Lymphotropic herpesvirus DNA detection in patients with active CMV infection - a possible role in the course of CMV infection after hematopoietic stem cell transplantation

• Published in: Medical science monitor 2011-08, Vol.17 (8), p.CR432-CR441
• Main Authors: Zawilinska, Barbara, Kopec, Jolanta, Szostek, Slawa, Piatkowska-Jakubas, Beata, Skotnicki, Aleksander B, Kosz-Vnenchak, Magdalena
• Format: Article
• Language: English
• Subjects: Adult; Clinical Research; Cytomegalovirus Infections - etiology; Cytomegalovirus Infections - virology; DNA, Viral - blood; Female; Graft vs Host Disease; Hematopoietic Stem Cell Transplantation - adverse effects; Herpesviridae Infections - etiology; Herpesvirus 6, Human - genetics; Herpesvirus 7, Human - genetics; Humans; Male; Viral Load; Young Adult
• ISSN: 1234-1010; 1643-3750
• DOI: 10.12659/MSM.881904

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). 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. 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. The results suggest that other herpesviruses, mainly HHV-7, could predispose CMV to cause chronic infection.