title: Cytomegalovirus viremia: risk factor for allograft cirrhosis after liver transplantation for hepatitis C.
abstract: BACKGROUND
  Despite recent advances in diagnosis and treatment, cytomegalovirus (CMV) infection continues to be a common cause of morbidity in liver transplant (LT) recipients. Because CMV infection suppresses cell-mediated immunity, which seems to be important in neutralizing hepatitis C virus (HCV) infection, we assessed the impact of CMV infection on histopathological HCV recurrence after LT.
  
  
  METHODS
  The study group was comprised of 43 consecutive LT recipients with at least 6 months of histologic follow-up. Group 1 consisted of the 8 patients who developed CMV viremia after LT; group 2 comprised the 35 patients without CMV viremia. There was no significant difference with regard to age, initial immunosuppression, incidence of rejection, distribution of HCV genotypes, or mean follow-up between the groups. Semiquantitative histopathologic assessment of allograft hepatitis was performed using the Knodell's score.
  
  
  RESULTS
  The mean total Knodell score of the final allograft biopsy was significantly greater in group 1 patients (P=0.016), with most of the difference due to periportal/bridging necrosis (P=0.009) and lobular activity subitem (P=0.01) scores. Half of the CMV viremic patients eventually developed allograft cirrhosis as compared with 11% of the CMV-negative patients (P=0.027). Accordingly, the cirrhosis-free actuarial survival by Kaplan-Meier estimates was significantly diminished in the CMV viremic patients. Glycoprotein B genotype analysis of CMV isolates revealed no significant differences between patients who did and those who did not develop allograft cirrhosis.
  
  
  CONCLUSIONS
  After LT for chronic HCV, patients who develop CMV viremia incur a significantly greater risk of severe HCV recurrence.
authors.affiliation: Department of Medicine, Oregon Health Sciences and Portland Veterans Affairs Medical Center, 97207, USA.
authors.forename: H R
authors.initials: HR
authors.lastname: Rosen
authors.forename: S
authors.initials: S
authors.lastname: Chou
authors.forename: C L
authors.initials: CL
authors.lastname: Corless
authors.forename: D R
authors.initials: DR
authors.lastname: Gretch
authors.forename: K D
authors.initials: KD
authors.lastname: Flora
authors.forename: A
authors.initials: A
authors.lastname: Boudousquie
authors.forename: S L
authors.initials: SL
authors.lastname: Orloff
authors.forename: J M
authors.initials: JM
authors.lastname: Rabkin
authors.forename: K G
authors.initials: KG
authors.lastname: Benner
mesh_terms: D000998:Antiviral Agents / Q000627:therapeutic use; D001706:Biopsy; D003587:Cytomegalovirus / Q000235:genetics; D003586:Cytomegalovirus Infections / Q000097:blood* / Q000517:prevention & control; D015774:Ganciclovir / Q000627:therapeutic use; D005838:Genotype; D006084:Graft Rejection / Q000401:mortality / Q000517:prevention & control; D016174:Hepacivirus / Q000235:genetics; D006526:Hepatitis C / Q000601:surgery; D006801:Humans; D008103:Liver Cirrhosis / Q000453:epidemiology / Q000209:etiology; D016031:Liver Transplantation / Q000009:adverse effects; D008875:Middle Aged; D012307:Risk Factors; D013997:Time Factors; D014184:Transplantation, Homologous / Q000009:adverse effects / Q000473:pathology
chemical_list: D000998:Antiviral Agents; D015774:Ganciclovir