Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The presence of hepatitis B surface protein (HBs) and hepatitis B core protein (HBc) was investigated, by flow cytometry, on the surface of peripheral mononuclear cells (PBMC) from cells of the following phenotype: CD3 (T lymphocytes), CD4 (T helper/ inducer), CD8 (T cytotoxic/suppressor), CD19 (B lymphocytes) and CD56 [natural killer (NK) cells] among eight patients suffering from chronic hepatitis B and five healthy HBV-negative subjects. This study demonstrated the presence of HBsAg and HBcAg on the lymphocyte surface for most of the patients. The mean percentage of labelled cells was 17% for HBsAg and 15% for HBcAg. Among the different lymphocyte subsets only B lymphocytes and the NK cells expressed HBsAg for 57% and 26% of cells, respectively. Similarly HBcAg was also detected among CD19 and CD56 cells only. Polymerase chain reaction (PCR) was used to search for the presence of hepatitis B virus (HBV) DNA and RNA in PBMC, using primers located in the S gene. HBV DNA was detected with variable intensity in the CD3, CD4, CD19 and CD56 subsets following their separation with a cell sorter. For HBV RNA the signal obtained after PCR and Southern blotting was higher for CD56 and CD19 cells than for CD3 cells and undetectable for CD4 cells. This study demonstrates that replication and transcription of the HBV can occur in CD19- and CD56-positive cells. Positive signals in CD3 cells may be due to contamination of this subpopulation by NK cells.
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PMID:Selective detection of human hepatitis B virus surface and core antigens in peripheral blood mononuclear cell subsets by flow cytometry. 879 May 58

The human herpes virus 7 (HHV-7) has been recently isolated from CD4 cells of healthy persons. The present study describes the antibody prevalence of this virus in a healthy Mexican population. Two hundred blood samples from candidates for blood donation at the Hospital General de Mexico were studied with the indirect immunofluorescence test (IFA) in HHV-7 infected SupT1 cells. The testing was done in the University of Cologne, Germany; 167 were males and 33 female; the donors came from 12 of the 31 states in the Mexican republican, predominantly from Mexico City (60.5%) and the State of Mexico (28%). Their mean age was 29.2 years. All but three samples were positive to the HHV-7 (98.5% positivity). Nearly 85% had high titers (> or = 1:80). Other serology testing in the samples revealed 1% positive tests to hepatitis B, 2% to syphilis, and 0.5% to brucella. Hepatitis C and the HIV test were negative in all. The high prevalence of HHV-7 in our donor population should be further studied in order to determine titers indicative of an active infection and of their association with illnesses.
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PMID:[Prevalence of human herpesvirus 7 in Mexican blood donors]. 885 Jan 45

Chronic hepatitis B viral infection is common in human immunodeficiency virus (HIV) carriers, but the effectiveness of interferon therapy is still unknown. We report the results of a long-term pilot study of five patients, who were infected with HIV and chronic hepatitis B, treated by interferon. Five males co-infected with HIV and hepatitis B virus (HBV) (mean age 27 years) were given a 6-month course of interferon (IFN)-alpha 2b 5 million units (MU) three times weekly. On initiating the treatment, their CD4 lymphocyte count was 340-553 mm-3, their CDC stage was IIa-III; all had histologically proven chronic hepatitis, with Knodell's score ranging from 6-10, and active HBV replication (HBV DNA and hepatitis B e antigen (HBeAg) were detectable). There was no associated hepatitis delta virus (H delta V) or hepatitis C virus (HCV) infection. Follow-up was for 53 months on average (24-74 months). After the treatment, hepatitis B e antibody (HBeAb) and hepatitis B s antibody (HBsAb) seroconversion was observed in one patient, HBeAb seroconversion alone in two patients, HBV DNA was absent from serum in three patients, and HBV DNA significantly decreased in one patient. The serum alanine aminotransferase (ALT) activity was normal in four patients. Histological improvement was obtained in four patients. The HIV stage remained unchanged in all patients during the whole follow-up. These preliminary results suggest that interferon can be successfully used in immunocompetent HIV carriers with chronic hepatitis B as well as in HIV-negative patients.
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PMID:Long-term effects of interferon-alpha in five HIV-positive patients with chronic hepatitis B. 891 5

