Human cytomegalovirus infection inhibits response of chronic hepatitis-C-virus-infected patients to interferon-based therapy

被引:21
|
作者
El Din, Noha G. Bader [1 ]
Abd El Meguid, Mai [1 ]
Tabll, Ashraf A. [1 ]
Anany, Mohamed A. [1 ]
Esmat, Gamal [2 ]
Zayed, Naglaa [2 ]
Helmy, Amr [5 ]
El Zayady, Abdel Rahman [3 ]
Barakat, Ahmed [4 ]
El Awady, Mostafa K. [1 ]
机构
[1] Natl Res Ctr, Dept Biomed Technol, Cairo, Egypt
[2] Cairo Univ, Fac Med, Dept Trop Med, Cairo, Egypt
[3] Ain Shams Univ, Fac Med, Dept Internal Med, Cairo, Egypt
[4] Ain Shams Univ, Fac Sci, Dept Microbiol, Cairo, Egypt
[5] Menoufia Univ, Natl Liver Inst, Dept Surg, Menoufia, Egypt
关键词
cytomegalovirus; hepatitis C virus; liver fibrosis; response to interferon therapy; LIVER-TRANSPLANTATION; B-VIRUS; ENDOTHELIAL-CELLS; SIGNAL-TRANSDUCTION; ALPHA-INTERFERON; COINFECTION; REPLICATION; DISEASE; MACROPHAGES; PERSISTENCE;
D O I
10.1111/j.1440-1746.2010.06319.x
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background and Aim: Cytomegalovirus (CMV) is a ubiquitous pathogen that infects the majority of humans. Co-infection of CMV and hepatitis C virus (HCV) may deteriorate the prognosis of HCV-infected patients. This study was conducted to examine the role of CMV reactivation in determining the response rate to treatment with interferon and ribavirin therapy in chronic HCV patients. Methods: Viral loads and genotyping were assessed using reverse transcription polymerase chain reaction and Innolipa systems, respectively. Reactivation of CMV in HCV patients who were all positive for CMV immunoglobulin G antibodies was tested by amplification of the gB1 gene using the end-point dilution quantitative-nested polymerase chain reaction method. Results: CMV DNA was detected in 89.7% of non-responders and in 34.6% of sustained virological responders. Patients with reactivated CMV had significantly higher fibrosis scores (72.7%) than those with undetectable CMV DNA (23.8%, P = 0.002). Patients with positive CMV had higher rates of non-response and relapse (79.5%) than those with negative CMV DNA (19%). Chronic HCV patients with latent CMV had higher rates of response (81%) to treatment than those with reactivated CMV (20.5%, P < 0.001). Therefore, HCV patients with reactivated CMV and advanced fibrosis were least likely to achieve a sustained virological response following interferon therapy. This possibility is reduced to 50% of its original value in patients with reactivated CMV without fibrosis. Conclusions: Besides the staging of liver fibrosis, CMV co-infection should be considered as an extremely important factor when designing predictive models for HCV response to interferon treatment.
引用
收藏
页码:55 / 62
页数:8
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