• 1.

    European Association for Study of Liver, 2014. EASL Clinical Practice Guidelines: management of hepatitis C virus infection. J Hepatol 60: 392420.

    • Search Google Scholar
    • Export Citation
  • 2.

    Negro F, 2014. Curbing hepatitis C virus spread in Egypt. Lancet Glob Health 2: e495e496.

  • 3.

    Lavanchy D, 2011. Evolving epidemiology of hepatitis C virus. Clin Microbiol Infect 17: 107115.

  • 4.

    Gryseels B, 2012. Schistosomiasis. Infect Dis Clin North Am 26: 383397.

  • 5.

    Colley DG, Bustinduy AL, Secor WE, King CH, 2014. Human schistosomiasis. Lancet 383: 22532264.

  • 6.

    Sanghvi MM, Hotez PJ, Fenwick A, 2013. Neglected tropical diseases as a cause of chronic liver disease: the case of schistosomiasis and hepatitis C co-infections in Egypt. Liver Int 33: 165168.

    • Search Google Scholar
    • Export Citation
  • 7.

    Attallah AM, Yones E, Ismail H, El Masry SA, Tabll A, Elenein AA, El Ghawalby NA, 1999. Immunochemical characterization and diagnostic potential of a 63-kilodalton Schistosoma antigen. Am J Trop Med Hyg 60: 493497.

    • Search Google Scholar
    • Export Citation
  • 8.

    Strickland GT, 2006. Liver disease in Egypt: hepatitis C superseded schistosomiasis as a result of iatrogenic and biological factors. Hepatol 43: 915922.

    • Search Google Scholar
    • Export Citation
  • 9.

    Van-Lume DS, Albuquerque M de F, Souza AI, Domingues AL, Lopes EP, Morais CN, Montenegro SM, 2013. Association between schistosomiasis mansoni and hepatitis C: systematic review. Rev Saude Publica 47: 414424.

    • Search Google Scholar
    • Export Citation
  • 10.

    Brady MT, MacDonald AJ, Rowan AG, Mills KH, 2003. Hepatitis C virus non‐structural protein 4 suppresses Th1 responses by stimulating IL‐10 production from monocytes. Eur J Immunol 33: 34483457.

    • Search Google Scholar
    • Export Citation
  • 11.

    Attallah AM, Omran MM, Nasif WA, Ghaly MF, El-Shanshoury AER, Abdalla MS, Sharada HM, Farid K, El-Shony W, Moussa ESM, El-Domany EB, Nour E, Eldosoky I, 2012. Diagnostic performances of hepatitis C virus-NS4 antigen in patients with different liver pathologies. Arch Med Res 43: 555562.

    • Search Google Scholar
    • Export Citation
  • 12.

    Chen CZ, Raghunath M, 2009. Focus on collagen: in vitro systems to study fibrogenesis and antifibrosis state of the art. Fibrogenesis Tissue Repair 2: 7.

    • Search Google Scholar
    • Export Citation
  • 13.

    Arthur MJP, 1994. Degradation of matrix proteins in liver fibrosis. Pathol Res Pract 190: 825833.

  • 14.

    Attallah AM, El-Far M, Abdel Malak CA, Omran MM, Farid K, Hussien MA, Albannan MS, Attallah AA, Elbendary MS, Elbesh DA, Elmenier NA, Abdallah MO, 2015. Fibro-check: a combination of direct and indirect markers for liver fibrosis staging in chronic hepatitis C patients. Ann Hepatol 14: 225233.

    • Search Google Scholar
    • Export Citation
  • 15.

    Poynard T, Bedossa P, Opolon P, 1997. Natural history of liver fibrosis progression in patients with chronic hepatitis C. The OBSVIRC, METAVIR, CLINIVIR, and DOSVIRC groups. Lancet 349: 825832.

    • Search Google Scholar
    • Export Citation
  • 16.

    Laemmli UK, 1970. Cleavage of structural proteins during the assembly of the head of bacteriophage T4. Nature 227: 680685.

  • 17.

    Towbin H, Staehelin T, Gordon J, 1979. Electrophoretic transfer of proteins from polyacrylamide gels to nitrocellulose sheets: procedure and some applications. Proc Natl Acad Sci USA 76: 43504354.

    • Search Google Scholar
    • Export Citation
  • 18.

    Lowry OH, Rosebrough NJ, Farr AL, Randall RJ, 1951. Protein measurement with the Folin phenol reagent. J Biol Chem 193: 265275.

  • 19.

    European Association for Study of Liver, 2015. EASL recommendations on treatment of hepatitis C 2015. J Hepatol 63: 199236.

  • 20.

    Strader DB, Wright T, Thomas DL, Seeff LB, 2004. Diagnosis, management, and treatment of hepatitis C. Hepatol 39: 11471171.

  • 21.

    Booth JC, O'Grady J, Neuberger J, 2001. Clinical guidelines on the management of hepatitis C. Gut 49: I1I21.

  • 22.

    Vilstrup H, 2003. Cirrhosis and bacterial infections. Rom J Gastroenterol 12: 297302.

  • 23.

    Mengshol JA, Golden-Mason L, Rosen HR, 2007. Mechanisms of disease: HCV-induced liver injury. Nat Clin Pract Gastroenterol Hepatol 4: 622634.

    • Search Google Scholar
    • Export Citation
  • 24.

    Bataller R, Paik YH, Lindquist JN, Lemasters JJ, Brenner DA, 2004. Hepatitis C virus core and nonstructural proteins induce fibrogenic effects in hepatic stellate cells. Gastroenterol 126: 529540.