The percentage of lymphocyte subsets from the peripheral blood of healthy adults and hepatitis B surface antigen (HBsAg) carriers were analyzed by flow cytometry. The five lymphocyte subsets studied were:- T (CD3) cells, B (CD19) cells, CD4 cells, CD8 cells, Natural Killer (CD3- CD16+/CD56+) cells (NK cells) and the CD4/CD8 ratio. The percentage (mean +/- SD) for the five lymphocyte subsets from the healthy adults were (67.5 +/- 8.5)%, (12.4 +/- 4.5)%, (35.5 +/- 7.8)%, (36.8 +/- 8.5)%, (17.9 +/- 8.1)% and 1.1 +/- 0.6, respectively. HBsAg carriers positive for HBV-DNA had a lower CD4/CD8 ratio than the healthy population (P = 0.030). The percentage of CD8 cells in HBsAg carriers increased significantly (r = 0.28; P = 0.019) with an increase in ALT levels but the values remained within normal range. The percentage of NK cells and CD4/CD8 ratio in HBsAg carriers positive for anti-HBe were higher than HBsAg carriers negative for anti-HBe (92% of which are HBeAg positive) (P = 0.045 and P = 0.035, respectively). The CD4/CD8 ratio in HBsAg carriers negative for anti-HBe (92% positive for HBeAg) was also lower than in the healthy population (P = 0.042). HBsAg carriers positive for HBV-DNA, HBeAg and raised ALT levels had a lower CD4/ CD8 ratio than did the healthy population. The lower ratio was due to an increase in the percentage of CD8 cells. This suggests an activated immune response triggered by the infection in an attempt to clear the virus. HBsAg carriers with normal ALT levels and who are negative for HBV-DNA may be in a state of tolerance.
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PMID:The cellular immune status of HBsAg-positive carriers in Malaysia. 898 Jul 96

Objective of the study was to determine whether there is any influence of hepatitis B virus (HBV) or hepatitis C virus (HCV) infection on CD4 count decline rate in HIV-infected individuals. Retrospective analysis of consecutive CD4 counts was conducted in 72 HIV-infected untreated individuals (including 57 intravenous drug addict (i.v.d.a.)) in relation to their serological markers of HBV and HCV infection and the history of i.v. substance abuse. Anti-HBc seropositive individuals had slower CD4 count decline rates compared to anti-HBc seronegative ones (-0.20%/month vs. -2.90%/month, Kruskal-Wallis H = 4.77, p = 0.029). Anti-HCV serostatus had no influence on CD4 count decline rates (-0.47%/month for anti-HCV seropositive persons vs. -0.61%/month for anti-HCV seronegative ones, p = 0.91). History of i.v. substance abuse did not affect the CD4 count decline rates too (-0.83 for i.v.d.a. vs +0.74 for non-i.v.d.a., p = 0.26). In our study HIV-infected individuals seropositive for anti-HBc tended to have substantially lower CD4 count decline rates compared to seronegative ones. Neither anti-HCV serostatus nor the history of i.v. substance abuse influenced the CD4 count decline rate. This observation arises question about the possible nature (molecular?, immune-based?) of potential mutual interactions between HIV and HBV infections.
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PMID:Does hepatitis B virus or hepatitis C virus infection influence CD4 count in HIV-positive individuals? 901 49

