Viral Liver Diseases Open Access
Copyright ©The Author(s) 2002. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Apr 15, 2002; 8(2): 298-300
Published online Apr 15, 2002. doi: 10.3748/wjg.v8.i2.298
mIL-2R, T cell subsets and hepatitis C
Chao-Pin Li, Ke-Xia Wang, Jian Wang, Bo-Rong Pan
Chao-Pin Li, Ke-Xia Wang, Jian Wang, Department of Aetiology and immunology, School of Medicine, Huainan University of Technology, Huainan 232001, Anhui Province, China
Bo-Rong Pan, the Fourth Military Medical University
Author contributions: All authors contributed equally to the work.
Supported by the Youth Scientific Foundation of the Ministry of Coal Industry of China, No. 96-072
Correspondence to: Dr. Chao-Pin Li, School of Medicine, Huainan Institute of Technology, Huainan 232001, Anhui Province, China.
Telephone: +86-554-6658770 Fax: +86-554-6662469
Received: September 14, 2001
Revised: October 3, 2001
Accepted: October 11, 2001
Published online: April 15, 2002


AIM: To study the levels of membrane interleukin-2 receptor (mIL-2R) and T cell subsets in peripheral blood mononuclear cells (PBMC) from patients with hepatitis C and their role in the pathogenesis of hepatitis C.

METHODS: The levels of mIL-2R and T cells subsets in PBMC were detected by biotin- streptatividin (BSA) technique before and after stimulation with PHA in 203 patients with hepatitis C with HCV-RNA (+), anti-HCV (+), anti-HCV (-).

RESULTS: The total expressive levels of mIL-2R before and after stimulation with PHA (0.03 ± 0.01, 0.03 ± 0.02, 0.04 ± 0.02, 0.36 ± 0.03), and T cell subsets in PBMC (0.62 ± 0.06, 0.37 ± 0.05, 0.35 ± 0.07) were all lower in patients with hepatitis C than those in normal controls (0.66 ± 0.07, 0.41 ± 0.06, 0.31 ± 0.05, P < 0.01). Among the patients, the levels of mIL-2R were lower in silence than those in situation of PHA inducting (P < 0.01). However, the levels of mIL-2R were similar in acute hepatitis C to that in chronic hepatitis C (P > 0.05). The levels of CD3+, CD4+, CD4+/CD8+ were lower and CD8+ was higher in patients with acute and chronic hepatitis C with anti-HCV (+) than those in normal controls (0.62 ± 0.06, 0.37 ± 0.05, 0.35 ± 0.07, 1.18 ± 0.30, 0.61 ± 0.07, 0.37 ± 0.05, 1.39 ± 0.33, 0.31 ± 0.05, P < 0.05 - P < 0.01).

CONCLUSION: The cellular immunity is obviously changed in patients with hepatitis C. The levels of mIL-2R and activation of T cells are closely associated with chronicity of hepatitis C.


In acute and chronic hepatitis C virus (HCV) infection liver damage is thought to be the results of T-lymphocyte-mediated destruction of virus infected liver cells[1-51]. The factors that affected the immune response to viral antigens, particularly those that regulate the function of virus-specific cytotoxic T-lymphocyte-mediated lymphocytes, most likely play an important role in determining the states of liver injury. Interleukin-2 (IL-2) has a crucial role in several immunologic functions and its effect is dependent on the interaction with IL-2 receptors (IL-2R) expressed on surface of activated T lymphocytes and other immunocompetent cells[52-54]. Decreased IL-2 activity in supernatants of mitogen-activated peripheral blood mononuclear cells (PBMC) has been measured in patients with chronic HCV infection who had active liver disease, while normal levels have been detected in chronic HCV carriers with milder or no liver damage. The impaired IL-2 activity of PBMC, which has been claimed to be associated with high levels of virus duplication, has been interpreted as the reflection of an immune regulatory disorder of chronic active hepatitis C, which may be responsible for reduced differentiation of cytotoxic, virus-specific T cells and could explain the failure to eliminate all infected cells. Recently, methods for detecting membrane interleukin-2 receptor (mIL-2R), which exists on surface of T cells and can be released from activated lymphocytes, have been available, and high levels of these serum factors have been detected in a variety of pathologic conditions. To analyze IL-2R dependent immunoregulatory function in viral hepatitis, the levels of mIL-2R in the course of acute and chronic HCV infection in relation to the activity of liver disease and of virus replication have been investigated. The results suggest that in chronic active hepatitis C there is a state of activation rather than of depression of the IL-2 system, and the pathogenesis is related to the cellular immune function of the patients. PBMC are aggregation of immune cells, which have a lot of T lymphocytes, and play an important role in the anti-HCV infection. The cellular immune function of the patients may be the reflection of the level of T cell subsets and mIL-2R. The method of biotin-streptavidin (BSA) has higher specificity and sensitivity. In order to study the influence on the cellular immune function after being infected by HCV in PBMC and the effect on the mechanism of hepatitis C, the T cell subsets and mIL-2R of 203 patients with acute and chronic hepatitis C were detected by the above methods.


