title: Absence of HBV and HCV, HTLV-I and -II, and human herpes virus-8 activation after allogeneic RBC transfusion in patients with advanced HIV-1 infection.
abstract: BACKGROUND
  The Viral Activation Transfusion Study was a prospective, randomized, double-blind comparison of transfusion with WBC-reduced versus non-WBC-reduced RBCs to HIV+ patients. The primary study characterized the effect of transfusion on HIV and CMV activation by monitoring viral load changes. The present study analyzed HBV, HCV, HTLV-I and -II, and human herpes virus-8 (HHV-8) viral load before and after transfusion to evaluate the further hypothesis that global immune stimulation following allogeneic RBC transfusion results in activation and increased viral proliferation of chronic viral infections other than HIV and CMV.
  
  
  METHODS
  Baseline samples from 519 to 523 subjects were screened for HBV, HCV, HTLV-I and -II, and HHV-8 infection, and baseline, serial weekly, and quarterly blood samples from infected subjects in the non-WBC-reduced arm were evaluated for changes from baseline in viral nucleic acid and ALT levels.
  
  
  RESULTS
  Seroprevalence of HBV, HCV, HTLV-I and -II, and HHV-8 was 68, 25, 5, and 30 percent, respectively. No significant induction of HBV, HCV, HHV-8, or HTLV-I and -II viral replication following allogeneic transfusion of non-WBC-reduced blood was observed. A significant, albeit small, association was observed between transfusion and ALT.
  
  
  CONCLUSIONS
  Based on these results and our previous finding that no adverse effect on HIV and CMV viral load and disease progression results from allogeneic transfusion, no evidence is found to support the selective use of WBC-reduced blood components for HIV-infected patients.
authors.affiliation: Department of Internal Medicine, Division of Infectious Diseases and Immunology, University of California-Davis Medical Center, 4150 V Street, Suite 6200 PSSB, Sacramento, CA 95817, USA. dasmuth@ucdavis.edu
authors.forename: David M
authors.initials: DM
authors.lastname: Asmuth
authors.forename: Leslie A
authors.initials: LA
authors.lastname: Kalish
authors.forename: Megan E
authors.initials: ME
authors.lastname: Laycock
authors.forename: Edward L
authors.initials: EL
authors.lastname: Murphy
authors.forename: Beth A
authors.initials: BA
authors.lastname: Mohr
authors.forename: Tzong-Hae
authors.initials: TH
authors.lastname: Lee
authors.forename: James
authors.initials: J
authors.lastname: Gallarda
authors.forename: Cristina
authors.initials: C
authors.lastname: Giachetti
authors.forename: Sheila C
authors.initials: SC
authors.lastname: Dollard
authors.forename: Charles M
authors.initials: CM
authors.lastname: van der Horst
authors.forename: Robert M
authors.initials: RM
authors.lastname: Grant
authors.forename: Michael P
authors.initials: MP
authors.lastname: Busch
mesh_terms: D000163:Acquired Immunodeficiency Syndrome / Q000628:therapy / Q000821:virology*; D000914:Antibodies, Viral / Q000097:blood; D004279:DNA, Viral / Q000097:blood; D004311:Double-Blind Method; D017707:Erythrocyte Transfusion; D016174:Hepacivirus / Q000235:genetics / Q000276:immunology / Q000502:physiology; D006515:Hepatitis B virus / Q000235:genetics / Q000276:immunology / Q000502:physiology; D019288:Herpesvirus 8, Human / Q000235:genetics / Q000276:immunology / Q000502:physiology; D015368:Human T-lymphotropic virus 1 / Q000235:genetics / Q000276:immunology / Q000502:physiology; D015367:Human T-lymphotropic virus 2 / Q000235:genetics / Q000276:immunology / Q000502:physiology; D006801:Humans; D011446:Prospective Studies; D019562:Viral Load; D014775:Virus Activation
chemical_list: D000914:Antibodies, Viral; D004279:DNA, Viral