The clinical and pathogenetic importance of a number of features characterizing cell-mediated immunity and nonspecific protective factors in acute virus hepatitis B. 124 patients with hepatitis B virus (HBV) infection were placed under observation. Of these, 115 patients had acute virus hepatitis B, 6 patients had acute virus hepatitis of mixed etiology (B + delta) and 3 patients had chronic virus hepatitis B. The study included, besides the detection of virus hepatitis markers and the biochemical analysis of blood, the determination of subpopulations of peripheral blood lymphocytes (CD3, CD4, CD8, CD57), the functional activity of natural killers, characteristics of the interferon status, serum neopterin and beta 2-microglobulin in blood serum. Considerable changes in cell-mediated immunity and the interferon system were found to occur and the optimum immune response in acute virus hepatitis B was characterized.
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PMID:[The characteristics of the immune response in acute viral hepatitis B]. 908 33

Twenty-two human immunodeficiency virus type 1 (HIV-1)-infected, asymptomatic volunteers with CD4 cell counts of >600 cells/mm3 who were enrolled in a phase I immunotherapy trial comparing two schedules of immunization of an HIV-1 IIIB-based recombinant gp160 (rgp160) experimental vaccine were evaluated for rgp160-specific antibodies in parotid saliva, genital secretions, and serum. When the study was unblinded, it was determined that five volunteers had received rgp160 on a month 0, 1, 2, 3, 4, and 5 immunization schedule, seven volunteers had received rgp160 on a month 0, 1, 2, and 5 schedule, five had received alum/deoxycholate placebo, and seven had received a licensed hepatitis B virus vaccine. Five volunteers consented to the donation of parotid saliva but not genital secretions. Prior to immunization, parotid saliva specimens were available for 11 of 22 volunteers, seminal plasma (SP) specimens were available for 7 of 22 volunteers, cervicovaginal lavage (CVL) specimens were available for 5 of 22 volunteers, and serum was available for 22 of 22 volunteers. These baseline specimens and specimens collected at 1 and 7 months after the final immunizations were assessed by enzyme-linked immunosorbent assay for immunoglobulin G (IgG) and IgA antibodies specific for HIV-1 LAI rgp160 or HIV-1 MN rgp160. No augmentation in HIV rgp160-specific IgG or IgA antibody production in either parotid saliva or serum specimens of vaccinees compared to that in controls was observed after immunization. There were insufficient numbers of SP or CVL specimens available for statistical comparisons between vaccinees and controls. Overall, anti-LAI rgp160 IgG antibodies were detected in the parotid saliva specimens of 20 of 22 volunteers, the seminal plasma specimens of 11 of 11 volunteers, and the CVL specimens of 6 of 6 volunteers and in 21 of 22 serum specimens. Fewer volunteers expressed anti-LAI rgp160 IgA antibodies in mucosal or serum specimens: 11 of 22 parotid saliva specimens, 3 of 11 SP specimens, 3 of 5 CVL samples, and 12 of 22 sera.
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PMID:Antibody to human immunodeficiency virus type 1 (HIV-1) gp160 in mucosal specimens of asymptomatic HIV-1-infected volunteers parenterally immunized with an experimental recombinant HIV-1 IIIB gp160 vaccine. The National Institute of Allergy and Infectious Diseases-sponsored AIDS Vaccine Evaluation Group. 914 68

We analyzed T-cell responses to mitogens and antigens and B-cell differentiation in response to T-cell dependent (TCD) and independent stimuli in 22 human immunodeficiency virus (HIV)-infected children (1 to 9 years of age) according to the presence of protective humoral immunity at a mean time of 18 months after vaccination with Haemophilus influenzae type b, hepatitis B, diphtheria, and tetanus vaccines. The 17 vaccine responders had a mean of 3.2 responses. However, their antibody levels were lower compared with healthy children. The 5 nonresponders had a mean of 0.84 responses. There were no significant differences between responders and nonresponders regarding age, Centers for Disease Control and Prevention (CDC) disease class, CDC immunologic class, serum immunoglobulin (Ig) levels, or in the use of antiretroviral therapy. However, responders tended to have higher age-adjusted absolute CD4 cell counts than nonresponders (p = 0.07). Nonetheless, there was no correlation between antibody levels and age-adjusted CD4 counts for each of the 4 TCD vaccines. Responders had conserved lymphoproliferative responses to mitogens and to candida antigen; 7 (41%) had normal responses to tetanus antigen. While nonresponders had some conserved responses to mitogens, only 1 had a response to antigen. Thirteen responders (77%) and only 1 nonresponder (20%) had normal responses to at least 2 of the 3 mitogens and 1 of the 2 antigens (p = 0.04). Although defects in B-cell differentiation were detected in both groups, they were profound and generalized in the nonresponders. Fourteen responders (82%) had at least 1 normal B-cell response compared with none of the 5 nonresponders (p = 0.002). There were no correlations between normal lymphoproliferative responses and age, CD4 counts, serum immunoglobulin G (IgG) levels, or the use of antiretroviral therapy. Immunologic function is important in the evaluation of HIV-infected children.
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PMID:Correlation of in vitro T-cell and B-cell function with responses to childhood vaccines in children with human immunodeficiency virus infection. 947 50