The 203 patients with confirmed diagnosis of hepatitis C (male 116 and female 87), aged 19-52 (average: 36.4 years), from our affiliated and teaching hospitals were chosen whose HCV-RNA in serum and PBMC were detected. Among them, the positive number of HCV-RNA in acute and chronic patients was 58 and 145 respectively. All diagnoses were made according to the diagnosis criterion of Chinese Hepatitis Conference 1995 (Beijing). The controls (n = 20) were normal blood donors from the local Central Blood Bank.

Reagents and instruments

The antibodies against T cell subsets, Ficoll-Hypaque sedimentation gradient were produced by Shanghai Jingan Medical Institute, the Second Reagent Factory of Shanghai, and Huamei Bioengineering Company of Shanghai (No. 981010, 980215, 980422). Carbon dioxide gas incubator (MDF-135) was made in Japan.


The peripheral vein blood 5 mL from each of the patients with hepatitis C was collected at 08:00, which was distributed 2.5 mL in a sterile test tube and an anticoagulant test tube with heparin respectively.

Separation of PBMC and detection of T cell subsets, mIL-2R

After the anticoagulant heparinized blood was mixed with equal volume of Hanks' liquid without Ca2+ and Mg2+, the PBMC were harvested from heparinized whole blood by centrifugation on Ficoll-Hypaque sedimentation gradient and diluted to (1-3) × 109•L⁻¹ cells suspension with RPMI 1640 culture liquid. The 10 μL suspension of PBMC was smeared on sheet glass pores so that the cells with CD3+, CD4+, CD8+ could be detected. Of the PBMC suspension, 0.5 mL was mixed with RPMI 1640 culture liquid, which had PHA 200 mg•L⁻¹. The cells were grown in continuous culture (37 °C, 50 mL•L⁻¹ CO2 in atmosphere) for 72 h and its mIL-2R induced by PHA could be measured by the antibodies against membrane of T cells.

Immunocytochemical method of Biotin- streptavidin system (BSA)

The different mAb against CD3, CD4, CD8 and Tac with biotin and SA-HRP were smeared on different sheet glasses. These smears were left dry naturally and fixed with acetone for 15-20 min. The cells were incubated in continuous culture (37 °C, 50 mL•L⁻¹ CO2 in atmosphere) for 30 min. The immune sheet glass pores were measured after being stained with the color-developing agent and several washings with Tris Buffer Solution (TBS). The total number of 200 PBMC was counted and its positive cells were statistically analyzed with the help of high power lens. The positive criterion was that the color of endoplasm or cell membrane was brown, if not being negative.

Statistical analysis was made by using Student's t test.


The results showed that the absolute positive rates of CD3+, CD4+ and CD4+/CD8+ were lower and CD8+ was higher in patients with anti-HCV (+) than those in normal controls (P < 0.01, Table 1). However, there was no significant difference between the patients with acute hepatitis C and normal controls (P > 0.05). But there was a higher significant difference between the patients with chronic hepatitis C and normal controls (P < 0.05). The reactivity of T cells in peripheral blood before and after being induced by PHA was all lower in acute, chronic hepatitis C than those in normal controls (P < 0.01).

