Lymphocyte subpopulations and level of the proinflammatory cytokines in the blood of patients with hepatitis C and with combined variant of hepatitis C and B

Subpopulation of cytotoxic lymphocytes CD8 having both secretory and cytolytic antiviral activity is supposed to play the essential role in the virus elimination. Inflammatory reactions are also of importance in the hepatitis C pathogenesis, their intensity being regulated by anti-inflammatory cytokins. This study was aimed at determination of lymphocyte subpopulation indices--the relative content of cells carrying markers CD4, CD8, CD16, CD19, CD72, the parameters of the phagocytic activity of granulocytes and monocytes, as well as serum concentrations of anti-inflammatory cytokines IL-1, IL-6 and TNF-alpha. These indices were evaluated in a group 132 patients with confirmed hepatitis C or mixed hepatitis B + C diagnosis, depending on the disease form and markers of the infectious process activity (as determined in the PCR test for hepatitis C virus RNA) in comparison with a group of healthy donors. In patients with variant hepatitis under study a growth in anti-inflammatory mediators concentration was observed along with decreased indices of lymphocyte subpopulations responsible for cell-mediated immunity and the phagocytosis parameters. In the case of mixed hepatitis these differences were shown to be more manifested.     

Interrelation between the activity of hepatitis, liver fibrosis and immune status in children with chronic hepatitis B and C

The lesion of the liver in viral hepatitis was found to depend on the state of the immune system. Relationship between the content of lymphocyte subpopulations (CD3+, CD4+, CD8+, CD20+) in the blood and immunoglobulins (IgG, IgM, IgA) with parameters of semi-quantitative evaluation of the activity of hepatitis and the stage of liver fibrosis in children with chronic virus hepatitis B, C, B + C was studied. The characteristic feature of all hepatitis was a decrease in the number of T lymphocytes CD4+ below the normal level and an increase in the content of B lymphocytes. The correlation between the morphological activity of hepatitis and the amount of T lymphocytes CD8+ was established only in chronic hepatitis B. In chronic hepatitis B and B + C the absolute amount of blood lymphocytes decreased with the increase of the age of the patients, but in chronic hepatitis B this was accompanied by the decrease of the morphological activity of hepatitis and in hepatitis B + C by its increase. The amount of lymphocytes CD4+ rose with the increase of liver fibrosis in chronic hepatitis B. In children with chronic hepatitis C and B + C the amount of blood lymphocytes was found to be unrelated to the morphological activity of hepatitis.     

Circulating and liver resident CD4+CD25+ regulatory T cells actively influence the antiviral immune response and disease progression in patients with hepatitis B

CD4+CD25+ regulatory T cells (Treg) have been shown to maintain immune tolerance against self and foreign Ags, but their role in persistent viral infection has not been well-defined. In this study, we investigated whether and where CD4+CD25+ Treg contribute to the development of chronic hepatitis B (CHB). One hundred twenty-one patients were enrolled, including 16 patients with acute hepatitis B, 76 with CHB, and 29 with chronic severe hepatitis B. We demonstrated that in chronic severe hepatitis B patients, the frequencies of CD4+CD25+ Treg in both PBMC and liver-infiltrating lymphocytes were significantly increased and there was a dramatic increase of FoxP3(+)-cell and inflammatory cell infiltration in the liver compared with healthy controls. In CHB patients, circulating CD4+CD25+ Treg frequency significantly correlates with serum viral load. In acute hepatitis B patients, circulating CD4+CD25+ Treg frequency was initially low and with time, the profile reversed to exhibit an increased number of circulating Treg in the convalescent phase and restored to normal levels upon resolution. In PBMC taken from infected patients, depletion of CD4+CD25+ Treg led to an increase of IFN-gamma production by HBV-Ag-stimulated PBMC. In addition, CD4+CD25+ Treg were capable of suppressing proliferation of autologous PBMC mediated by HBV Ags, which probably reflects the generation of HBV-Ag-specific Treg in circulation and in the liver of HBV-infected patients. Together, our findings suggest that CD4+CD25+ Treg play an active role not only in modulating effectors of immune response to HBV infection, but also in influencing the disease prognosis in patients with hepatitis B.     

