Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A major epidemic of human immunodeficiency virus type 1 (HIV-1) infections has developed in Thailand since 1988. The blood banks in Chiang Mai began screening donors for HIV-1 antibodies in February 1988 and for p24 antigen in April 1992. The trends of HIV-1 antibody prevalence were analyzed by type of donor (i.e., paid, replacement, and voluntary) for the period of 1988 through 1993. In addition, the prevalence of HIV-1 p24 antigen and of antibodies to syphilis, hepatitis B surface antigen, and hepatitis C virus was evaluated among blood donors at Chiang Mai University Hospital and the Thai Red Cross blood banks in Chiang Mai. The prevalence of HIV-1 antibodies in donor sera increased from 0.84% in 1988 to 3.23% in 1989. It continued to increase in subsequent years, reaching a maximum of 4.04% in 1991; the prevalence declined slightly in 1992 and 1993. In the first year of screening, the prevalence of HIV antibodies was highest in paid professional donors. The use of paid donors was discontinued on July 1, 1992, largely because of their high rates of HIV seropositivity. This action lowered the prevalence of HIV infection in the overall donor population in 1992 to 3.61%, from the peak of 4.04% in 1991. Antibody prevalence in replacement donors increased from 0.56% in 1988 to 5.82% in 1991. Screening for p24 antigen, introduced on April 29, 1992, identified 48 infected donors (among the 44,446 donors tested in 1992 and 1993) who were HIV p24 antigen positive. Altogether, 7 (0.016%) donors tested repeatedly reactive for p24 antigen, had positive p24 antigen neutralization tests, and were negative for antibodies to HIV. The exclusion of paid donors and the use of p24 antigen testing are justified in northern Thailand. Additional strategies to exclude donors at very high risk and to attract those at low risk for infection should be developed.
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PMID:Infectious disease markers in blood donors in northern Thailand. 787 21

A progressive significant decrease of CD28 surface antigen expression on CD4+ (mean, 90, 86, 79, 68% in stages I, II, III, and IV, respectively, versus 96% in normals), as well as on CD8+ T lymphocytes (mean, 38, 32, 31, and 29% in stages I, II, III, and IV, respectively, versus 47% in normals) was observed during HIV-1 infection. The increase of cytotoxic/suppressor T cells, in both percentage and absolute numbers, that was observed in almost all HIV-1 patients, was associated with an increase of the CD8+ cells lacking the CD28 surface antigen. The loss of CD28 antigen expression was parallel to the increase of CD38, human leukocyte antigen (HLA)-DR, and CD45RO antigen expression on T lymphocytes throughout the disease. Furthermore, a positive significant correlation within the CD4+ but not the CD8+ subset was observed between the percentage of cells lacking the CD28 antigen and the percentage of cells expressing the HLA-DR and CD38 antigens, a finding suggesting that the loss of CD28 antigen expression on CD4+ lymphocytes may be associated with T-lymphocyte activation. Patients treated with zidovudine showed no significant differences in the percentages of either CD4+CD28+ or CD8+CD28+ T-cell subsets when compared to untreated patients. These phenotypic changes may be associated with the functional defects of T lymphocytes in HIV-1 infected individuals.
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PMID:Downregulation of CD28 surface antigen on CD4+ and CD8+ T lymphocytes during HIV-1 infection. 790 2

Pygmies remain isolated from other tribes and urban communities in central Africa. This study was undertaken among the Baka pygmies of the Eastern Province of Cameroon in an effort to redress the lack of published information on the health needs of that population. 141 adults aged 18-45 years were tested for the hepatitis B surface antigen (HBsAg), antibody to the surface antigen (anti-HBs), antibody to the core antigen (anti-HBc), and antibody to the hepatitis C virus (anti-HCV). HBsAg-positive sera were tested for the hepatitis B e antigen and antibody, while the presence of antibodies to the hepatitis D virus was determined in most of the anti-HBs-positive sera and some of the HBsAg-positive sera. Furthermore, previous infection with syphilis, measles, HIV-1 and HIV-2, and HTLV were determined by looking for the specific antibodies. Test results identified HBsAg in 14.2%, anti-HBc in 93.6%, anti-HBs in 52.2%, anti-HCV in 7.9%, hepatitis D in 46%, measles antibody in 99.3%, antibody to Treponema pallidum in 13.4%, antibody to HTLV-1 in 10.9%, and antibody to HIV-1 in 0.7% of sera tested. This prevalence of HIV-1 infection is lower than the estimated 1-1.5% projected for the sexually active general population.
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PMID:Infections among pygmies in the Eastern Province of Cameroon. 790 63