Table 1 The detective results of T cell subsets and mIL-2R in peripheral blood of patients with hepatitis C (¯x ± s).
Anti-HCV (+)AH580.62 ± 0.05a0.37 ± 0.05b0.35 ± 0.07a1.18 ± 0.300.03 ± 0.01b0.34 ± 0.02b
Anti-HCV (-)CH1450.61 ± 0.07b0.37 ± 0.05b0.36 ± 0.06b1.04 ± 0.42b0.03 ± 0.01b0.35 ± 0.02b
Normal controls200.66 ± 0.070.41 ± 0.060.31 ± 0.051.39 ± 0.330.04 ± 0.020.36 ± 0.03
P< 0.01< 0.01< 0.01< 0.01< 0.01< 0.01
MS within group40.34726.18632.0220.1501.395.354

The chronicity of hepatitis is easier in patients with hepatitis C than that with hepatitis B[6,12,20,26,36]. The T cell subsets of the 203 patients with hepatitis C were detected by the method of BSA, and the results showed that the positive rate of T cell subsets and their mutual proportion were significantly different (P < 0.01), and there were significant disorders of cellular immune function and obvious pathologic injury.

It seems probable that mIL-2R is an important symbol of active T cells and plays a key role in biologic effect and its expression level can reflect the course of T cells activity and immune situation. The expressive level of T cells in silence was lower in hepatitis C patients than in normal controls (P < 0.01), which showed that the T cell activity was interfered. The possible reasons seemed to be as follows: (1)The mIL-2R on surface of T cells of the patients was inhibited by HCV; (2)The infection, duplication, proliferation of HCV in PBMC promoted the soluble interleukin-2 receptor to (sIL-2R) produced and released from T cells and inhibited the expression of mIL-2R[55-59]. This manifestation was caused by the low inducing cellular immune ability. Some active Tc cells could be combined tightly with the complex of HCV antigen-MHC-Imolecule on the surface of liver cells by T cells receptor (TCR) and released perforin. This irrevocable and progressive injury was one of the important reasons for chronicity of hepatitis C; (3)sIL-2R and mIL-2R could competitively combine with IL-2, and sIL-2R, being an immunosupperssive factor (similar to blocking factor), which could activate the IL-2 around the T cells so that the self-secretion effect of T cells decreased and the disorder of cellular immune function was enforced and the infection of HCV would be persisted[60-62]. These conclusions were in agreement with the concept that both acute and chronic active hepatitis C liver cell damages were caused mainly by cytotoxic T lymphocytes directed against viral antigens expressed on the surface of infected cells and that CD8+ lymphocytes were abundant in the infiltrates of the liver.

The present study demonstrates that the receptor of PHA exists on the surface of T cells. The level of mIL-2R obviously increased after stimulation with PHA, which showed that mIL-2R could be induced by PHA and was significantly different between acute hepatitis C patients and chronic hepatitis C patients (P < 0.05). The more serious the patient's condition, the longer the course of disease, and the lower the level of mIL-2R. The low level of mIL-2R was not beneficial for clearing away HCV and easy to reduce chronicity of hepatitis C.

CD3+, CD4+ and CD8+ are major function subsets of T cells and play a key role in response to HCV. Its counts and mutual relationship could be used to identify the cellular immune level and immunoregulation and is one of the valuable immunologic targets to forecast the change of patients' condition. The results showed that the lower positive rate of CD3+ in chronic hepatitis C and the immunity to HCV were partly deficient. The lower positive rate and poor activation of CD4+ are important reasons for the disorder of the immune function and can not clean HCV in time. Another key reason is the high level of CD8+ in chronic active hepatitis C, which can cause injury of liver cells and increase of ALT persistently. The proportion of CD4+/CD8+ could play an important role in the network of immunoregulation. The high level of CD8+ identified the injury of liver cells caused by CTL. These findings indicated that the immune response of the body to HCV was limited, and the infection of HCV existed persistently so that the patient's condition would change from acute to chronic.


