Abstract
We investigated the effect of β-herpesviruses on allograft failure and mortality, hepatitis C virus (HCV) replication, and liver histologic characteristics among 92 HCV-infected liver transplant recipients. Reactivation of cytomegalovirus (CMV) but not of human herpesvirus 6 (HHV-6) was independently associated with allograft failure and mortality (risk ratio, 3.71; 95% confidence interval, 1.64-8.39); allograft failure and mortality was observed in 48% of patients with CMV disease, 35% of patients with subclinical CMV infection, and 17% of patients without CMV infection (P = .0275). CMV reactivation was highly predictive of mortality (P<.001), regardless of whether it remained subclinical or evolved into CMV disease. Patients with CMV disease had a higher fibrosis stage (P = .05) and had a trend toward a higher hepatitis activity index (P = .10) and HCV load (P = .10) at 16 weeks after liver transplantation. The pathogenesis of HCV is influenced by its interaction with CMV but not with HHV-6.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 974-981 |
| Number of pages | 8 |
| Journal | Clinical Infectious Diseases |
| Volume | 35 |
| Issue number | 8 |
| DOIs | |
| State | Published - Oct 15 2002 |
Fingerprint
ASJC Scopus subject areas
- Immunology
Cite this
The pathogenesis of hepatitis C virus is influenced by cytomegalovirus. / Razonable, Raymund R; Burak, Kelly W.; Van Cruijsen, Hester; Brown, Robert A.; Charlton, Michael R.; Smith, Thomas F.; Espy, Mark J.; Kremers, Walter K; Wilson, Jennie A.; Groettum, Cynthia; Wiesner, Russell; Paya, Carlos V.
In: Clinical Infectious Diseases, Vol. 35, No. 8, 15.10.2002, p. 974-981.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - The pathogenesis of hepatitis C virus is influenced by cytomegalovirus
AU - Razonable, Raymund R
AU - Burak, Kelly W.
AU - Van Cruijsen, Hester
AU - Brown, Robert A.
AU - Charlton, Michael R.
AU - Smith, Thomas F.
AU - Espy, Mark J.
AU - Kremers, Walter K
AU - Wilson, Jennie A.
AU - Groettum, Cynthia
AU - Wiesner, Russell
AU - Paya, Carlos V.
PY - 2002/10/15
Y1 - 2002/10/15
N2 - We investigated the effect of β-herpesviruses on allograft failure and mortality, hepatitis C virus (HCV) replication, and liver histologic characteristics among 92 HCV-infected liver transplant recipients. Reactivation of cytomegalovirus (CMV) but not of human herpesvirus 6 (HHV-6) was independently associated with allograft failure and mortality (risk ratio, 3.71; 95% confidence interval, 1.64-8.39); allograft failure and mortality was observed in 48% of patients with CMV disease, 35% of patients with subclinical CMV infection, and 17% of patients without CMV infection (P = .0275). CMV reactivation was highly predictive of mortality (P<.001), regardless of whether it remained subclinical or evolved into CMV disease. Patients with CMV disease had a higher fibrosis stage (P = .05) and had a trend toward a higher hepatitis activity index (P = .10) and HCV load (P = .10) at 16 weeks after liver transplantation. The pathogenesis of HCV is influenced by its interaction with CMV but not with HHV-6.
AB - We investigated the effect of β-herpesviruses on allograft failure and mortality, hepatitis C virus (HCV) replication, and liver histologic characteristics among 92 HCV-infected liver transplant recipients. Reactivation of cytomegalovirus (CMV) but not of human herpesvirus 6 (HHV-6) was independently associated with allograft failure and mortality (risk ratio, 3.71; 95% confidence interval, 1.64-8.39); allograft failure and mortality was observed in 48% of patients with CMV disease, 35% of patients with subclinical CMV infection, and 17% of patients without CMV infection (P = .0275). CMV reactivation was highly predictive of mortality (P<.001), regardless of whether it remained subclinical or evolved into CMV disease. Patients with CMV disease had a higher fibrosis stage (P = .05) and had a trend toward a higher hepatitis activity index (P = .10) and HCV load (P = .10) at 16 weeks after liver transplantation. The pathogenesis of HCV is influenced by its interaction with CMV but not with HHV-6.
UR - http://www.scopus.com/inward/record.url?scp=0037108614&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0037108614&partnerID=8YFLogxK
U2 - 10.1086/342911
DO - 10.1086/342911
M3 - Article
C2 - 12355385
AN - SCOPUS:0037108614
VL - 35
SP - 974
EP - 981
JO - Clinical Infectious Diseases
JF - Clinical Infectious Diseases
SN - 1058-4838
IS - 8
ER -