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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A total of 219 sera from HIV-infected patients were tested by a competitive immunoassay for the presence of antibodies to env and core protein. Whereas antibodies to the HIV envelope protein (gp41) were detected in all patients, only 84% of the patients with latent infection, 73% of the patients with LAS and 48% of the patients with AIDS had antibodies to the core protein (p 24). The prognostic importance of the decline of antibody reactivity to HIV core protein was further investigated in patients with lymphadenopathy syndrome or AIDS-related complex and correlated with other serological and immunological parameters. In those patients with no detectable anti-core reactivity, we found more frequently pathological and significantly higher serum levels of beta-2-microglobulin and IgA, but significantly lower numbers of leucocytes and lymphocytes and T4/T8 ratio than in patients with both gp41 env and p24 core antibodies. These results demonstrate that the determination of antibodies to HIV core proteins in sera of HIV-infected patients, especially with lymphadenopathy syndrome or AIDS-related complex, appears to be of great value for monitoring prognosis and disease activity.
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PMID:[Prognostic significance of antibodies to HIV nuclear proteins in patients with the lymphadenopathy syndrome]. 316 27

Different stages of HIV infection are marked by expression of HIV genes, production of HIV antibodies, formation of antigen/antibody complexes and clearance of such complexes. Transient HIV antigenemia appearing generally 6-8 weeks prior to HIV antibody (HIV-Ab) seroconversion and lasting 3-4 months is generally seen in acute infection. If IgG antibodies to both envelope and core protein persist in the absence of HIV-Ag the short-term prognosis is relatively good. However, HIV-Ag seroconversion may appear at any time after HIV-Ab seroconversion. Progression to AIDS is strongly associated with declining or absent levels of IgG antibodies to p24. Titers of antibodies to HIV p24 below 64 are strongly associated with the presence of HIV antigen and a poor clinical outcome. HIV antigen may be less efficiently detected with the present assays in sera from regions where the prototype strains of HIV (HTLV-III and LAV) are less prevalent, like Central Africa. Levels of HIV-Ag in serum, and possibly in CSF, can be decreased by nucleoside analogues, like AZT. This indicates HIV-Ag and possibly antibody to HIV core protein p24 as suitable markers for selecting individuals for antiviral therapy as well as monitoring the efficacy of such therapy.
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PMID:Serodiagnostic profiles of HIV and HIV pathogenesis in vivo. 316 47

The autopsied brains of three homosexual men with acquired immune deficiency syndrome (AIDS), progressive encephalopathy and widespread multinucleated giant cell encephalitis were investigated by lectin and immunohistochemical methods to ascertain the cellular distribution of a human immunodeficiency virus (HIV) core protein, p25. Abundant viral antigen was present in all brains, limited to perivascular macrophages, microglial and multinucleated cells, some bearing elongated cytoplasmic processes. The multinucleated cells were consistently labelled by the lectin Ricinus communis agglutinin-1, a marker for microglia, which demonstrated process-bearing variants of these cells. The prominent staining of microglia for viral antigen and the morphological suggestion that they fuse with other microglia and/or macrophages to form the multinucleated cells characteristic of HIV encephalitis indicate that microglia are probably direct targets of HIV infection and serve to propagate and amplify this retroviral encephalitis.
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PMID:Microglia in the giant cell encephalitis of acquired immune deficiency syndrome: proliferation, infection and fusion. 317 3

The specific cellular immune response toward envelope and core proteins of human immunodeficiency virus-1 (HIV-1) was investigated in gibbon apes chronically infected with the HTLV-IIIB isolate. After in vitro stimulation of PBMC from infected and control animals with HIV-1 Ag, DNA synthesis, IL-2R expression and IL-2 release were assayed. Cells from infected gibbon apes demonstrated a group-specific response toward whole virus preparations from three divergent HIV-1 isolates (HTLV-IIIB, HTLV-IIIRF, HTLV-IIIMN). Consistent responses were also detected against purified HIV-1 Ag, i.e., native gp120 envelope glycoprotein, recombinant gp160 glycoprotein, a synthetic peptide (peptide 7) representing a highly conserved region of gp120, and purified native core protein p24. In addition, lymphocytes from infected gibbon apes displayed a specific, MHC-restricted, cytotoxic activity against autologous cells expressing HIV-1 envelope or gag proteins. The specific T cell reactivity toward HIV-1 proteins observed in infected gibbons contrasts with findings in HIV-1 infected humans, and may help to explain the apparent discrepancy in the natural history of the infection between the two species.
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PMID:Cell-mediated immune response toward viral envelope and core antigens in gibbon apes (Hylobates lar) chronically infected with human immunodeficiency virus-1. 326 61