Edited by Hu DK

1.  Chen YD, Tao QM, Zhang CY. The treatment of oral interferon for thirty patients with hepatitis C. Xin Xiaohuabingxue Zazhi. 1996;4:12-14.  [PubMed]  [DOI]  [Cited in This Article: ]
2.  Liu YJ, Cong WM, Xie TP, Wang H, Shen F, Guo YJ, Chen H, Wu MC. Detecting the localization of hepatitis B and C virus in hepatocellular carcinoma by double in situ hybridization. China Natl J New Gastroenterol. 1996;2:187-189.  [PubMed]  [DOI]  [Cited in This Article: ]
3.  Wei L, Wang Y, Chen HS, Tao QM. Sequencing of hepatitis C virus cDNA with polymerase chain reaction directed sequencing. China Natl J New Gastroenterol. 1997;3:12-15.  [PubMed]  [DOI]  [Cited in This Article: ]
4.  Gao JE, Tao QM, Guo JP, Ji HP, Lang ZW, Ji Y, Feng BF. Preparation and application of monoclonal antibodies against hepatitis C virus nonstructural proteins. China Natl J New Gastroenterol. 1997;3:114-116.  [PubMed]  [DOI]  [Cited in This Article: ]
5.  Yu SJ. A comparative study on proliferating activity between HBV related and HCV related small HCC. China Natl J New Gastroenterol. 1997;3:236-237.  [PubMed]  [DOI]  [Cited in This Article: ]
6.  Zhang LF, Peng WW, Yao JL, Tang YH. Immunohistochemical detection of HCV infection in patients with hepatocellular carcinoma and other liver diseases. World J Gastroenterol. 1998;4:64-65.  [PubMed]  [DOI]  [Cited in This Article: ]
7.  Tong WB, Zhang CY, Feng BF, Tao QM. Establishment of a nonradioactive assay for 2'-5' oligoadenylate synthetase and its application in chronic hepatitis C patients receiving interferon-alpha. World J Gastroenterol. 1998;4:70-73.  [PubMed]  [DOI]  [Cited in This Article: ]
8.  Liu YH, Zhou RL, Rui JA. Detection of hepatoma cells in peripheral blood of HCC patients by nested RT-PCR. World J Gastroenterol. 1998;4:106-108.  [PubMed]  [DOI]  [Cited in This Article: ]
9.  Zhu FL, Lu HY, Li Z, Qi ZT. Cloning and expression of NS3 cDNA fragment of HCV genome of Hebei isolate in E. coli. World J Gastroenterol. 1998;4:165-168.  [PubMed]  [DOI]  [Cited in This Article: ]
10.  Yang JM, Wang RQ, Bu BG, Zhou ZC, Fang DC, Luo YH. Effect of HCV infection on expression of several cancer-associated gene products in HCC. World J Gastroenterol. 1999;5:25-27.  [PubMed]  [DOI]  [Cited in This Article: ]
11.  Chen SB. The infection of HCV and primary hepatocellular carcinoma. Xin Xiaohuabingxue Zazhi. 1994;2:239-240.  [PubMed]  [DOI]  [Cited in This Article: ]
12.  Sun ZQ, Wang YJ. The positive and negative growth factors for modulate on replication of hepatocellular. Xin Xiaohuabingxue Zazhi. 1994;2:247-248.  [PubMed]  [DOI]  [Cited in This Article: ]
13.  Deng C, Su XS. The studied advance on growth factors of hepatocellular. Xin Xiaohuabingxue Zazhi. 1994;2:61.  [PubMed]  [DOI]  [Cited in This Article: ]
14.  Chen SB. The relationship between hepatic disease and heredity. Xin Xiaohuabingxue Zazhi. 1995;3:1-2.  [PubMed]  [DOI]  [Cited in This Article: ]
15.  Li JX, Sun DY, Li H, Zhu XZ, Liou QK, Su SL, Zhang D, Shen XY. Detection the marker of hepatitis virus and cytonmegalovirus for blood donors with ELISA. Xin Xiaohuabingxue Zazhi. 1995;3:181.  [PubMed]  [DOI]  [Cited in This Article: ]
