The late protein U14 of HHV-6A can induce the pro-inflammatory transcription factor NFκB, and NFκB, in turn, can encourage the replication of HHV-6A.
While CD134 remains the more important receptor for HHV-6B, HHV-6B can use the CD46 receptor when a T cell has the C1 isoform of CD46.
If confirmed, finding could explain ability of HHV-6B to infect salivary, liver and neural cells.
A small pediatric study found that adoptive NK cell infusions eliminated HHV-6B encephalitis, while maintaining a low rate of GVHD. At a ratio of NK/CD4 >2, the HHV-6B reactivation rate dropped dramatically.
Failure to distinguish HHV-6A from HHV-6A/B, and questions about assay sensitivity, make results difficult to interpret.
A prospective study of children transplanted for both malignant and nonmalignant disease found HHV-6 viremia in 53% of cases.
Among infectious agents, HHV-6 was found to be an independent risk factor for thrombotic microangiopathy (TMA) and only HHV-6 infection was associated with TMA-related mortality.
The tetraspanin CD9 promotes CD46-dependent cellular infection by HHV-6A and impairs CD46-independent infection by HHV-6B.
Pattern consistent with clinical studies suggesting these viruses may be one trigger of systemic sclerosis.
HHV-6A was found to both enhance expression and inhibit degradation of amyloid precursor protein in vitro.
40% of the patients with HHV-6 DNA had CNS symptoms, compared to 14.3% of the HHV-6 negative patients.
OX40 levels distinguished DIHS/DRESS from other inflammatory dermatologic conditions, and were associated with HHV-6 reactivation
Systematic review and meta-analysis confirm an association, but not a causal link, between HHV-6 and CFS
HHV-6 was the most prevalent virus in febrile neutropenia episodes among pediatric patients
Significant positive correlations were found between HERV family proteins and antibodies to HHV-6A/B but not antibodies to EBV