Elevated numbers of Fc gamma RIIIA+ (CD16+) effector CD8 T cells with NK cell-like function in chronic hepatitis C virus infection

CTL are crucial in the defense against viral infections. In the course of investigating peripheral blood and intrahepatic CD8 T cells in patients with chronic hepatitis C virus (HCV) infection, we observed a significant population of CD8 T cells expressing the FcgammaRIIIA (CD16) receptor. This observation led us to characterize these cells with respect to their phenotype and function in a cohort of patients with chronic HCV infection as well as in healthy blood donors. On average, 10% of peripheral blood CD8 T cells from HCV-infected patients expressed CD16 compared with only a few percent in healthy donors. CD16(+) CD8 T cells displayed a late-stage effector phenotype with high levels of perforin. These cells exhibited a restricted TCR profile suggesting underlying clonal expansion. Stimulation of CD16 on CD8 T cells evoked a vigorous response similar to that of CD16 stimulation in NK cells. Our data suggest that CD8 T cells, during chronic HCV infection in humans, continue to differentiate beyond defined stages of terminal effector cells, acquiring CD16 and NK cell-like functional properties.     

Profiling blood lymphocyte interactions with cancer cells uncovers the innate reactivity of human gamma delta T cells to anaplastic large cell lymphoma

Quantifying the contacts that circulating lymphocytes have with cancer cells is useful, because their deficit favors malignancy progression. All normal lymphocytes contact, scan, and acquire membrane fragments (trogocytosis) from foreign cells for their immunosurveillance. So in this study, we used the in vitro trogocytosis of PKH67-stained cancer cell lines as a measure of their interactions with bulks of PBMC freshly isolated from healthy donors. Allogeneic PBMC mixed and coincubated in vitro for 1 h did not trogocytosis, whereas in the same conditions CD20(+), CD4(+), CD8(+), gammadelta T, and CD16(+) PBMC interacted strongly with the cancer cells. Although most unprimed lymphoid effectors of innate (NK) and adaptive (B and T) immunity from healthy donors spontaneously trogocytosed different tumoral cell lines, some carcinoma cell lines could escape them in the coculture. This also uncovered the strong interactions of circulating Vgamma9/Vdelta2(+) central memory gammadelta T cells with anaplastic large cell lymphoma. These interaction profiles were stable upon time for healthy blood donors but were different with other tumors and blood donors. This profiling provides interaction signatures for the immunomonitoring of cancer.     

不同临床类型乙型病毒感染者外周血T 细胞亚群与血清HBV DNA 载量 及HBeAg 滴度相关性分析

目的:探讨慢性乙型肝炎病毒(HBV)感染患者外周血T细胞亚群与血清HBV DNA载量及HbeAg滴度的关系。方法:选取103名HBV感染患者和20名健康者为研究对象。流式细胞术检测外周血T细胞亚群,聚合酶链式反应及酶免疫分析法分别检测血清HBV DNA载量及HbeAg滴度。结果:慢性乙型肝炎患者和慢性HBV携带者外周血CD3+T、CD4+T淋巴细胞亚群百分数低于健康对照组,结果有统计学意义(P<0.05或0.01;而CD8+T细胞亚群则呈现相反趋势,结果亦有统计学意义(P<0.05或0.01)。HBeAg阴性组中,HBVDNA水平与CD8+T细胞亚群百分数呈正相关(r=0.567,P<0.01),与CD4+/CD8+T细胞亚群百分数比值呈负相关(r=-0.601,P<0.01),而与CD3+T、CD4+T细胞亚群百分数无相关性。HBeAg阳性组中,HBV DNA水平及HbeAg滴度与CD3+T、CD4+T、CD8+T细胞百分数及CD4+/CD8+T细胞百分数均无相关性(P>0.05)。结论:不同临床类型的慢性乙型肝炎病毒感染患者外周血T细胞亚群存在不同程度细胞免疫功能降低和细胞免疫调节异常。HbeAg阴性的HBV感染患者,其血清HBV DNA水平与外周血T淋巴细胞免疫存在相关性。     