16.  Li XY, Yin FQ, Hou YF. The treatment of Ligalong dilution for 68 patients with hepatitis C. Xin Xiaohuabingxue Zazhi. 1995;3:116.  [PubMed]  [DOI]  [Cited in This Article: ]
17.  Tian SB, Li DG, Lu HM. Transformation growth factor α and hepatic disease. Xin Xiaohuabingxue Zazhi. 1995;3:55.  [PubMed]  [DOI]  [Cited in This Article: ]
18.  Jia KL, Zhang XF. Analysis on the detection of anti-HCV and ALT for 1050 blood donors. Xin Xiaohuabingxue Zazhi. 1995;3:154.  [PubMed]  [DOI]  [Cited in This Article: ]
19.  An P, Yuan F, Han CF. Risk factos of hepatitis C virus infevtion in hemodialysis patients. Xin Xiaohuabingxue Zazhi. 1996;4:12-14.  [PubMed]  [DOI]  [Cited in This Article: ]
20.  Li JQ, Si PR, Yang LG, Liu BY, Min JR, Sun ZH, Cheng SM. Superifection and mutual relation of hepatitis B and C virus. Xin Xiaohuabingxue Zazhi. 1996;4:15-17.  [PubMed]  [DOI]  [Cited in This Article: ]
21.  Dong SX, Chen SB. Tumor necrosis factor and chronic hepatic disease. Xin Xiaohuabingxue Zazhi. 1996;4:44-45.  [PubMed]  [DOI]  [Cited in This Article: ]
22.  Li JX, Zhu XZ, Li H. The detective rate of HBV, HCV, HDV in fresh serum of HBsAg () and ALT (-). Xin Xiaohuabingxue Zazhi. 1996;4:52.  [PubMed]  [DOI]  [Cited in This Article: ]
23.  Li C, Zhan SL, Wang BN. The significance of detection of anti-HCV and hematometachysis. Xin Xiaohuabingxue Zazhi. 1996;4:55-56.  [PubMed]  [DOI]  [Cited in This Article: ]
24.  Ren ZX, Pei WX, Wang LS, Liou JX. The change of viral marker in serum for overlapping infection of HBV and HCV. Xin Xiaohuabingxue Zazhi. 1996;4:379-380.  [PubMed]  [DOI]  [Cited in This Article: ]
25.  Li JQ, Si PR, Yang LG, Liou BY, Min JR. Study on the viral marker in serum of 311 patients with hepatitis. Xin Xiaohuabingxue Zazhi. 1996;4:387-388.  [PubMed]  [DOI]  [Cited in This Article: ]
26.  Zhang SL, Lan SM, Li YF. The diagnosis and treatment of chronic hepatitis C. Xin Xiaohuabingxue Zazhi. 1996;4:397-398.  [PubMed]  [DOI]  [Cited in This Article: ]
27.  Cheng SQ. The advance of hepatic manifesta- tion of viral disease. Xin Xiaohuabingxue Zazhi. 1996;4:401-402.  [PubMed]  [DOI]  [Cited in This Article: ]
28.  Tang ZN, Hao LJ. The treatment of interferon on hepatitis C. Xin Xiaohuabingxue Zazhi. 1996;4:403-404.  [PubMed]  [DOI]  [Cited in This Article: ]
29.  Zhan SL, Li C, Wang BN. The manifestation of auto-antibody in serum of patients with positive of anti-HCV. Xin Xiaohuabingxue Zazhi. 1996;4:382.  [PubMed]  [DOI]  [Cited in This Article: ]
30.  Ji JM, Li JX. The detective rate of anti-HCV in serum of patients in hospital. Xin Xiaohuabingxue Zazhi. 1996;4:411.  [PubMed]  [DOI]  [Cited in This Article: ]
31.  Wang M, Li JX. Detection of viral marker of patients with hematometachysis and hemodialysis. Xin Xiaohuabingxue Zazhi. 1996;4:413-414.  [PubMed]  [DOI]  [Cited in This Article: ]
32.  Zhang YR, Ding SZ, Li HB, Fan XM, Yang YX. The influence of HBV, HCV on liver function. Xin Xiaohuabingxue Zazhi. 1996;4:417-418.  [PubMed]  [DOI]  [Cited in This Article: ]
