Herpesvirus co-infections, particularly HHV-6 and CMV, cause severe lymphopenia, pneumonia, and an increased risk of acquiring bacterial and fungal infections in non-transplant acute leukemia patients undergoing chemotherapy.
C. trachomatis infection activates latent HHV-6, and HHV-6 in turn promotes persistence of C. trachomatis. Both have been reported in cases of ovarian cancer, leaving the authors to wonder if a co-infection might increase the risk for developing ovarian cancer.
The U94 “latency” gene of HHV-6, interferes with breast cancer proliferation and potentiates chemotherapy.
A Chinese group found HHV-6 direct repeat 7 in 48% of glioma tumors. Furthermore, they determined that DR7 overexpression could promote glioma cell migration, invasion and angiogenesis. Expression profiles showed that DR7 created an inflammatory microenvironment that enhanced degradation of the extracellular matrix.
Since its discovery, HHV-6 has been studied in the context of lymphoproliferative disorders and various types of cancer. Several obstacles, particularly the ubiquitous nature of the virus, have made it difficult to determine exactly how HHV-6 might, or might not, be involved in tumor development.
Investigators from Japan looked at HHV-6 and HHV-7 DNA levels in saliva to see if they might be biomarkers for cancer-related fatigue (CRF) in multiple myeloma patients.
Investigators at the National Cancer Institute found that HHV-6+ lymph nodes can be identified in biopsies from both lymphadenopathy and malignancies. They warn that failing to identify HHV-6 in these biopsies can lead to misdiagnosis in lymphoma cases.
Using a novel serological assay that can differentiate HHV-6A from HHV-6B, investigators found HHV-6A immediate early antibodies to be associated with an increased risk of non-Hodgkin lymphoma.
German investigators conducted a broad scale analysis of CD8 T cell responses to HHV-6B, identifying novel epitopes with potential for immunotherapy or vaccines. The strongest responses were directed against an epitope from IE-2.
The authors discuss how HHV-6 may contribute to the progression of reactive lymphoproliferative disorders by spurring a dysfunctional immune response.
A broadscale investigation of the ovarian cancer oncobiome using a microarray system PathoChip found HHV-6A sequences at or near genes associated with tumorigenesis in ovarian cancer tissue samples.
A team at University of Pittsburgh analyzed a large database of deep sequencing data from tumor and control tissues to look for viral sequences in 22 different cancers. They were surprised to find several herpesviruses in gastrointestinal cancers but not in control tissues.
A higher prevalence of inherited virus was found in patients
Investigators at Fred Hutchinson Cancer Center determined that transplant patients with inherited ciHHV-6 were twice as likely to develop acute graft vs host disease and three times more likely to develop high level CMV viremia. Transplant patients were also significantly more likely to have inherited ciHHV-6 than donors.
Italian investigators found that HHV-6 latency-associated gene U94, inserted in a HSV1 vector, inhibited the development of breast cancer, cervical cancer, and lung metastasis. It also impaired tumor driven angiogenesis.
Human papillomavirus 4 is a benign strain not associated with cancer. However, in a woman with inherited chromosomally integrated HHV-6A, a high grade vaginal squamous lesion developed rapidly. The authors warn that there may be a synergistic effect between HPV4 and iciHHV6A.
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