title: Plasma triglyceride levels may modulate hepatitis C viral replication.
abstract: BACKGROUND
  Plasma and hepatic lipid abnormalities are frequent in hepatitis C infected individuals.
  
  
  METHODS
  Plasma lipid and medical records profiles were prospectively obtained in 130 consecutive individuals seen by a single hepatologist in a university liver disease clinic. The relationships between viral load, genotype, plasma lipid fractions, HDL, LDL particle number and particle size were examined.
  
  
  RESULTS
  Of 130 individuals studied, 74 had hepatitis C while 15 had NAFLD/NASH and 30 had alcohol related liver disease. The LDL particle number and LDL-C levels did not differ between those with and without hepatitis C although the number of small LDL particles was greater in those with hepatitis C infection. The HDL-C and total cholesterol levels were greater in those without hepatitis C than those with hepatitis C (P = 0.009). In contrast, the serum triglyceride level was greater in the hepatitis C viral group (P = 0.013). Importantly, the hepatitis C viral load regardless of the genotype correlated directly with the triglyceride and VLDL levels with r values of 0.73 and 0.84, respectively.
  
  
  CONCLUSIONS
  There are: (1) important differences in lipid classes, number and the size of lipid particles exist between hepatitis C virus infected and noninfected liver disease groups, (2) the serum total triglyceride and the LDL levels correlate significantly with the hepatitis C viral load and, (3) Serum triglyceride level may play an important role in viral replication. These data further suggest that therapies directed at lowering plasma triglyceride levels may enhance the efficacy of current antiviral treatment regimens.
authors.affiliation: Rush University Medical Center, Chicago, IL, USA, dvanthiel@dr.com.
authors.forename: David H
authors.initials: DH
authors.lastname: Van Thiel
authors.forename: Magdalena
authors.initials: M
authors.lastname: George
authors.forename: Bashar M
authors.initials: BM
authors.lastname: Attar
authors.forename: Giuliano
authors.initials: G
authors.lastname: Ramadori
authors.forename: Niculae
authors.initials: N
authors.lastname: Ion-Nedelcu
mesh_terms: D000328:Adult; D002784:Cholesterol / Q000097:blood*; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D015243:Cholesterol, VLDL / Q000097:blood; D015897:Comorbidity; D003924:Diabetes Mellitus, Type 2 / Q000453:epidemiology; D005234:Fatty Liver / Q000097:blood* / Q000453:epidemiology; D005260:Female; D005838:Genotype; D016174:Hepacivirus / Q000235:genetics / Q000502:physiology*; D006526:Hepatitis C / Q000453:epidemiology; D006801:Humans; D008108:Liver Diseases, Alcoholic / Q000097:blood* / Q000453:epidemiology; D008297:Male; D008875:Middle Aged; D065626:Non-alcoholic Fatty Liver Disease; D010316:Particle Size; D011446:Prospective Studies; D014280:Triglycerides / Q000097:blood*; D014779:Virus Replication / Q000502:physiology*
chemical_list: D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D015243:Cholesterol, VLDL; D014280:Triglycerides; D002784:Cholesterol