不同临床类型乙型病毒感染者外周血T细胞亚群与血清HBVDNA载量及HBeAg滴度相关性分析

目的：探讨慢性乙型肝炎病毒（HBV）感染患者外周血T细胞亚群与血清HBVDNA载量及HbeAg滴度的关系。方法：选取103名HBV感染患者和20名健康者为研究对象。流式细胞术检测外周血T细胞亚群,聚合酶链式反应及酶免疫分析法分别检测血清HBVDNA载量及HbeAg滴度。结果：慢性乙型肝炎患者和慢性HBV携带者外周血CD3可、CD4T淋巴细胞亚群百分数低于健康对照组,结果有统计学意义（P〈0．05或0．01;而CD8＋T细胞亚群则呈现相反趋势,结果亦有统计学意义（P〈0．05或0．01）。HBeAg阴性组中,HBVDNA水平与CD8T细胞亚群百分数呈正相关（r=0．567,P〈0．01）,与CD47CD8＋T细胞亚群百分数比值呈负相关（r=-0．601,P〈0．01）,而与CD3＋T、CD4＋T细胞亚群百分数无相关性。HBeAg阳性组中,HBVDNA水平及HbeAg滴度与cD3＋1r、cD41、CD8叮细胞百分数及CD47CD8＋T细胞百分数均无相关性（P〉0．05）。结论：不同临床类型的慢性乙型肝炎病毒感染患者外周血T细胞亚群存在不同程度细胞免疫功能降低和细胞免疫调节异常。HbeAg阴性的HBV感染患者,其血清HBVDNA水平与外周血T淋巴细胞免疫存在相关性。     

Production of profibrotic cytokines by invariant NKT cells characterizes cirrhosis progression in chronic viral hepatitis

Invariant (inv)NKT cells are a subset of autoreactive lymphocytes that recognize endogenous lipid ligands presented by CD1d, and are suspected to regulate the host response to cell stress and tissue damage via the prompt production of cytokines. We investigated invNKT cell response during the progression of chronic viral hepatitis caused by hepatitis B or C virus infection, a major human disease characterized by a diffused hepatic necroinflammation with scarring fibrotic reaction, which can progress toward cirrhosis and cancer. Ex vivo frequency and cytokine production were determined in circulating and intrahepatic invNKT cells from controls (healthy subjects or patients with nonviral benign or malignant focal liver damage and minimal inflammatory response) or chronic viral hepatitis patients without cirrhosis, with cirrhosis, or with cirrhosis and hepatocellular carcinoma. invNKT cells increase in chronically infected livers and undergo a substantial modification in their effector functions, consisting in the production of the type 2 profibrotic IL-4 and IL-13 cytokines, which characterizes the progression of hepatic fibrosis to cirrhosis. CD1d, nearly undetectable in noncirrhotic and control livers, is strongly expressed by APCs in cirrhotic ones. Furthermore, in vitro CD1d-dependent activation of invNKT cells from healthy donors elicits IL-4 and IL-13. Together, these findings show that invNKT cells respond to the progressive liver damage caused by chronic hepatitis virus infection, and suggest that these cells, possibly triggered by the recognition of CD1d associated with viral- or stress-induced lipid ligands, contribute to the pathogenesis of cirrhosis by expressing a set of cytokines involved in the progression of fibrosis.     

