Preservation of immune function and anti-hepatitis C virus (HCV) immune responses after liver transplantation in HIV–HCV coinfected patients (ANRS-HC08 “THEVIC” trial)

Fibrosing Cholestatic Hepatitis in HIV/HCV Co-Infected Transplant Patients—Usefulness of Early Markers After Liver Transplantation

“…We recently demonstrated that the median HCV viral load rose from 5.83 log 10 /mL before transplantation to 6.58 log 10 /mL posttransplantation, without there being any changes to CD4 counts and T-cell subsets (20). If only one patient with FCH was included in this latter study, no HCV-specific responses were detectable in patients with severe hepatitis or a fibrosis score higher than F2 (20).…”

“…This severe complication is characterized histologically by extensive dense portal fibrosis with immature fibrous bands extending into sinusoidal spaces, ductular proliferation, marked canalicular and cellular cholestasis and mononuclear inflammation (11,18). However, a broad spectrum of FCH may exist with different degrees of mononuclear inflammation and ductular reaction and the possible coexistence of an expansion of portal fibrosis (20).…”

“…We recently demonstrated that the median HCV viral load rose from 5.83 log 10 /mL before transplantation to 6.58 log 10 /mL posttransplantation, without there being any changes to CD4 counts and T-cell subsets (20). If only one patient with FCH was included in this latter study, no HCV-specific responses were detectable in patients with severe hepatitis or a fibrosis score higher than F2 (20). The present report demonstrates that the HCV viral load could constitute an important feature because a significantly higher load was observed at the time of FCH diagnosis, which occurred within a mean delay of 7 months post-LT, when compared with the HCV viral load at 6 months post-LT in the non-FCH group.…”

“…The mean age of these predominantly male patients (82%) at LT was 44 years [range: 29-63]; three patients had a previous history of alcohol abuse and one patient suffered from hepatopulmonary syndrome. The principal indication for LT was hepatic insufficiency (Child C = 10 patients) with a mean MELD score of 17.5 [range: [6][7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24] except for the patient with hepatopulmonary syndrome who was Child A and had a MELD score of nine at the time of LT. As shown in Table 3, there were no differences in terms of the severity of liver disease (MELD score), virological characteristics (genotype 1 frequency, HCV viral load), CD4 cell count and donor age. Interestingly, in the FCH group, we observed a higher level of HLA-A, B, DR matching (≥2) and acute rejection episodes (54% vs. 35%; p = 0.3) but no more requirement for steroid boluses (36% vs. 33%; p = 1).…”

Outcome and management of HCV/HIV coinfection pre- and post-liver transplantation. A 2015 update

“…However, these antiretroviral drugs are no longer used. With current ART regimens, most HCV/HIV-coinfected liver transplant recipients are virologically suppressed, with a CD4 cell count remaining above 200 cell/mm 3 over time [21]. The CD4 cell count at inclusion on the waiting list was not identified as a poor prognostic factor [8,9].…”