33.  Wang YJ, Wang XH, Wang YM, Li MD. Ultrastructural changes of neutrophils in patients with chronic severe viral hepatitis. Xin Xiaohuabingxue Zazhi. 1996;4:452-453.  [PubMed]  [DOI]  [Cited in This Article: ]
34.  Lin SM, Zhang SL, Di PC, Liang XS. The significance of recombinant immunoblot assay in acute hepatitis C. Xin Xiaohuabingxue Zazhi. 1996;4:511-512.  [PubMed]  [DOI]  [Cited in This Article: ]
35.  Zhao YY, Yang HY, Liu GX, Li ZQ, Liu L, He LL, Deng WJ. Hepatitis C virus infection in patients with primary liver cancer. Xin Xiaohuabingxue Zazhi. 1996;4:43-44.  [PubMed]  [DOI]  [Cited in This Article: ]
36.  Jiang ZK, Zhang XF, Zhang C, Li LH, Yan MH. Study on the aetiology of posthepatitic cirrhosis. Xin Xiaohuabingxue Zazhi. 1997;5:136.  [PubMed]  [DOI]  [Cited in This Article: ]
37.  Shen J, Xu YC, Gao Z, Niu JY, Shen HB, Ye FF. Epidemiological statocellulaudy on the etiologic synergistic interaction of HCV and HBV in the development of hepar carcinoma. Xin Xiaohuabingxue Zazhi. 1997;5:72-74.  [PubMed]  [DOI]  [Cited in This Article: ]
38.  Li SL, Ma XX, Jing XJ. Investigation on HCV contamination of blood products in hospitals. Xin Xiaohuabingxue Zazhi. 1997;5:94-95.  [PubMed]  [DOI]  [Cited in This Article: ]
39.  Tang ZY, Qi JY, Shen HX, Yang DL, Hao LJ. Short_and long term effect of interferon therapy of patients with chronic hepatitis C. Xin Xiaohuabingxue Zazhi. 1997;5:104-105.  [PubMed]  [DOI]  [Cited in This Article: ]
40.  Luo YQ, Wu MC. Hepatocyte growth fuctor. Xin Xiaohuabingxue Zazhi. 1997;5:198-199.  [PubMed]  [DOI]  [Cited in This Article: ]
41.  Liang XS, Zhang SL, Di PC, Lin SM. Serum hepatitis C virus RNA in patients with chronic hepatitis C virus infection treated with interferon α. Xiaohuabingxue Zazhi. 1997;5:311-312.  [PubMed]  [DOI]  [Cited in This Article: ]
42.  Lin SM, Zhang SL. Diagnostic value of RIBA and RIA-2 in detection of anti HCV in chronic hepatitis C. Xin Xiaohuabingxue Zazhi. 1997;5:444-445.  [PubMed]  [DOI]  [Cited in This Article: ]
43.  Tang W, Du SC, Tao QM, Zhu L. A study on anticontamination of RT-PCR in detection of HCV-RNA. Xin Xiaohuabingxue Zazhi. 1997;5:638-639.  [PubMed]  [DOI]  [Cited in This Article: ]
44.  Yan XB, Wei L, Wu WT. Clinical analysis on gene-type and different type of HCV overlapping infection of HBV. Xin Xiaohuabingxue Zazhi. 1997;5:805-806.  [PubMed]  [DOI]  [Cited in This Article: ]
45.  Li SL, Su K, Fang JT. Epidemiologic analysis of HBV, HCV and HDV infection in natural population in Fushun. Xin Xiaohuabingxue Zazhi. 1997;5:42-43.  [PubMed]  [DOI]  [Cited in This Article: ]
46.  Li LF, Zhou Y, Xia S, Zhao LL, Wang ZX, Wang CQ. The epidemiologic feature of HCV prevalence in Fujian. World J Gastroenterol. 2000;6:80.  [PubMed]  [DOI]  [Cited in This Article: ]
47.  Du JH, Cha WZ. Interrelation between hepatitis C and primary hepatocellular carcinoma. Shijie Huaren Xiaohua Zazhi. 1999;7:176.  [PubMed]  [DOI]  [Cited in This Article: ]
48.  Worman HJ, Lin F. Molecular biology of liver disorders: the hepatitis C virus and molecular targets for drug development. World J Gastroenterol. 2000;6:465-469.  [PubMed]  [DOI]  [Cited in This Article: ]