The prevalence of serum markers of delta hepatitis was determined prospectively in 82 intravenous drug abusers at various stages of human immunodeficiency virus (HIV) disease. Seventeen were HIV negative, 30 were HIV positive without acquired immunodeficiency syndrome (AIDS) and 35 had been diagnosed as having AIDS. Antihepatitis D virus (HDV) in serum was measured by a commercially available enzyme-linked immunosorbent assay (ELISA) and also by solid phase capture radioimmunoassays (RIAs) for immunoglobulin G (IgG) and immunoglobulin M (IgM) anti-HDV. HDV antigen and hepatitis B virus (HBV) DNA were also measured. Hepatitis B surface antigen (HBsAg) and anti-HBs were determined by using a commercially available RIA. Anti-HDV (RIA) was only detected in serum that contained HBsAg. These anti-HDV (RIA) positive samples also tested positive with the commercial anti-HDV electroimmunoassay. In addition, the commercial anti-HDV ELISA detected anti-HDV in some serum samples that were negative for HBsAg; these anti HDV-positive HBsAg-negative samples were frequently lipemic or contained rheumatoid factor. The prevalence of HBsAg and anti-HBs did not differ significantly with the stage of HIV disease. HBsAg was detected in 3 of 13 (23%) HIV-negative, 5 of 29 (17%) HIV-positive, and 4 of 18 (22%) patients with AIDS. IgG and IgM anti-HDV (RIA) was positive in 2 of 3 HIV-negative and 4 of 5 HIV-positive pre-AIDS HBsAg-positive subjects. However, none of 4 AIDS patients had anti-HDV. The difference between AIDS and non-AIDS patients was statistically significant (Fisher's exact test, p = 0.03). HDV antigen was detected in serum from one AIDS patient.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of HIV disease on serum markers of hepatitis delta infection in intravenous drug abusers. 793 Aug 80

Human recombinant adenoviruses (Ad) have been employed to develop experimental vaccines against a number of infectious agents. Ad-vectored vaccines express recombinant proteins, including any post-translational modifications, into functioning replicas of the native proteins capable of eliciting neutralizing antibodies in both abortive and permissive animal models. Human Ad types 4, 5, and 7 were used to construct recombinant viruses that express the respiratory syncytial virus F or G glycoproteins, the hepatitis B surface antigen, and the HIV env or gag genes. The recombinant Ad-HIV viruses are of particular interest and have been examined for their immunogenicity in dogs and chimpanzees. Dogs were immunized intratracheally with Ad-env recombinants (10(9) pfu/dog). Excellent humoral anti-HIV responses, including neutralizing antibodies, were detected in the sera following booster immunization (12-18 weeks after primary immunization) with a second Ad-env recombinant made in a different Ad serotype (heterotypic booster). Chimpanzees were immunized in two ways, orally with lyophilized virus (10(9) to 10(10) pfu/virus) in enteric-coated capsules or intranasally (10(7) pfu/virus). Intranasal immunization was superior to oral immunization with respect to replication of recombinant viruses as well as induction of anti-Ad and anti-HIV antibodies. Administration by both routes resulted in stimulation of cellular immune responses, as measured by antigen proliferation assays. Anti-HIV antibodies were detected in chimpanzee secretions (salivary, nasal, rectal, vaginal) taken from animals following intranasal immunization with a heterotypic recombinant. Intranasal administration effectively primed chimpanzees to produce high-titred (320-640) serum neutralizing antibodies to HIV following boosting with a baculovirus-derived env (gp160) subunit vaccine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adenovirus vectored vaccines. 795 85

Peripheral blood lymphocytes from healthy HIV-1 seronegative donors were immunized in vitro with the following synthetic peptides: (i) an octameric poly-L-lysine conjugated peptide of the HIV-1MN V3 loop and (ii) a resin bound synthetic peptide aa642-665 of HIV-1 gp41. Lymphoblastoid cell lines (LCL) were obtained by immortalization with Epstein-Barr virus (EBV). We produced four LCL secreting human monoclonal antibodies (HuMoAbs) of the IgM isotype: three were directed against the V3 domain (FC10, FC81 and CF41) and one against aa642-665 (CA45C). Two of these HuMoAbs (FC81 and CA45C) reacted to viral surface antigen on HIV-1-infected cells. All the HuMoAbs inhibited 40-53% of cell fusion induced by HIV-1-infected H9 cells at 5 micrograms/ml. They also neutralized, at lower concentrations, cell-free infection with HIV-1MN, HIV-1IIIB and four primary clinical HIV-1 isolates. No enhancing activity of the HuMoAbs in the presence of complement was observed. The results presented here show the feasibility of generating neutralizing human monoclonal antibodies against HIV-1 by primary in vitro immunization with selected synthetic peptides of HIV-1 envelope glycoproteins. This approach has provided tools for further studies of synergistic neutralization assays, and generated potential immunoglobulin candidates for passive immunotherapy.
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PMID:Primary in vitro immunization with multimeric synthetic peptides of HIV-1 envelope glycoproteins: generation of neutralizing human monoclonal antibodies. 796 97