Anti-interferon activity of peripheral blood leukocytes in patients infected with HIV-1

The study was aimed at anti-interferon activity of different components of the in vitro system cells MT-4--HIV-1 as well as the culture fluid of peripheral blood leukocytes from patients at different stages of HIV infection and from patients with mixed infection (HIV and chronic hepatitis C) in comparison with patients infected with hepatitis C virus alone and healthy persons. Anti-interferon activity was detected in all groups of patients, its detection rate varying within 33% and 68%. The tendency towards increased detection rate of anti-interferon activity in HIV-infected patients in parallel with decreased number of CD4+ lymphocytes was noted. These data made it possible to suggest that increased detection rate of anti-interferon activity in the culture fluid of peripheral blood leukocytes from HIV-infected patients in parallel with decreased number of CD4+ lymphocytes could result from pathogenetic processes in the body, leading to a decrease in therapy effectiveness of HIV-infected patients with the preparations of alpha-interferon, especially in patients with a low content of CD4+ cells.     

Cell-mediated and humoral immunity in HBS-Ag carriers]

The presence of HBs--Ag in the blood was established in 1.8% of practically healthy persons, in 29.7% of virus hepatitis patients and in 86.0% of serum hepatitis patients. The immunological study of clinically healthy HBs--Ag carriers revealed a statistically significant decrease in the number of T and B lymphocytes and an increased level of serum IgA, IgM and IgG in the blood. Among donors, 7.6% were found to have lymphocytes sensitized to HBs--Ag and 15.4% were found to have lymphocytes sensitized to liver antigen, while for HBs--Ag carriers these data were 62.5% and 50%, respectively.     

Anti-IFN autoantibodies are present in healthy Egyptian blood donors at low titer

Autoantibody against interferon is associated in many viral and non-viral diseases. This study aimed to determine the prevalence of anti-IFN-alpha autoantibodies in healthy Egyptian blood donors. The study included 558 (100 females (17.92%) and 458 males (82.08%)) Egyptian healthy blood donors who showed normal levels of liver enzymes and kidney tests and were conformed negative for hepatitis B surface antigen (HBsAg), hepatitis C virus (HCV) antibodies (Abs), HIV-1/2 Abs, anti-HBc and Treponema Abs. Autoantibody against IFN-alpha-1a and IFN-alpha-2b were screened using ELISA. Anti-IFN-alpha-1a positive cases were found to be 43 subject (7.76%; 6 females (1.08%); 37 males (6.68%)) and anti-IFN-alpha-2b positive cases were found to be 3 (0.54%; all males). Combined positivity against both IFN-alpha-1a and IFN-alpha-2b was 38 (6.86%; 7 females (1.26%) and 31 males (6.60%)). From these findings we can conclude that antibodies against IFN-alpha are present in considerable number at low titer in accepted blood donors.     

