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Lymphotropic herpesvirus DNA detection in patients with active CMV infection – a possible role in the course of CMV infection after hematopoietic stem cell transplantation
BACKGROUND: The natural history of cytomegalovirus (CMV) infection and disease in transplant recipients prompts researchers to look for other factors contributing to this infection. The ubiquity of lymphotropic herpesviruses (EBV, HHV-6, and HHV-7) and the possibility of their activation during immu...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
International Scientific Literature, Inc.
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3539614/ https://www.ncbi.nlm.nih.gov/pubmed/21804462 http://dx.doi.org/10.12659/MSM.881904 |
Sumario: | BACKGROUND: The natural history of cytomegalovirus (CMV) infection and disease in transplant recipients prompts researchers to look for other factors contributing to this infection. The ubiquity of lymphotropic herpesviruses (EBV, HHV-6, and HHV-7) and the possibility of their activation during immunosuppression may suggest their participation in progression of CMV infection in patients after hematopoietic stem cell transplantation (HSCT). MATERIAL/METHODS: The presence of CMV, EBV, HHV-6 and HHV-7 was confirmed through detection of viral DNA isolated from leukocytes. Allo-HSCT recipients (n=55) were examined repeatedly within the average period of 14±7.3 months post-transplant. RESULTS: CMV DNA was detected in 24% of samples, while EBV, HHV-6 and HHV-7 were detected in 20%, 15% and 14% of samples, respectively. Based on the presence of CMV infection at particular time-points (months) after transplantation, the recipients were divided into 3 groups: Group I (N=15) with persistent infection, Group II (N=20) with transient infection, and Group III (N=20) without CMV infection. In Group I, the mean CMV load was significantly higher than in Group II, and the clinical condition of Group I patients was poorer. All these patients manifested clinical symptoms, and all had episodes of GvHD. All Group I patients developed multiple infections; EBV in 80%, HHV-6 in 47% and HHV-7 in 87% of patients. In the remaining groups, with the exception of HHV-6 in group II, the frequency of infected patients was lower. In addition, CMV presence was often preceded by another herpesvirus. CONCLUSIONS: The results suggest that other herpesviruses, mainly HHV-7, could predispose CMV to cause chronic infection. |
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