D. Laszlo

Human polyomaviruses DNA detection in peripheral blood leukocytes from immunocompetent and immunocompromised individuals

Peripheral blood leukocytes from immunocompetent and immunocompromised individuals were analyzed for human polyomarivus BK and JC DNA presence. A nested polymerase chain reaction which amplify the transcriptional control region of the genome of both viruses was employed. The immunocompromised patients included bone marrow transplantation recipients and AIDS patients. BKV sequences were detectable in 52.8-62.5% of the individuals included in this study, whereas the percentage of individuals with JCV sequences in peripheral blood lymphocytes varied from 38.8% to 50%. The frequency of reactivations of BKV and JCV were also determined by detection of shedding in urine of viral DNA. The highest frequency of reactivations of either BKV or JCV was demonstrable in the group of bone marrow transplantation recipients, but reactivations occurred also in immunocompetent individuals. JCV sequences amplified from urine samples showed a restriction pattern similar to the archetype one, whereas sequences obtained from lymphocytes showed rearranged pattern as well as archetype pattern. Finally all JCV sequences from cerebrospinal fluid seemed to be rearranged. These observations suggest that peripheral blood lymphocytes have a fundamental role in the persistence of polyomaviruses infection and in the dissemination at least of JCV within the organism allowing that rearranged variants, better adapted to grow in brain tissue, emerge.

Fatal herpesvirus 6 encephalitis after unrelated bone marrow transplant.

A complex pattern of neurological dysfunctions with generalized seizures and visual allucinations, but without focal signs, suddenly arose 20 days after an unrelated bone marrow transplant for chronic myelogenous leukemia (CML) in a 13-year-old girl, accompanied by signs of acute skin graft-versus-host disease (GVHD). Magnetic resonance imaging (MRI) revealed multiple bilateral foci of signal abnormalities, which were exclusively localized in the grey matter, sparing the white. Extensive microbiological and virological assays of cerebrospinal fluid (CSF) allowed the identification of HHV-6, variant A, DNA. Further progression of both neurological alterations and of skin and gut GVHD led to a fatal outcome 2 weeks later. A retrospective analysis of both the recipient and donor mononuclear cell suspensions supported the hypothesis that HHV-6 had been acquired from the donor with the bone marrow graft. This report suggests a pathogenetic role of HHV-6 in viral encephalitis in immunocompromised bone marrow transplant (BMT) recipients, and its possible association with GVHD.