Cytomodulin can induce Peyronie's-like condition in the rat penis, which may explain the role of TGF-beta in the pathogenesis of Peyronie's disease.

TGF-beta1 protein expression is significantly associated with Peyronie's disease, which may provide a new insight and the potential for the prevention and treatment of this disease.

TGF-beta1 protein expression is significantly associated with Peyronie's disease, which may provide a new insight and the potential for the prevention and treatment of this disease.

Hepatitis G virus (HGV) is prevalent in patients with chronic liver disease and has been previously detected in liver specimens. However, it is unknown whether the virus is replicating in the liver or is simply a contaminant from serum. We sought to determine whether HGV was hepatotropic and to determine whether coinfection with HGV and hepatitis C virus (HCV) influenced the level of either virus. Virus was quantitated using branched DNA (bDNA) assay for both HGV and HCV in the liver explants and pre‐transplant serum samples from 30 transplant recipients: Group I, HGV/HCV coinfection (n  = 10); group II, HCV infection alone, (n = 8); group III, HGV alone (n = 12). In patients with coinfection HCV (RNA) titers in liver were consistently higher than those for HGV RNA (median 1.13 × 108 and 360,000 Eq/g respectively, P < .01). The ratio of liver/serum viral RNA was significantly higher for HCV than for HGV (median 129 and 0.3 respectively, P < .01). Levels of HCV RNA were similar in patients with HCV infection alone versus those with HGV/HCV coinfection (median; liver = 1.15 × 107 vs. 1.13 × 108 Eq/g, serum = 500,000 vs. 200,000 Eq/mL) and levels of HGV RNA in liver and serum were similar in patients with HGV infection alone compared to those with HGV/HCV coinfection (median; liver = 1.2 × 106 vs. 4.0 × 105 Eq/g, serum = 4.5 × 106 vs. 2.6 × 106 Eq/mL). Levels of either virus appeared unaffected by the presence of an additional virus. The high ratio of HCV RNA levels in liver compared to serum is consistent with its known hepatotropism, but this pattern was not observed for HGV. The median liver/serum ratio of HGV RNA was less than unity, a finding consistent with serum contamination of liver tissue. Thus we conclude that the liver is not the main site of HGV replication.

Evolution of hepatitis C quasispecies may be one mechanism by which fibrosing cholestatic hepatitis develops after liver transplantation. In this study, we compared changes in quasispecies complexity and/or divergence in (1) hepatitis C-infected immunosuppressed transplant recipients and in immunocompetent controls; (2) transplant recipients with mild recurrence, and in those with the most severe form of posttransplantation recurrence. Quasispecies were measured in 12 hepatitis C-infected patients pretransplantation and posttransplantation (6 with mild and 6 with severe recurrence), and in 5 immunocompetent patients with similar follow-up, and characterized by heteroduplex mobility and sequence analysis of the hypervariable region. Although the number of variants (complexity) did not change with time in either group, there was a qualitative change in the variants with time (divergence) in immunocompromised, but not in immunocompetent patients. These changes were most marked with severe recurrence, and preceded the development of severe disease. Phylogenetic analysis confirmed that most posttransplantation variants were unrelated to those detected pretransplantation. These observations suggest that in the absence of immune suppression, there is minor evolution of quasispecies. With immune suppression, divergence of quasispecies is enhanced, resulting in selection/emergence of many new variants, particularly in those with fibrosing cholestatic hepatitis. Thus, quasispecies may influence disease progression in immune suppressed populations. (HEPATOLOGY 1999;30: 1513-1520.)Hepatitis C virus (HCV)-related end-stage liver disease has become the leading indication for liver transplantation in the majority of transplant centers. 1 Unfortunately, recurrence of infection is universal 2 and recurrent HCV disease is the most common cause of chronic hepatitis after transplantation. 3,4 Although within 1 year of follow-up only about 50% of transplant recipients will develop histological evidence of HCV-related disease, 3,5 with longer follow-up, the majority of patients evolve to a slowly progressive form of chronic hepatitis. 6,7 There is a subset of patients, albeit the minority, who develops an extremely severe form of posttransplantation hepatitis, characterized by cholestasis and progressive fibrosing hepatitis, which typically results in allograft failure in less than 1 year. 8,9 Such cases have been compared with the fibrosing cholestatic variant of hepatitis B, also described in the setting of transplantation. 10