不同病毒载量慢性乙型肝炎患者树突状细胞 B7-H1 表达及对 免疫功能的影响 *

摘要 目的： 观察慢性乙型肝炎患者外周血树突状细胞表面共刺激分子 B7-H1 的表达及对免疫功能的影响。方法： 检测慢性乙型 肝炎患者肝功能、 HBV-DNA 水平, 将患者分为高病毒载量高 ALT 组 （ A 组） 、 高病毒载量低 ALT 组 （B 组） 、低病毒载量组 （C 组） 及正常对照组 （D 组）。 流式细胞术检测各组患者外周血树突状细胞表面 HLA-DR、 CD80、 CD86、 CD83、 CD1a、 B7-H1 表达, 酶联免 疫吸附试验 （ELISA ） 检测 DC 培养上清液和混合淋巴细胞培养上清液中细胞因子 IL-12、 IL-10 水平。结果： 慢性乙肝患者的树突 状细胞膜表面分子 HLA-DR、 CD80、 CD86、 CD83、 CD1a 的表达均明显降低 (A、 B、 C 组与 D 组比较分别为 42.3± 4.9%、 46.7± 7.0 %、 52.5 ± 6.3 % vs 94.5± 3.5%; 34.5 ± 5.3%、 39.9 ± 6.4%、 45.6 ± 5.2 % vs 90.6± 6.5%; 38.2 ± 8.6%、 36.1 ± 5.4%、 42.5 ± 6.8 % vs 87.7 ± 5.1%; 28.3 ± 6.5%、 25.6 ± 3.4%、 33.5 ± 4.3% vs 82.6 ± 4.8%; 32.3 ± 5.8%、 29.3 ± 5.3%、 48.3 ± 4.9 % vs 68.2 ± 5.2 % P< 0.05), B7-H1 表达水平明显升高(27.48± 21.4%、 21.83± 20.2%、 15.43± 10.32 % vs 4.23± 2.2 % P<0.05)。B7-H1 表达水平与 ALT 呈正相关, 与 IL-12 水平呈负相关。 结论： 慢性乙型肝炎患者树突状细胞功能低下, 其机制可能与树突状细胞高表达 B7-H1 有关。 B7-H1 高表达抑制了淋巴细胞的功能, 导致乙型肝炎病毒持续感染。     

不同病毒载量慢性乙型肝炎患者树突状细胞B7-H1表达及对免疫功能的影响

目的：观察慢性乙型肝炎患者外周血树突状细胞表面共刺激分子B7-H1 的表达及对免疫功能的影响。方法：检测慢性乙型肝炎患者肝功能、HBV-DNA 水平,将患者分为高病毒载量高ALT 组（A 组）、高病毒载量低ALT 组（B 组）、低病毒载量组（C 组）及正常对照组（D 组）。流式细胞术检测各组患者外周血树突状细胞表面HLA-DR、CD80、CD86、CD83、CD1a、B7-H1 表达,酶联免疫吸附试验（ELISA）检测DC 培养上清液和混合淋巴细胞培养上清液中细胞因子IL-12、IL-10 水平。结果：慢性乙肝患者的树突状细胞膜表面分子HLA-DR、CD80、CD86、CD83、CD1a的表达均明显降低（A、B、C组与D组比较分别为42.3± 4.9 %、46.7± 7.0%、52.5± 6.3 %vs 94.5± 3.5 %;34.5± 5.3 %、39.9± 6.4 %、45.6± 5.2 %vs 90.6± 6.5 %;38.2± 8.6 %、36.1± 5.4 %、42.5± 6.8 % vs87.7± 5.1 %;28.3± 6.5 %、25.6± 3.4 %、33.5± 4.3% vs 82.6± 4.8 %;32.3± 5.8 %、29.3± 5.3 %、48.3± 4.9 % vs 68.2± 5.2 % P〈0.05）,B7-H1 表达水平明显升高（27.48± 21.4 %、21.83± 20.2 %、15.43± 10.32 %vs 4.23± 2.2%P〈0.05）。B7-H1 表达水平与ALT呈正相关,与IL-12 水平呈负相关。结论：慢性乙型肝炎患者树突状细胞功能低下,其机制可能与树突状细胞高表达B7-H1 有关。B7-H1 高表达抑制了淋巴细胞的功能,导致乙型肝炎病毒持续感染。     

Apoptosis and oxidative status in peripheral blood mononuclear cells of diabetic patients

We have compared the concentrations of intracellular glutathione (GSH), glutathione-dependent antioxidative enzymes, the cell death rate and immunophenotype profile of peripheral blood mononuclear cells (PBMC) from healthy donors and from patients with insulin-dependent type I (IDDM) or non insulin-dependent type II (NIDDM) diabetes mellitus. The IDDM and NIDDM patients had above-normal absolute lymphocyte counts, whereas the percentages of CD3, CD4 and CD8 T lymphocytes were significantly reduced. In contrast, the absolute number and percentage of B lymphocytes was higher in diabetic patients than in healthy donors. The low intracellular reduced glutathione (GSH) and the unbalanced profile of key enzymes involved in GSH metabolism, gamma glutamyltransferase (-GT) and glutathione-S-transferase (GST), account for the increased oxidative status of PBMC from diabetic patients. The plasma membranes of PBMC from diabetic patients were less permeable to propidium iodide than those of PBMC from healthy donors, indicating that the apoptotic cell death rate was lower in the cells from diabetic patients. These differences are potentially useful markers of pathogenic metabolic changes which occur during clinical diabetes and if they are confirmed could be used to identify the onset of diabetes.     

