encoded superantigen. The human endogenous retrovirus K-18 (HERV-K18) encodes a superantigen that causes deregulation of the immune system. Because Epstein-Barr Virus (EBV), a member of the herpesvirus family, induces HERV-K18, a group led by Brigitte Huber of Tufts University looked at HHV-6A to determine if it would have similar transactivation properties. They found that HHV-6A (GS strain), in both latent form and during acute infection, induces the transcription of HERV-K18 in HSB2 cells. They thus concluded that HHV-6A is likely to lead to superantigen production, similarly to EBV. See Abstract from the Journal of Clinical Virology.

HHV-6 variants in pediatric brain tumors. John Crawford and his group provided the first reported series of HHV-6 detection in pediatric brain tumors. Based on screening for HHV-6 by nested polymerase chair reaction, in situ hybridization and immunohistochemistry, they found that 44-72% of the tumors were positive for HHV-6. Their findings do not suggest HHV-6 as a direct cause of brain tumors but the findings show that there is an association of HHV-6 in brain tumors, specifically glial tumors and thus worth further investigation. See Abstract from the Journal of Clinical Virology.

Differential effect of HHV-6A on T cell subsets. Dr. Sudhir Gupta and his colleagues at the University of California, Irvine investigated the response of naïve T cells and various subsets of memory CD4 and CD8+ cells to HHV-6A. They found that HHV-6A has very specific effects on different types of CD4+ and CD8+ T cells. It induces cell division in effector memory CD4+ and CD8+ T cells (which are resistant to apoptosis) whereas naïve and central memory CD4+ and CD8+ T cells showed minimal or no cell division and increased sensitivity to HHV-6A induced apoptosis. These findings show that HHV-6A differentially regulates the immune responses of naïve T cells and different memory subsets of CD4+ and CD8+ T cells. See Abstract from the Journal of Virology.

CIHHV-6 in congenital infection. Caroline Hall and associates at University of Rochester found that 86% of congenital infections were caused by CIHHV-6 or chromosomally integrated HHV-6. They also report that 8% of the CIHHV-6 infants had mRNA, suggesting that these infants either have a reduced immune response to HHV-6, or that CIHHV-6 may activate in some individuals.See abstract from the September issue of Pediatrics.

HHV-6A linked to syncytial giant-cell hepatitis. At the onset of the disease in a transplant patent, HHV-6A (but not HHV-6B) DNA was found in plasma, in affected liver tissue, and in the syncytial giant cells. Viremia disappeared with the resolution of symptoms. See abstract from the August issue of New England Journal of Medicine.

High levels of HHV-6B found in pediatric dilated cardiomyopathy. A team in Italy found high levels of HHV-6 DNA in  44% of pediatric specimens from explanted hearts.  This supports similar findings by several German groups on the evidence of HHV-6 in adult DCM samples. The same specimens had previously tested negative for other cardiotropic viruses. See abstractin Journal of Clinical Pathology.