PMID- 9049223
OWN - NLM
STAT- MEDLINE
DCOM- 19970320
LR  - 20111117
IS  - 0270-9139 (Print)
IS  - 0270-9139 (Linking)
VI  - 25
IP  - 3
DP  - 1997 Mar
TI  - Cytotoxic T lymphocyte response and viral load in hepatitis C virus infection.
PG  - 705-12
AB  - A cytotoxic T lymphocyte (CTL) response to the hepatitis C virus (HCV) 
      nucleoprotein residues 88-96 that are the minimal and optimal epitope for human 
      leukocyte antigen (HLA) B44-restricted CTLs was assessed in 27 HLA B44-positive 
      patients with chronic HCV infection. Serum HCV RNA concentration and the amino 
      acid sequence of the residues 81-100 were also determined. Three patients were 
      infected with HCV with uncommon amino acid substitutions within the epitope. One 
      was infected with HCV with an amino acid substitution in the flanking residues of 
      the epitope. To stimulate CTLs in the peripheral blood, 9-mer peptides that 
      corresponded to the residues 88-96 of the individual patients were synthesized 
      and used. Seven of the 27 patients demonstrated a CTL response to the residues 
      88-96 with specific cytotoxic activities higher than 20%. The CTL activities were 
      significantly higher in patients with a low titer of serum HCV RNA than in those 
      with a high titer of serum HCV RNA (P = .0006). Some of the patients that 
      demonstrated a CTL response to the residues 88-96 also demonstrated a CTL 
      response to a newly identified HLA B44-restricted CTL epitope or a known HLA 
      A11-restricted CTL epitope or both. No apparent association was observed between 
      the CTL response and the stage of disease, or between the CTL response and the 
      grade of necroinflammatory activity. The results suggest that the HLA 
      B44-restricted CTLs together with other HCV-specific CTLs may inhibit the 
      outgrowth of HCV and that high-titer infection with HCV may suppress the CTL 
      responses.
FAU - Hiroishi, K
AU  - Hiroishi K
AD  - Hepatology Division, Jichi Medical School, Tochigi, Japan.
FAU - Kita, H
AU  - Kita H
FAU - Kojima, M
AU  - Kojima M
FAU - Okamoto, H
AU  - Okamoto H
FAU - Moriyama, T
AU  - Moriyama T
FAU - Kaneko, T
AU  - Kaneko T
FAU - Ishikawa, T
AU  - Ishikawa T
FAU - Ohnishi, S
AU  - Ohnishi S
FAU - Aikawa, T
AU  - Aikawa T
FAU - Tanaka, N
AU  - Tanaka N
FAU - Yazaki, Y
AU  - Yazaki Y
FAU - Mitamura, K
AU  - Mitamura K
FAU - Imawari, M
AU  - Imawari M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Hepatology
JT  - Hepatology (Baltimore, Md.)
JID - 8302946
RN  - 0 (Epitopes)
RN  - 0 (HLA-B Antigens)
RN  - 0 (HLA-B44 Antigen)
RN  - 0 (RNA, Viral)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Epitopes/immunology
MH  - Female
MH  - Genotype
MH  - HLA-B Antigens/*immunology
MH  - HLA-B44 Antigen
MH  - Hepatitis C/genetics/*immunology/*virology
MH  - Humans
MH  - Male
MH  - Middle Aged
MH  - RNA, Viral/analysis
MH  - T-Lymphocytes, Cytotoxic/*immunology
EDAT- 1997/03/01 00:00
MHDA- 1997/03/01 00:01
CRDT- 1997/03/01 00:00
PHST- 1997/03/01 00:00 [pubmed]
PHST- 1997/03/01 00:01 [medline]
PHST- 1997/03/01 00:00 [entrez]
AID - S0270913997001420 [pii]
AID - 10.1002/hep.510250336 [doi]
PST - ppublish
SO  - Hepatology. 1997 Mar;25(3):705-12. doi: 10.1002/hep.510250336.