The expression profile of Fc receptor-like Y in B lymphocytes with hepatitis B virus induced diseases

The Fc Receptor-like Y (FcRY) molecule is preferentially expressed by B lymphocytes and has recently been considered as a potential therapeutic target for B cell malignancies. In this study, we investigated the correlation between FcRY expression profile, B lymphocytes population and different HBV infection disease status. The FcRY expression level on B lymphocytes and the number of B lymphocytes population from peripheral blood in 27 healthy controls (HC) and 65 patients with HBV-induced diseases, including chronic hepatitis B (CHB), liver cirrhosis (LC) and hepatocellular carcinoma (HCC), were analyzed using quantitative real-time PCR and flow cytometry. The results showed the level of FcRY expression and frequency of germinal center (GC) B lymphocytes from peripheral blood were significantly correlated with the HBV-related disease status, which was highest in HCC and LC patients, lowest in healthy donors, and in the middle in patients with CHB. Our study indicates that there is a significant correlation between FcRY expression profile, B lymphocytes population and HBV-induced diseases. However, the roles of FcRY and B lymphocytes in HBV-induced diseases are unclear and need further investigation.     

Cytotoxic lymphocytes in B-cell chronic lymphocytic leukemia. A flow cytometric study of peripheral blood, lymph nodes and bone marrow.

The occurrence of cytotoxic lymphocyte subpopulations (i.e., CD 16+, CD 57+ and cytotoxic CD 8+) wa studied in the peripheral blood of 18 B-cell chronic lymphocytic leukemia (B-CLL) patients. The absolute numbers of CD 57+, CD 16+ and cytotoxic CD 8+ lymphocytes were increased in the peripheral blood of untreated patients as compared with healthy donors, suggesting a causal relation with the accumulation of malignant B-cells. For 5 B-CLL patients and 5 hematological normal donors, the lymphocyte subpopulations in peripheral blood, lymph nodes and bone marrow were determined. A significant immune response was observed in the lymph nodes of the patients, as reflected by the CD 3+ lymphocytes, which were 1.7-27 times larger in the patients lymph nodes than in their peripheral blood and bone marrow. In contrast, with peripheral blood this was mainly caused by an increase in CD 4+ lymphocytes. The CD 57 lymphocytes in the lymph nodes of the patients had abnormal orthogonal light-scattering signals and an abnormal density of CD 57+ receptors in comparison with their peripheral blood CD 57+ lymphocytes or the CD 57+ lymphocytes in the peripheral blood, bone marrow and tonsils of the hematological normal donors. This study shows that although a significant increase of cytotoxic lymphocytes in the peripheral blood of B-CLL patients is observed, the actual distributions of the non-malignant lymphocytes can be quite different at the actual tumor sites, i.e., bone marrow and lymph nodes.     

Clinical evaluation of the structural characteristics of peripheral blood leukocyte DNA in patients with viral hepatitis B

The DNA structure of peripheral blood leukocytes in healthy donors and in viral hepatitis B patients was studied by the rate of the alkaline denaturation of DNA in cell lysates. An increased rate of the DNA alkaline denaturation of cell lysates was established, which was indicative of the damages in their DNA. The most pronounced damages of DNA were found in granulocytes of patients with highly active chronic hepatitis and hepatic cirrhosis, especially in cases of simultaneous delta-virus infection. The damage of leukocyte DNA reflected probably the accumulation of cells, committed to apoptosis, in peripheral blood. Apoptosis may be induced by cytotoxic lymphocytes recognizing HBV-infected cells.     

