Findings suggest role in evading host immune defenses.
Both HHV-6 and specific microRNAs may correlate with neurological symptoms in COVID-19.
Transcription of HHV-6 genes was rare, but occurred most often in cells with the highest levels of EBV transcription.
Advance may aid the study of integration and excision and might ultimately have clinical application.
Unclear if viral gene expression signature confers prognostic information that is independent of host cell gene expression signatures.
Genes U12 and U51 encode homologues of human G-protein-coupled receptors, and are potential triggers of autoimmunity.
A large study of iciHHV-6 integration sites found integration at 9q more common in hematologic malignancies—but the study lacked power to draw firm conclusions.
Isolating DNA fragments less than 120 base pairs enriches for viral vs. cellular DNA.
The presence of HHV-6 and EBV DNA in nasal secretions correlates with the degree of adenoid hypertrophy in children.
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.
The tetraspanin CD9 promotes CD46-dependent cellular infection by HHV-6A and impairs CD46-independent infection by HHV-6B.
U20/21 genes may help HHV-6A evade immune response
Chromatin interactions help silence transcription of HHV-6A genes following integration
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