RT Book, Section
A1 Dienstag, Jules L.
A2 Jameson, J. Larry
A2 Fauci, Anthony S.
A2 Kasper, Dennis L.
A2 Hauser, Stephen L.
A2 Longo, Dan L.
A2 Loscalzo, Joseph
SR Print(0)
ID 1178426876
T1 Chronic Hepatitis C Pathophysiology and Clinical Features
T2 Harrison's Principles of Internal Medicine, 20e
YR 2018
FD 2018
PB McGraw-Hill Education
PP New York, NY
SN 9781259644016
LK accesspharmacy.mhmedical.com/content.aspx?aid=1178426876
RD 2024/04/24
AB Regardless  of  the  epidemiologic  mode  of  acquisition  of  hepatitis  C  virus  (HCV)  infection,  chronic  hepatitis  follows  acute  hepatitis  C  in  50−70%  of  cases;  chronic  infection  is  common  even  in  those  with  a  return  to  normal  in  aminotransferase  levels  after  acute  hepatitis  C,  adding  up  to  an  85%  likelihood  of  chronic  HCV  infection  after  acute  hepatitis  C.  Few  clues  had  emerged  to  explain  host  differences  associated  with  chronic  infection  until  recently,  when  variation  in  a  single  nucleotide  polymorphism  (SNP)  on  chromosome  19,  IL28B  (which  codes  for  IFN-λ3),  was  identified  that  distinguished  between  responders  and  nonresponders  to  IFN-based  antiviral  therapy  (see  below).  The  same  variants  correlated  with  spontaneous  resolution  after  acute  infection:  53%  in  genotype  C/C,  30%  in  genotype  C/T,  but  only  23%  in  genotype  T/T.  The  association  with  HCV  clearance  after  acute  infection  is  even  stronger  when  IL28B  haplotype  is  combined  with  haplotype  G/G  of  a  SNP  near  human  leukocyte  antigen  (HLA)  Class  II  DBQ1*03:01.