    • Search Google Scholar
    • Export Citation
  • 25.

    Shin JY, Hur W, Wang JS, Jang JW, Kim CW, Bae SH, Jang SK, Yang SH, Sung YC, Kwon OJ, Yoon SK, 2005. HCV core protein promotes liver fibrogenesis via up-regulation of CTGF with TGF-beta1. Exp Mol Med 37: 138145.

    • Search Google Scholar
    • Export Citation
  • 26.

    Arthur MJ, Mann DA, Iredale JP, 1998. Tissue inhibitors of metalloproteinases, hepatic stellate cells and liver fibrosis. J Gastroenterol Hepatol 13: S33S38.

    • Search Google Scholar
    • Export Citation
  • 27.

    Leroy V, Monier F, Bottari S, Trocme C, Sturm N, Hilleret MN, Morel F, Zarski JP, 2004. Circulating matrix metalloproteinases 1, 2, 9 and their inhibitors TIMP-1 and TIMP-2 as serum markers of liver fibrosis in patients with chronic hepatitis C: comparison with PIIINP and hyaluronic acid. Am J Gastroenterol 99: 271279.

    • Search Google Scholar
    • Export Citation
  • 28.

    Bataller R, Brenner DA, 2005. Liver fibrosis. J Clin Invest 115: 209218.

  • 29.

    Kamal SM, Turner B, He Q, Rasenack J, Bianchi L, Al Tawil A, Nooman A, Massoud M, Koziel MJ, Afdhal NH, 2006. Progression of fibrosis in hepatitis C with and without schistosomiasis: correlation with serum markers of fibrosis. Hepatol 43: 771779.

    • Search Google Scholar
    • Export Citation
  • 30.

    Inagaki Y, Okazaki I, 2007. Emerging insights into transforming growth factor beta Smad signal in hepatic fibrogenesis. Gut 56: 284292.

  • 31.

    Jarcuska P, Janicko M, Veseliny E, Jarcuska P, Skladaný L, 2010. Circulating markers of liver fibrosis progression. Clin Chim Acta 411: 10091017.

  • 32.

    Knittel T, Mehde M, Kobold D, Saile B, Dinter C, Ramadori G, 1999. Expression patterns of matrix metalloproteinases and their inhibitors in parenchymal and non-parenchymal cells of rat liver: regulation by TNF-alpha and TGF-beta1. J Hepatol 30: 4860.

    • Search Google Scholar
    • Export Citation
Past two years Past Year Past 30 Days
Abstract Views 0 0 0
Full Text Views 171 83 3
PDF Downloads 49 25 0
 
 
 
 
 
 
 
 
 
 
 
 
 
 

 

 

 

Impact of Hepatitis C Virus/Schistosoma mansoni Coinfection on the Circulating Levels of HCV-NS4 Protein and Extracellular-Matrix Deposition in Patients with Different Hepatic Fibrosis Stages

View More View Less
  • 1 Biotechnology Research Center, New Damietta, Egypt.
  • | 2 Faculty of Science, Cairo University, Giza, Egypt.
  • | 3 Faculty of Science, Helwan University, Cairo, Egypt.
  • | 4 Faculty of Medicine, Mansoura University, Mansoura, Egypt.
Restricted access

Hepatitis C virus (HCV)/Schistosoma mansoni coinfection is common in Egypt and other developing countries. This study aimed to investigate the influence of HCV/S. mansoni coinfection on the concentration of HCV–nonstructural protein-4 (NS4) in addition to collagen III and matrix metalloproteinase-1 (MMP-1) in different hepatic fibrosis stages. We found that coinfected patients (N = 186) showed significantly (P < 0.05, Mann–Whitney U test) higher concentrations of HCV-NS4, collagen III, and collagen III/MMP-1 ratio (CMR) than those with HCV monoinfection (N = 104) in different fibrosis stages. Conversely, coinfected patients showed significantly lower concentrations of MMP-1 when compared with HCV monoinfection. The elevated levels of CMR in case of HCV monoinfection yielded an estimated odds ratio of 1.8 and 2.6 for developing significant fibrosis (F2-F4) and cirrhosis (F4), respectively. HCV/S. mansoni coinfection increased the risk for developing F2-F4 and F4 several fold yielding an estimated odds ratio of 11.1 and 5.2, respectively. This means that coinfected patients have a 6-fold and 2-fold increased risk of developing F2-F4 and F4, respectively, over HCV-monoinfected patients. Thus, elevated levels of HCV-NS4 and CMR in HCV/S. mansoni coinfection suggest increased susceptibility of coinfected patients, compared with those with HCV monoinfection, for accelerating hepatic fibrosis progression.

Author Notes

* Address correspondence to Abdelfattah M. Attallah, Biotechnology Research Center, P.O. Box 14, 23 July Street, Industrial Zone, New Damietta 34517, Egypt. E-mail: amattallah@hotmail.com

Authors' addresses: Abdelfattah M. Attallah, Mohamed S. Albannan, and Ahmed A. Attallah, Biotechnology Research Center, New Damietta, Egypt, E-mails: amattallah@hotmail.com, mohamedalbannan@yahoo.com, and ahmedattallah2009@hotmail.com. Sanaa O. Abdallah, Faculty of Science, Cairo University, Giza, Egypt, E-mail: sanaa.osman@gmail.com. Mohamed M. Omran, Faculty of Science, Helwan University, Cairo, Egypt, E-mail: drmmomran@yahoo.com. Khaled Farid, Faculty of Medicine, Mansoura University, Mansoura, Egypt, E-mail: khaled_som@mans.edu.eg.

Save