Outcomes worse for the subtype linked to EBV and HHV-6.
Although 28% of children undergoing chemotherapy develop herpesvirus viremia, there is minimal clinical impact
HHV-6, CMV and HSV1/2 were the most likely to reactivate, but herpesvirus reactivation was just as likely prior to chemotherapy.
How frequent are HHV-6-related complications with CAR-T cell therapy?
A combination of studies find that both reactivation and disease are infrequent after CAR-T therapy.
HHV-6B DNA associated with worse clinical outcomes in high grade serous epithelial ovarian cancer
Multiplex assay for 113 viruses in tumor tissue finds six viruses, including HHV-6B, linked to reduced overall survival.
HHV-6A infection of thyroid cancer cells induces various growth-promoting changes
Oncogene activation, pro-inflammatory cytokines, genomic instability, expression of oncogenic miRNAs are induced by infection.
HHV-6 detectable in some urine samples, but not linked to disease
In contrast, human papillomavirus found more often in urine of bladder cancer patients than in urine of patients with non-cancerous urinary tract conditions.
Part 1: Latent HHV-6 is reactivated in patients receiving CAR-T cell therapy
Investigators urge careful monitoring for HHV-6 and ciHHV-6.
Part 2: CAR-T cell therapy and its complications
Could some complications of CAR-T cell therapy be secondary to HHV-6 infection?
Part 3. HHV-6 Encephalitis in CAR-T Cell therapy
Clearly documented cases of HHV-6 encephalitis have been reported, but some are missed because they were classified as ICAN or because HHV-6 testing was not performed in patients with mental status changes.
Part 4. Might HHV-6 contribute to some cases of cytokine release syndrome, pneumonia, and cytopenias in CAR-T Cell therapy?
While unlikely to trigger the cytokine storm, HHV-6 infection may perpetuate it, and contribute directly to cytopenias and pneumonia.
Differentially expressed HHV-6A/B and HHV-7 genes may have prognostic value in gliomas
Unclear if viral gene expression signature confers prognostic information that is independent of host cell gene expression signatures.
HHV-6 encephalitis following CAR-T cell therapy
A growing number of case reports reveal reactivation similar to that seen after hematopoietic stem cell therapy. Could CAR-T cells be a source of lytic HHV-6?
HHV-6A promotes inflammation in astrocytoma cells by dysregulating autophagy
Infection increases ROS, induces ER stress and activates STAT3, NF-κB and mTOR pathways.
Does inherited chromosomal integration of HHV-6 at 9q increase the risk of malignancy?
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.
Adult patients with lower levels of anti-HHV-6 IgG are significantly more likely to experience HHV-6 reactivation following cord blood transplant
Patients with low levels of HHV-6 antibodies might benefit from treatment from IVIG or novel neutralizing antibodies before cord blood transplantation