The aims of this study were to analyze the mortality directly attributable to chronic viral hepatitis in HIV-1 infected patients and to investigate the influence of hepatitis virus infections on the survival of this population. A cohort of 328 HIV-1 infected, antiretroviral-treated patients, followed up from 1989 to 1996, was investigated in the study. The median follow-up period of the cohort was 120 weeks. The median baseline CD4 + cell count of the cohort was 303 cells/mm3. Hepatitis C virus, hepatitis B virus and hepatitis D virus infections were present in 214 (65%), 16 (4.9%) and 9 (2.7%) patients, respectively. Sixty-seven (20.4%) subjects died but there was no information on the vital status of 36 patients (11%). The causes of mortality were AIDS in 49 (73%), liver failure in 3 (4.5%) and other causes in 15 (22.4%). The cohort was divided into two groups for survival analysis, the groups consisting of persons infected by a hepatitis virus and persons without hepatitis virus infection. There was no difference in survival between the two groups (p = 0.31, log-rank). It is concluded that mortality among HIV-1/hepatitis virus coinfected patients with moderate to severe immunosuppression is mostly due to AIDS, and that the survival of these subjects is not influenced by the presence of hepatitis virus infections, particularly hepatitis C virus.
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PMID:Influence of hepatitis C virus infection on the mortality of antiretroviral-treated patients with HIV disease. 966 97

High viral and/or antigen load may be an important cause of the T cell hyporesponsiveness to hepatitis B virus (HBV) antigens that is often observed in patients with chronic HBV infection. Reduction of viral and antigen load by lamivudine treatment represents an ideal model for investigating this hypothesis. HLA class II restricted T cell responses and serum levels of HBV-DNA, HBsAg, and HBeAg were studied before and during lamivudine treatment in 12 patients with hepatitis B e antigen positive chronic active hepatitis B to assess possible correlations between viral and/or antigen load and vigor of the T cell response. Cell proliferation to HBV nucleocapsid antigens and peptides and frequency of circulating HBV nucleocapsid-specific T cells were assessed to characterize CD4-mediated responses. A highly significant enhancement of the CD4-mediated response to HBV nucleocapsid antigens was already detectable in most patients 7-14 d after the start of lamivudine treatment. This effect was dramatic and persistent in 10 patients but undetectable in 2. It occurred concomitant with a rapid and marked reduction of viremia. Interestingly, lamivudine also enhanced the responses to mitogens and recall antigens, showing that its effect was not limited to HBV-specific T cells. In conclusion, an efficient antiviral T cell response can be restored by lamivudine treatment in patients with chronic hepatitis B concurrently with reduction of viremia, indicating the importance of viral load in the pathogenesis of T cell hyporesponsiveness in these patients. Since lamivudine treatment can overcome T cell hyporeactivity, combining lamivudine with treatments directed to stimulate the T cell response may represent an effective strategy to induce eradication of chronic HBV infection.
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PMID:Lamivudine treatment can restore T cell responsiveness in chronic hepatitis B. 972 53


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