Details

Autor(en) / Beteiligte

• Vahidnia, Farnaz
• Petersen, Maya
• Rutherford, George
• Busch, Michael
• Assmann, Susan
• Stapleton, Jack
• Custer, Brian

Titel

Transfusion Transmission of GB Virus Type C (HGV) In a Cohort of HIV Infected Patients

Ist Teil von

• Blood, 2010-11, Vol.116 (21), p.3341-3341

Ort / Verlag

Elsevier Inc

Erscheinungsjahr

2010

Link zum Volltext

Quelle

Electronic Journals Library - Freely accessible e-journals

Beschreibungen/Notizen

• Abstract 3341 GB virus type C (GBV-C) infection is common with 3–5% rates of viremia in blood donors and a much higher prevalence in HIV infected patients. GBV-C is transmitted by sexual or blood exposure. Although infection may persist, most immune competent individuals clear viremia within 2 years. Few data describe the clinical course of acute GBV-C infection following transfusion in HIV infected patients. We estimated risk of GBV-C RNA acquisition following transfusion. We used a limited access database from the National Heart Lung and Blood Institute from the Viral Activation Transfusion Study (VATS). A RCT of leukoreduced (LR) vs. non-LR transfusion, VATS collected blood samples from U.S. HIV infected transfusion naïve patients. GBV-C RNA in pre- and post transfusion samples was tested after completion of VATS. GBV-C RNA acquisition up to 120 days post-transfusion was examined in 294 patients who were GBV-C RNA and antibody negative before transfusion. Discrete hazard of GBV-C RNA acquisition as a function of cumulative units transfused was estimated using pooled logistic regression. GBV-C RNA was detected in 22 (7.5%) of 294 subjects within 120 days following first transfusion. Viremia was detected within the first 30 days in 12 (4.1%) subjects and between 31 and 120 days in 10 (3.4%) subjects. Median (IQR) follow-up duration and total blood units transfused for subjects who acquired GBV-C RNA or stayed negative were: 88.5 (80-108) and 77.5 (32-100) days; and 4 (2-7) and 4 (2-6) units, respectively (Table 1). Discrete hazard of GBV-C RNA acquisition increased with each additional unit transfused (OR=1.09, 95% CI=1.06, 1.11) (Table 2). In pooled logistic regression models, lower baseline HIV viral load and use of antiretroviral therapy (ART) predicted subsequent GBV-C RNA acquisition after controlling for units of blood transfused. Leukoreduction status was not associated with GBV-C transmission. Table 1Subject characteristics by GBV-C acquisition status, VATS (n=294)CharacteristicGBV-C RNA acquisition n=22GBV-C RNA negative n=272p-valueFollow-up time in daysMean (SD)85.0 (28.9)71.2 (34.4)0.06Median (IQR)88.5 (80–108)77.5 (32–100)0.04Baseline HIV viral load per ml, log10Mean (SD)4.1 (1.4)4.7 (1.1)0.02Baseline CD4 cells per uLMean (SD)70.5 (86.7)55.5 (105.5)0.54Median (IQR)30.5 (7.5–95.5)14 (3–56)0.20Baseline ART exposure, n (%)6 (27.3)58 (21.3)0.51Units transfused, mean (SD)Mean (SD)7.2 (9.3)5.2 (4.5)0.08Median (IQR)4 (2–7)4 (2–6)0.59 Blood transfusion is associated with significant risk of GBV-C acquisition in HIV infected patients. Establishing evidence for transfusion transmission of GBV-C will allow additional studies on the impact of acute acquisition on the course of HIV infection in co-infected patients. No relevant conflicts of interest to declare.