Human herpesvirus 6 (HHV–6) is one of many infectious agents that have been implicated in the pathogenesis of multiple sclerosis (MS). Request the document from your library. The mean HHV-6 DNA load (log10 copies)/hair follicle was 4.2 (≥1 copies/hair follicle cell), demonstrating that viral integration is not confined to blood cells. IF: 1/10 – 1/50. Five of 36 patients without prophylactic GCV showed clinical manifestations including skin rash, interstitial pneumonitis, persistent thrombocytopenia, enterocolitis and thrombotic microangiopathy, respectively. Antibody titers did not correlate with HHV-6 DNA levels in PBMCs or saliva (P = 0.27 and P = 0.44, respectively). Limitations of the available experimental techniques and perspectives for future research are discussed.
In addition, one further specimen with evidence of EBV-involvement was from a patient who died 3 months after biopsy with fatal infectious mononucleosis (IM). These five samples had HHV-6 DNA by PCR and ISH. Two specimens without specific histologic abnormalities showed evidence of HHV-6 only by PCR but not by ISH. Both high grade malignant lymphomas showed clonal proliferations, one of monoclonal B-cells and the other of clonal T-cells. All the other HHV-6-positive samples presented a polyclonal pattern. The malignant lymphomas positive for HHV-6 had a supprising clinical course. After the initiation of anti-tumor therapy, both showed complete remission, one with a follow-up of 3 years and the other of 1 year.
Yoshikawa T, Suga S, Asano Y, Yazaki T, Kodama H, et al. (1999) proposed a novel latent form for HHV-6, in which integrated viral genome can be chromosomally transmitted. The latter has a typical morphology and clinical behavior, which in the patients studied, showed rapid regression after therapy.