Similar findings with EBV and CMV reactivation; causation vs. correlation unclear.
Could HHV-6 reactivation in drug hypersensitivity trigger fulminant type 1 diabetes?
Small study demonstrates increased HHV-6 antibodies in all patients shortly before the onset of DIHS-associated fulminant diabetes.
International expert panel publishes guidelines for management of DRESS
Guidelines recommend routinely assessing HHV-6 viral load, but not antiviral treatment when HHV-6 reactivation identified.
Increased expression of HHV-6B receptor CD134/OX40 found in DIHS/DRESS skin lesions
The severity of DIHS/DRESS cases was significantly correlated with the frequency of CD134+ cells.
Thorough review of the role of HHV-6 in DIHS/DRESS
HHV-6 reactivation much more frequent than reactivation of other herpesviruses.
Investigators find HHV-6 in the skin of DRESS patients two weeks before it is found in the blood in a large, multi-center case series
HHV-6 reactivation in both skin and blood was found frequently in severe cases.
DRESS, a syndrome linked to viral reactivation, may be triggered by several antivirals
Ribavarin, ritonavir, abacavir and lamivudine were the primary triggers.
The role of OX40 in DIHS/DRESS and HHV-6 reactivation
OX40 levels distinguished DIHS/DRESS from other inflammatory dermatologic conditions, and were associated with HHV-6 reactivation
In DRESS/DIHS, early treatment with high dose steroids may suppress HHV-6; late treatment may prolong viremia
High dose steroids given in the first week appears to prevent HHV-6 reactivation in DRESS/DIHS patients by suppressing T-cell activation and serum interleukin-2 receptor (sIL-2R) levels. In contrast, a late start of steroid therapy resulted in a persistently high viral load for at least three weeks.
An explanation for why HHV-6 reactivation and DRESS lead to autoimmunity
Patients with DRESS/DIHS hypersensitivity reactions and active HHV-6 often develop autoimmune diseases such as type 1 diabetes and autoimmune thyroiditis. Investigators at National Taiwan University Hospital believe that IP-10 is key to this process.
Single-cell RNA sequencing analysis implicates HHV-6B in DIHS/DRESS.
RNA-Seq analysis of cells from skin and blood identified both HHV-6 and JAK-STAT pathways inhibitors as potential targets. Central memory CD4+T cells were enriched with HHV-6B.
HHV-6 interacts with HLA-B*13:01 to confer a 92-fold increased risk of trichloroethylene hypersensitivity reaction
Chinese investigators determined that human leukocyte antigen polymorphism HLA-B*13:01 and HHV-6 DNA blood positivity were not only independently associated with occupational trichloroethylene hypersensitivity, they had an interactive effect, increasing the odds ratio to 92.
HHV-6 and lymphoproliferative syndromes: a review
The authors discuss how HHV-6 may contribute to the progression of reactive lymphoproliferative disorders by spurring a dysfunctional immune response.
HHV-6 reactivation tied to early hypogammaglobulinemia in drug hypersensitivity syndrome
A Spanish study of drug-induced eosinophilia found that early hypogammaglobulinemia was associated with subsequent HHV-6 reactivation in patients with severe drug hypersensitivity syndromes. This study of 274 cases at La Paz University Hospital in Madrid confirms earlier reports from Japan and France that described transient reductions of total IgG at the outset of drug hypersensitivity reactions leading to HHV-6 reactivation.
Does CD134 upregulation explain why HHV-6 reactivates preferentially in DRESS/ DIHS?
It has long been a mystery why HHV-6 is preferentially reactivated in drug reaction with eosinophilia and systemic symptoms (DRESS), also known as drug induced hypersensitivity syndrome (DIHS). HHV-6 reactivation occurs in over 60% of severe cases and is part of the definition of DIHS in Japan. Investigators in Japan suspect that the explanation may lie with the CD134 receptor on activated CD4 cells.
- Page 1 of 2
- 1
- 2