A research team from Riga Stradins University in Latvia has reported that the activation of HHV-6B and HHV-7 in patients with gastrointestinal cancer may lead to a marked decrease in lymphocytes and worsening of immunosuppression. Furthermore, a detailed analysis of viral interactions and specific cellular subpopulation levels among their cohort suggests an abnormal antiviral response that could lead to an accelerated progression of co-infections and worse outcomes in these patients.
Overall, 65 patients with gastrointestinal cancer (GIC) were enrolled in the study, which showed that the activation of HHV-6 & HHV-7 is significantly more frequent among patients with lymphopenia (p=0.003). All HHV-6 positive patients were identified as having HHV-6B, corresponding with previous studies of patients with GI tract complications (Lempinen 2012).
A more detailed analysis demonstrated that subpopulations of specific lymphocytes are decreased among patients with lymphopenia and active viral infection, particularly those known to be betaherpesvirus target cells (CD3+, CD8+ and CD38+ subpopulations). In addition, the activation of HHV-6 and HHV-7 in patients with GIC contributed to a significantly increased expression of the immunomodulatory factors IL-6 and sIL-2R, while simultaneously decreasing the expression of TNF-alpha. Taken together, both findings (decrease in lymphocyte subpopulations and the observed changes immunomodulatory factors), could contribute to viable mechanisms that predict how HHV-6 and HHV-7 influence the course of the disease.
In light of their findings, the authors propose two primary mechanisms for interaction: the first is through direct influence on lymphocytes by direct infection and induction of cell lyses; the second is through influencing the host’s immunomological capabilities by altering the expression of naturally-occuring factors such as interleukins. Both routes would ultimately lead to worse clinical outcomes for patients with GIC. The authors propose that combining studies of both virus and cancer-mediated immune suppressive mechanisms in the future (and importantly, the evaluation of not only changes in pro-inflammatory cytokines but also the expression of anti-inflammatory cytokines) will further elucidate the specific role of HHV-6 & HHV-7 in host-tumour interactions.
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