Recent advances in the understanding of the pathogenesis of infection with human immunodeficiency virus (HIV) stems from the demonstration that the membrane glycoprotein, CD4, is the cellular receptor for HIV. This glycoprotein is found mainly on the surface of a major subpopulation of T lymphocytes and also on macrophages, natural killer cells, some B lymphocytes, and neuronal cells. Cells infected with HIV may be destroyed or have their normal function impaired. Host immune responses to HIV are poor and are not sustained. Neutralizing antibody often is not produced, or HIV may escape from normal immunosuppressive mechanisms through the process of rapid antigenic variation. Factors and markers that may be important in the outcome or that may predict progression of HIV infection are genetic (Gc type), environmental (nutritional status or intercurrent sexually transmitted diseases sustained by the host), and immunologic (rate of decline in number and impairment of function of CD4 lymphocytes and of decline in antibody titers to HIV core protein, p24). A recombinant vaccine will probably be developed for testing in future clinical trials.
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PMID:Immunology of human immunodeficiency virus infection and the acquired immunodeficiency syndrome. An update. 330 Apr 61

We conducted anti-HIV testing on follow-up samples obtained at a mean interval of 20 weeks from 150 blood donors who had previously tested anti-HIV ELISA positive and Western blot atypical. Of 93 donors who demonstrated reactivity to HIV core protein p24, 4 progressed to positive Western blots. Most of the remaining donors showed a persistent p24 reactivity on Western blot and had no risk factors for HIV infection. Immunofluorescence testing of the initial sample from 93 donors could not definitively separate seroconverters from those with persistent p24 reactivity. Of 57 donors with p18 reactivity, none were positive on follow-up anti-HIV testing. Our findings suggest policies and strategies for notifying donors of atypical anti-HIV Western blot results.
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PMID:Follow-up testing and notification of anti-HIV Western blot atypical (indeterminant) donors. 336 39

Viral particles have been demonstrated by electron microscopy in lymph nodes from patients with acquired immune deficiency syndrome AIDS-related persistent generalized lymphadenopathy (PGL) syndrome. Immunohistochemical and in situ hybridization studies have identified these viruses as the human immunodeficiency virus (HIV). In this study, we examined 20 PGL lymph nodes and found viral particles in 18 cases. Immunohistochemical studies on these cases revealed positive staining for the HIV core protein P24 within germinal centers of secondary follicles. In addition we found viral particles, morphologically indistinguishable from those observed in PGL lymph nodes, in 13 of 15 non-HIV related reactive lymph nodes. Immunohistochemical staining of these lymph nodes for the P24 core protein was negative. None of the patients in this group had risk factors for developing AIDS and none exhibited clinical evidence of immune deficiency. We conclude that the viral particles observed in PGL lymph nodes are most likely HIV, but similar particles can be seen in reactive lymph nodes not associated with HIV infection. The discrete localization of these particles within germinal centers has been observed for other viruses and immune complexes and a possible mechanism of this antigen deposition is discussed.
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PMID:The ultrastructural and immunohistochemical demonstration of viral particles in lymph nodes from human immunodeficiency virus-related and non-human immunodeficiency virus-related lymphadenopathy syndromes. 337 79

