No increased incidence for GB‐virus C infection in a cohort of HIV‐positive lymphoma patients

Abstract

Dear Sir, Until recently no pathogenic potential could be demonstrated in humans infected with GB-Virus C (GBV-C). In contrast, replicative GBV-C infection in HIV-infected individuals correlated with reduced progression to immunodeficiency (Tillmann, NEJM 2001). We therefore read with great interest, the article by Krajden et al. published recently in the International Journal of Cancer, in which the authors described a cohort of 553 patients with Non-Hodgkin lymphoma and 438 controls for evidence of serum GBV-C RNA. GBV-C RNA was found in 4.5% of NHL patients and in 1.8% of controls, a difference which under analysis achieved statistical significance (odds ratio 1⁄4 2.72, confidence interval1⁄4 1.22–6.69). This study however exclusively included apparently immunocompetent patients and therefore does not offer insight into the potential role of replicative GBV-C infection contributing to the preexisting increased risk of lymphoma in HIVinfected patients. To further clarify the prevalence of GBV-C infection in our cohort of HIV-infected patients with and without lymphoma, we performed a retrospective analysis. In total 33 HIV-positive patients with lymphoma were recruited from the HIV-outpatient clinic at Hanover Medical University for GBV-C RNA and the frequency of viremia was compared with 584 HIV-infected patients without lymphoma. From the 33 patients in the lymphoma group with a mean CD4þ T cell count of 371/lL (range 7–970 cells/lL) 7 had Hodgkin Lymphoma (HL) and 26 Non-Hodgkin Lymphoma (NHL). In total ten patients (30.3%) tested GBV-CRNA positive. In our control group 138 of 584 HIV-positive patients tested positive for GBV-C-RNA (23.6%). These results however failed to achieve statistical significance regarding an association between positive GBV-C-Status and lymphoma (p 1⁄4 0.39). Interestingly the updated results in our cohort revealed an increase in the overall incidence of GBV-C viremia from 16.8% (Tillmann et al. 2001) to 23.6%. This might indicate a general spread of GBV-C infection in our cohort with known elevated risks for parenteral or mucosal transmission of viral infections. Hence the elevated GBV-C incidence in lymphoma patients, described by Krajden et al. could be explained and a confounding phenomenon indicating elevated risks for transmission of other hypothetically oncogenic viruses. On the other hand, the persistence of GBV-C viremia in HIV-positive individuals has been explained by the prevalence of T-cellular immunodeficiency. Therefore it cannot be ruled out that an elevated incidence of GBV-C replication in lymphoma patients rather indicates a secondary or preexisting alteration of T-cell immunity than a causal factor for tumor ontogenesis. Yours sincerely, Diana Ernst Sven Pischke Mark Greer Heiner Wedemeyer Matthias Stoll