Hepatitis B surface antigen (HBsAg) produced by recombinant DNA technology is now widely and safely used worldwide for hepatitis B vaccination. We used the HBsAg particle as a carrier molecule for presentation of selected human immunodeficiency virus type 1 (HIV-1) determinants to the immune system. Immunization studies carried out in primates showed that the particles elicit HIV specific virus neutralizing antibodies as well as T cell proliferative responses to both pathogens. As an experimental approach to active immunotherapy for hepatitis B virus (HBV) chronic carriers, we evaluated the efficiency of such hybrid antigen to overcome B cell tolerance in HBV transgenic mice.
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PMID:Immunogenicity of hybrid hepatitis B surface antigen particles. 804 75

Serum samples from 51 patients with malaria, 35 patients with hepatitis B virus infection, 111 patients with tuberculosis, and 166 healthy controls were studied to determine any associations between tuberculosis, malaria, hepatitis B, and AIDS in Nigeria, West Africa. All serum samples were examined for the presence of HIV-1/HIV-2, hepatitis B virus surface antigen (HBsAg), and malaria antibodies. Only one patient was HIV-1 antibody-positive and none HIV-2 antibody-positive. Statistical associations were found between the presence of malaria antibody titres on the one hand and a diagnosis of hepatitis B virus infection (P < 0.05) or tuberculosis (P < 0.05). A stronger association (P < 0.001) was found between the presence of HBsAg and tuberculosis suggesting that HBsAg carriers are at higher risk of contracting tuberculosis.
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PMID:Seroepidemiological associations between tuberculosis, malaria, hepatitis B, and AIDS in West Africa. 804 26

The CD4:CD8 ratio in peripheral T lymphocytes was determined in 123 Papua New Guineans aged over 5 years from Rumginae, a rural area of the Western Province. 18 people had a ratio less than 1.0. No antibody response to human immunodeficiency virus 1 (HIV 1) was found within the group. Hepatitis B surface antigen was more commonly associated with a CD4:CD8 ratio less than 1.0 than were microfilaraemia or a positive Mantoux test. Hepatitis B infection may be one of the causes of the CD4:CD8 ratio reduction within the community. Irrespective of the cause, other studies in Papua New Guinea have shown that a CD4:CD8 ratio less than 1.0 may result more from an increase in the CD8 cell count than a reduction in the CD4 cell count.
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PMID:A study of the CD4: CD8 ratio in peripheral T lymphocytes of rural Papua New Guineans: a reduced ratio assessed with regard to infectious agents. 805 46

A high percentage of HIV-1-infected infants and children in Romania are coinfected with hepatitis B virus. Little information is available on the impact of concurrent hepatitis B infection on the course of HIV-1 infection. We conducted a prospective cohort study over 1 year in a group of 68 HIV-1-infected infants and children to determine whether hepatitis B surface antigenemia, neopterin, and beta 2-microglobulin (B2M) predicted death. Among the 44 hepatitis B surface antigen-positive (HBsAg+) subjects at enrollment, 13 (30%) died during 1 year of follow-up. In comparison, two of 24 (8%) HBsAg-negative subjects died (RR = 7.7; p = 0.05). Higher initial serum concentrations of neopterin and B2M were negatively associated with survival. After stratifying by baseline clinical evidence of HIV-related disease, survival was negatively associated with HBsAg+ status (p = 0.04) in 33 children in stage P-2, adjusting for age, serum neopterin, and serum B2M levels. The results of this study suggest that serum neopterin is a marker for severity of clinical illness and that HBsAg+ status increases the mortality rate among children with clinical evidence of HIV infection.
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PMID:A prospective study of the association of serum neopterin, beta 2-microglobulin, and hepatitis B surface antigenemia with death in infants and children with HIV-1 disease. 808 26


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