Immunopathogenesis of hepatitis C virus infection

Hepatitis C virus, a recently identified member of the family Flaviviridae, is an important cause of chronic viral hepatitis and cirrhosis. There are similarities in the nature of the immune response to this pathogen with immunity in other flavivirus and hepatotropic virus infections, such as hepatitis B. However, the high rate of viral persistence after primary hepatitis C infection, and the observation that neutralizing antibodies are not protective, would suggest that there are a number of important differences between hepatitis C, other flaviviruses, and hepatitis B. The phenomenon of quasispecies evolution and other viral factors have been proposed to contribute to immune evasion by hepatitis C virus. In the face of established persistent infection, virus-specific cytotoxic T lymphocytes may exert some control over viral replication. However, these same effectors may also be responsible for the progressive liver damage characteristic of chronic hepatitis C infection. The nature of protective immunity, including the role of innate immune responses early after hepatitis C exposure, remains to be defined.     

T cells with a CD4+CD25+ regulatory phenotype suppress in vitro proliferation of virus-specific CD8+ T cells during chronic hepatitis C virus infection

Chronic hepatitis C virus (HCV) infection is associated with impaired proliferative, cytokine, and cytotoxic effector functions of HCV-specific CD8(+) T cells that probably contribute significantly to viral persistence. Here, we investigated the potential role of T cells with a CD4(+)CD25(+) regulatory phenotype in suppressing virus-specific CD8(+) T-cell proliferation during chronic HCV infection. In vitro depletion studies and coculture experiments revealed that peptide specific proliferation as well as gamma interferon production of HCV-specific CD8(+) T cells were inhibited by CD4(+)CD25(+) T cells. This inhibition was dose dependent, required direct cell-cell contact, and was independent of interleukin-10 and transforming growth factor beta. Interestingly, the T-cell-mediated suppression in chronically HCV-infected patients was not restricted to HCV-specific CD8(+) T cells but also to influenza virus-specific CD8(+) T cells. Importantly, CD4(+)CD25(+) T cells from persons recovered from HCV infection and from healthy blood donors exhibited significantly less suppressor activity. Thus, the inhibition of virus-specific CD8(+) T-cell proliferation was enhanced in chronically HCV-infected patients. This was associated with a higher frequency of circulating CD4(+)CD25(+) cells observed in this patient group. Taken together, our results suggest that chronic HCV infection leads to the expansion of CD4(+)CD25(+) T cells that are able to suppress CD8(+) T-cell responses to different viral antigens. Our results further suggest that CD4(+)CD25(+) T cells may contribute to viral persistence in chronically HCV-infected patients and may be a target for immunotherapy of chronic hepatitis C.     

The comparative characteristics of the indices of lymphocyte and neutrophil functional activity in patients with HIV infection and chronic viral hepatitis B]

In 34 patients with human immunodeficiency virus (HIV) infection at the asymptomatic stage and 29 patients with chronic viral hepatitis B at the period of exacerbation (of these 14 patients had chronic persistent hepatitis and 15 patients had chronic active hepatitis) the complex study of the functional activity of lymphocytes and neutrophils was carried out by cytochemical methods with the simultaneous determination of the content of immunoregulating lymphocyte subpopulations. In patients with chronic active hepatitis a decrease in the percentage and the absolute number of helper T-lymphocytes and the ratio of CD4/8 in comparison with those in patients with HIV infection were revealed. At the same time patients with HIV infection exhibited more pronounced decrease in the activity of all lymphocytic enzymes under study (neutrophil esterase, acidic phosphatase and succinate dehydrogenase in lymphocytes), as well as in the activity of myeloperoxidase and the content of cation proteins and glycogen in neutrophils in comparison with patients having chronic active hepatitis.