Blood donors reactive by enzyme-linked immunosorbent assay for antibody to the human immunodeficiency virus (HIV) who showed atypical patterns of viral core protein reactivity on Western blot were monitored for several months. Characterization of their antibodies was performed by 1) use of recombinant HIV proteins; 2) determination of cross-reactivity to HTLV-I, HTLV-II, and HTLV-IV: 3) assessment of immune status; and 4) identification of potentially interfering autoantibodies. Nineteen of 20 donors maintained the same HIV antibody reactivity throughout the follow-up period; the other donor became fully antibody-positive. Eighteen of 20 donors' sera showed clear reactivity with HIV recombinant core proteins. Ten of 19 donor samples demonstrated cross-reactivity to HTLV-IV; 3 of these 10 also cross-reacted with HTLV-I. The immune status of all donors was normal, although the medical histories and HLA antibody screens suggested possible autoimmune reactivity in 9 of 18 donors. During follow-up interviews, three donors reported possible risk factors for HIV infection that had not been acknowledged at the time of blood donation. We conclude that exclusion of donors with these atypical serologic test results is warranted while further studies to determine significance are being conducted.
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PMID:Evaluation of atypical human immunodeficiency virus immunoblot reactivity in blood donors. 342 Jun 68

53 individuals negative for anti-HIV by screening test and 79 individuals positive for anti-HIV were prospectively surveyed for clinical progression and by quantitatively measuring anti-p24 (antibodies against an HIV core protein), anti-gp41 (antibodies against an HIV surface protein) and HIV-(p24) antigen. The patients were classified into four categories of HIV-markers: 1. Anti-p24 in high concentrations, HIV-Ag negative, 2. anti-p24 in high concentrations, HIV-Ag positive (most often transitory only), 3. anti-p24 absent/deficient, HIV-Ag negative and 4. anti-p24 absent/deficient and HIV-AG positive. Within a minimum of 18 months, 4 of the 53 (8%) initially anti-HIV negative individuals contracted HIV infection. 17 of the 79 (22%) initially anti-HIV positive individuals showed disease progression. 8 of the patients in category 4 already had AIDS when entering the study, and 3 of the 6 (5%) remaining patients of this category developed AIDS. Amongst the 19 patients in the third category 2 individuals (11%) developed AIDS and in a further 5 (26%) individuals the disease progressed but in no case to AIDS. None of the patients of the categories 1 and 2 developed AIDS but 2 of the 10 (20%) individuals in the second category and 3 of the 29 (10%) in the first category showed disease progression but not to AIDS. In conclusion, the quantitative measurement of anti-p24 and of HIV-Ag affords prognostic pointers for the clinical outcome of HIV infection.
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PMID:[HIV serological parameters in the prognosis and follow-up assessment of an HIV infection]. 342 61

Human immunodeficiency virus (HIV) is lymphotropic and neurotropic. In vivo clinical and immunological abnormalities develop in a large proportion of long-term HIV antibody seropositive persons. Different stages of HIV infection are marked by expression of HIV genes, production of HIV antibodies, formation of antigen/antibody complexes and clearance of such complexes. Transient HIV antigenemia appearing generally 6-8 wk prior to HIV antibody (HIV-Ab) seroconversion and lasting 3-4 mth is generally seen in acute infection. IgM antibodies predominantly to core proteins may occasionally be detectable when, or just before, IgG antibodies appear. If IgG antibodies to both envelope and core proteins persist in the absence of HIV-Ag the short-term prognosis is relatively good. However, HIV-Ag seroconversion may appear at any time after HIV-Ab seroconversion. Progression to AIDS is strongly associated with declining or absent levels of IgG antibodies to p24. IgG2 and IgG4 antibodies to HIV, which are mainly directed to p24, disappear most dramatically. Titers of antibodies to HIV p24 below 64 are strongly associated with the presence of HIV antigen and a poor clinical outcome. HIV antigen was detected frequently in sera from children in all stages of infection in contrast to adults whose sera were generally HIV-Ag negative when asymptomatic and positive when AIDS was apparent. HIV antigen may be less efficiently detected with the present assays in sera from regions where the prototype strains of HIV (HTLV-III and LAV) are less prevalent, like Central Africa. Persistence of HIV-Ag in cerebrospinal fluid (CSF) appears to be pathognomonic for progressive encephalopathy, particularly in children. Levels of HIV-Ag in serum, and possibly in CSF, can be decreased by nucleoside analogues, such as AZT. This indicates HIV-Ag and possibly antibody to HIV core protein p24 as suitable markers for selecting individuals for antiviral therapy as well as monitoring the efficacy of such therapy.
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PMID:Pathogenesis of HIV and its implications for serodiagnosis and monitoring of antiviral therapy. 347 46


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