Table 1.

HCV-specific CTL can be detected in the majority of subjects with chronic HCV infection in whom CTL had previously been detected in the livera

StatusSubjectStimulationExpansion (fold)No. of clones/no. tested
Chronic HCV infection with intrahepatic CTLP1 (94F)HCV-H36.832/120
12F652.9
P2 (91E)HCV-H0.33/165
12F645.6
P3 (94I)HCV-H1.730/120
P4 (93K)HCV-H1.27/147
P5 (95I)HCV-H2.63/168
12F652.60/84
P6 (93I)HCV-H1.20/120
12F655.0
P7 (95K)HCV-H0.50/120
12F653.0
Chronic HCV infection without intrahepatic or PBMC CTLP8 (95L)HCV-H4.60/179
12F668.0
P9 (97B)HCV-H11.80/140
12F686.0
Seronegative controls N1 (BW)HCV-H6.70/126
N2 (MK)HCV-H21.80/97
12F630.8
N3 (CCW)HCV-H0.20/120
12F638.9
  • a Cryopreserved PBMC were subjected to one round of stimulation with HCV-H antigens expressed on autologous B-LCL using a recombinant vaccinia virus infection system. On day 14, the cells were counted to assess the degree of expansion. The cells were also tested for HCV-specific CTL activity using a standard 4-h chromium release assay. Assays were scored as positive if the total percent specific lysis was greater than 20% and at least 15% greater than the background nonspecific lysis. The cells were then subcloned and tested for HCV-specific CTL activity. HCV-specific CTL activity was detected from five of seven subjects with chronic HCV in whom CTL had previously been detected from the liver. HCV-specific PBMC CTL were not detected in two subjects with chronic HCV in whom CTL had also not been detected in the liver or in three HCV-seronegative control subjects. These negative results were not due to poor cell viability, as cells expanded after stimulation with the anti-CD3 monoclonal antibody 12F6.