Abstract number: S532
Human Adenoviruses (HAdV) are a highly genetically divergent group of DNA viruses consisting of seven species with 54 types. A few of these HAdV types (1, 2, 5 and 31) are clearly associated with infections of immunosuppressed patients as for example haematopoietic stem cell recipients. These HAdV types are not typical opportunistic agents but also cause less severe diseases in immunocompetent patients.
HAdV can persist for several months to years after an acute infection even in immunocompetent hosts and are more prevalent in children than in adults. Complications due to HAdV in haematopoetic stem cell recipients may originate from HAdV persistence and de novo infections. Due to HAdV persistence, diagnosis of HAdV disease cannot be made by mere detection of HAdV DNA. In case of organ related HAdV diseases, diagnosis is feasible by HAdV detection at the putative infection site, e.g. in case of cystitis by HAdV detection in urine. HAdV infection can also lead to potentially fatal disseminated HAdV disease. Main risk factors are young age, lymphopenia, T cell depletion and high dosage of immunosuppressive drugs. Diagnosis of the disseminated HAdV disease has been simplified by HAdV load testing in peripheral blood samples using quantitative HAdV PCR. High virus loads (>1e6 genome equivalents/ml) were clearly associated with disseminated disease whereas low virus loads (<1e4 genome equivalents/ml) can be observed in case of HAdV latency. However, a precise threshold HAdV load value has not yet been determined. Disseminated disease may be predicted in case of rapidly rising HAdV loads in blood.
Pathophysiology of HAdV disseminated disease includes massive virus replication in affected organs as for example the liver which may be infected by interaction of HAdV capsids with clotting factor X. Furthermore binding of HAdV capsids to platelets, formation of immune complexes with preformed HAdV specific antibodies as well as induction of cytokines may contribute to the pathophysiology of disseminated HAdV disease.
An antiviral treatment for HAdV disease has not yet been established. Cidofovir may have beneficial effects if applicated early but may fail if applicated in case of very high virus loads. HAdV specific T-lymphocytes seem to be a promising therapeutic approach because risk of disseminated HAdV disease is clearly associated with lymphopenia. However, HAdV specific T lymphocytes must be prepared before onset of disease in order to be available in time.
|Session name:||Abstracts 20th European Congress of Clinical Microbiology and Infectious Diseases|
|Location:||Vienna, Austria, 10 - 13 April 2010|
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