title: SEN Virus infection in HIV/HCV coinfected patients.
abstract: BACKGROUND
  Chronic Hepatitis C Virus (HCV) infection is currently one of the most relevant coinfections in HIV positive patients. The influence of SEN Virus (SENV) on the outcome of HCV therapy in HIV/HCV coinfected patients who underwent combination therapy with pegylated interferon (PEG-IFN) and ribavirin is unclear.
  
  
  METHODS
  SENV DNA was determined by polymerase chain reaction in 67 HIV/HCV coinfected patients, 77 HIV monoinfected patients, 95 treatment naive HCV monoinfetcted patients, and 122 healthy blood donors. Quantitative analysis was done for SENV H DNA.
  
  
  RESULTS
  SENV DNA was detected in 8 of 67 (12%) HIV/HCV coinfected patients, in 9 of 77 (11.7%) HIV monoinfected patients, in 21 of 95 (22%) HCV monoinfected patients, and 12 of 122 (9.8%) healthy blood donors. HIV monoinfected patients showed the highest mean SENV H DNA level. The mean SENV H DNA was significantly lower in HIV/HCV coinfected patients compared to all other groups. The sustained virological response rates to combination therapy of HCV in HIV/HCV coinfected patients did not differ between patients with detectable SENV 5/8 (62.5%) and without SENV 28/59 (47.5%; p = 0.47). We found no significant difference in SENV H DNA pretreatment levels between nonresponders and responders to combination therapy (112 +/- 144 copies vs. 8 +/- 7 copies/ml; p = 0.27).
  
  
  CONCLUSIONS
  Coinfection with HCV may reduce SENV H replication in HIV positive patients and results in significantly lower SENV H DNA levels in HIV/HCV coinfected patients. SENV infection has no influence on the outcome of HCV combination therapy in HIV/HCV coinfected patients.
authors.affiliation: Klinik für Gastroenterologie, Hepatologie und Infektiologie, Universitätsklinik Düsseldorf, Moorenstr. 5, 40225 Düsseldorf, Germany. sagir@med.uni-duesseldorf.de
authors.forename: A
authors.initials: A
authors.lastname: Sagir
authors.forename: O
authors.initials: O
authors.lastname: Adams
authors.forename: M
authors.initials: M
authors.lastname: Oette
authors.forename: M
authors.initials: M
authors.lastname: Vogel
authors.forename: B
authors.initials: B
authors.lastname: Kupfer
authors.forename: J
authors.initials: J
authors.lastname: Emmelkamp
authors.forename: J
authors.initials: J
authors.lastname: Rockstroh
authors.forename: D
authors.initials: D
authors.lastname: Häussinger
mesh_terms: D000328:Adult; D000998:Antiviral Agents / Q000627:therapeutic use; D015897:Comorbidity; D004266:DNA Virus Infections / Q000453:epidemiology* / Q000821:virology; D004279:DNA, Viral / Q000032:analysis; D024882:Drug Resistance, Viral; D004359:Drug Therapy, Combination; D005260:Female; D005838:Genotype; D015658:HIV Infections / Q000453:epidemiology* / Q000821:virology; D016174:Hepacivirus / Q000187:drug effects* / Q000235:genetics; D019698:Hepatitis C, Chronic / Q000188:drug therapy* / Q000453:epidemiology* / Q000821:virology; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D011092:Polyethylene Glycols / Q000627:therapeutic use; D015995:Prevalence; D012367:RNA, Viral / Q000032:analysis; D011994:Recombinant Proteins; D012254:Ribavirin / Q000627:therapeutic use; D022783:Torque teno virus / Q000235:genetics; D014779:Virus Replication
chemical_list: D000998:Antiviral Agents; D004279:DNA, Viral; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D012367:RNA, Viral; D011994:Recombinant Proteins; D011092:Polyethylene Glycols; D012254:Ribavirin; C100416:peginterferon alfa-2a