49.  Jiang RL, Lu QS, Luo KX. Cloning and expression of core gene cDNA of Chinese hepatitis C virus in cosmid pTM3. World J Gastroenterol. 2000;6:220-222.  [PubMed]  [DOI]  [Cited in This Article: ]
50.  Zhou YX, Feng ZH, Jia ZS, Lian JQ, Li JG, Li WB. A study of gene immunization with recombinant expression plasmid of hepatitis C virus core antigen. Huaren Xiaohua Zazhi. 1998;6:966-968.  [PubMed]  [DOI]  [Cited in This Article: ]
51.  Guo YH, Yan XJ, Hou Y, Ren FL, Zhao JR, Cuei DX, Han FC, Duan J, Li XQ, Su CZ. Quantitative detection HCV-RNA in serum of Chinese people with RT-PCR. Huaren Xiaohua Zazhi. 1999;7:810-811.  [PubMed]  [DOI]  [Cited in This Article: ]
52.  Zhao XM, Duan DL, Zhang AL, Wang ZG, Zhu M, Hu R. Effect of antineoplastic agent huisheng oral liquid on human IL-2 level and activity of LAK cells. Huaren Xiaohua Zazhi. 1998;6:409-411.  [PubMed]  [DOI]  [Cited in This Article: ]
53.  Jing DD, Qiu DK. Relationship between IL-2 activity, IL-2R expression and liver function in patients with post hepatitis B cirrhosis. Huaren Xiaohua Zazhi. 1998;6:900-901.  [PubMed]  [DOI]  [Cited in This Article: ]
54.  Zhao CY, Liu JX, Tang HH, Feng ZJ, Zhen Z, Zhang SH. Significance of IL-2 and related indexes in patients with hepatitis and hepatocellular carcinoma. Huaren Xiaohua Zazhi. 1998;6:479-481.  [PubMed]  [DOI]  [Cited in This Article: ]
55.  Liu YH, Zhou RL, Rui JA. Detection of hepatoma cells in peripheral blood of HCC patients by nested RT-PCR. World J Gastroenterol. 1998;4:106-108.  [PubMed]  [DOI]  [Cited in This Article: ]
56.  Wu HB, Li ZW, Li Y. Clinical significance of detection of positive and negative strands of HCV RNA in peripheral blood mononuclear cells. Shijie Huaren Xiaohua Zazhi. 1999;7:220-221.  [PubMed]  [DOI]  [Cited in This Article: ]
57.  Zhao XP, Shen HX, Tian DY, Zhang DS, Peng ZH, Yang DL, Hao LJ. Expression and significance of HCV RNA and HCV NS5 antigen in liver tissues of patients with hepatitis C. Shijie Huaren Xiaohua Zazhi. 1999;7:516-518.  [PubMed]  [DOI]  [Cited in This Article: ]
58.  Fan XG, Tang FQ, Ou ZM, Zhang JX, Liu GC, Hu GL. Lymphoproliferative response to hepatitis C virus (HCV) antigens in patients with chronic HCV infection. Shijie Huaren Xiaohua Zazhi. 1999;7:1038-1040.  [PubMed]  [DOI]  [Cited in This Article: ]
59.  Liou WN, Tan DM, Fan XG, Zhang Z, Ou YK. The significance of detection of HCV in peripheral blood mononuclear cells of patients. Shijie Huaren Xiaohua Zazhi. 2001;9:235.  [PubMed]  [DOI]  [Cited in This Article: ]
60.  Wang JP, Li XH, Zhu Y, Wang AL, Lian JQ, Jia ZS, Xie YM. Detection of serum sIL-2R, IL-6, IL-8, TNF-αand lymphocytes subsets, mIL-2R in patients with chronic hepatitis B. Shijie Huaren Xiaohua Zazhi. 2000;8:763-766.  [PubMed]  [DOI]  [Cited in This Article: ]
61.  Huang PC. Clinical manifestation of detection of sIL-2Rin serum and ascites for the patients with cirrhosis and hepatocellular carcinoma. Huaren Xiaohua Zazhi. 1998;6:455-456.  [PubMed]  [DOI]  [Cited in This Article: ]
62.  Zhang SL, Liang XS, Lin SM, Qiu PC. Relation between viremia level and liver disease in patients with chronic HCV infection. China Natl J New Gastroenterol. 1996;2:115-117.  [PubMed]  [DOI]  [Cited in This Article: ]