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

During 1989, 316 members of a cohort of homosexual men were tested for HIV-specific DNA by the polymerase chain reaction (PCR) using a pair of gag-region primers. Of 125 HIV-seronegative subjects, 123 (98.4%) were PCR-negative while 158 (82.7%) of 191 HIV-seropositive subjects were PCR-positive. Fewer of the 33 subjects who were seropositive and PCR-negative were at Centers for Disease Control (CDC) stage IV than the seropositive, PCR-positive subjects (6 versus 25%; P = 0.030). The seropositive, PCR-negative group had higher mean CD4 counts (640 versus 490 x 10(6) cells/l; P = 0.006), higher CD4: CD8 ratios (0.92 versus 0.64; P = 0.004), lower immunoglobulin (Ig) G levels (1290 versus 1645 mg/dl; P = 0.002), lower IgA levels (168 versus 251 mg/dl; P less than 0.001), and lower C1q binding activity (8 versus 14%; P = 0.010) than the seropositive, PCR-positive subjects. The median rate of CD4 cell decline in the 3 years preceding the PCR sample was less marked in the seropositive, PCR-negative group than the seropositive, PCR-positive group (-58 versus -77 x 10(6) cells/l per year; P = 0.028). To control for duration of infection, we restricted the analysis to the subgroups of 11 seropositive, PCR-negative subjects and 34 seropositive, PCR-positive subjects who had seroconverted earlier in the cohort study. Both subgroups had similar durations of infection, yet the same pattern of differences persisted.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Low HIV-1 proviral DNA burden detected by negative polymerase chain reaction in seropositive individuals correlates with slower disease progression. 167 80

Markers of immune function present before infection may determine the subsequent course of disease in HIV-infected individuals. In 1983, we measured immune function in a group of haemophiliacs in Edinburgh. In 1984, 18 of these patients became infected with HIV-1 from contaminated factor VIII. We have followed-up these patients since their seroconversion. The rate of disease progression, as assessed by the appearance or not of AIDS symptoms or signs within five years of seroconversion, was related both to the concentration of total plasma IgM before exposure to infection and to the pattern of specific IgM and IgA anti-HIV response around the time of IgG seroconversion. Disease progression also correlated with concentrations of plasma interleukin-2 receptor (a marker of lymphocyte activation) and with the number and percentage of circulating DR + ve (activated) T cells. Our findings show that the extent of host immune reactivity, which may be genetically determined, is a powerful factor in the pathogenesis of HIV-associated disease.
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PMID:Determinants of HIV disease progression: six-year longitudinal study in the Edinburgh haemophilia/HIV cohort. 134 60

Human immunodeficiency virus type 1 (HIV-1) exhibits extensive genomic and antigenic diversity, which is thought to contribute to the failure of the host's immune response to control infection and prevent clinical progression. Part of this failure may be due to utilization by the virus of antigenic variation as a means to escape protective immune responses. Antibody-escape variants of HIV-1 were studied here using fresh clinical isolates and autologous plasmas. HIV-1 was isolated from the plasma of seven people who were all seropositive for at least 2 years, and symptomatic sometime during that period. Isolated viruses were confirmed as HIV-1 by the presence of reverse transcriptase activity in infected culture supernatants, and by positive immunofluorescence using human monoclonal antibody to HIV-1 core protein. Plasma from these people were positive by Western immunoblot (DuPont) for most major HIV-1 (strain IIIB) antigens. These plasmas neutralized three laboratory strains of HIV-1 (i.e., IIIB, RF, and MN) but did not neutralize the homotypic strain in five cases, and had greatly reduced neutralizing titers against the homotypic strain in two cases. Homotypic neutralizing antibodies were absent in autologous plasma obtained 3 months later. When antibody titers were measured by fixed-cell indirect immunofluorescence assays (IFAs), high titers of IgG (1:6400 to 1:25,600) were detected against HIV-1 IIIB, while low titers of only 1:20 to 1:160 were detected against homotypic viral antigens at the time of virus isolation, and remained low 12 and 16 weeks later. No class IgA, IgD, IgE, or IgM antibodies to homotypic viral antigens, as possible IgG-blocking antibodies, were detected by fixed-cell IFAs. Cross-reactions with heterologous donor's plasmas were observed in some cases, and in these cases the cross-reactions were unidirectional. Live-cell IFAs detected IgG in patient's plasma to HIV-1 IIIB-infected cells but not to cells infected with homotypic isolates. These results suggest that it is common for neutralization-resistant HIV-1 variants to appear during the course of infection, and that all or most antigens of these variants are capable of escaping antibody recognition.
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PMID:Homotypic antibody responses to fresh clinical isolates of human immunodeficiency virus. 170 33

Peripheral blood lymphocytes (PBL) were obtained from HIV-1-infected patients at different stages of disease. The absolute number of IgM-, IgG-, and IgA-producing lymphocytes per 10(6) PBL was increased 2.8-, 3.4-, and 1.9-fold, respectively, compared with normal controls. 2-17% of IgG-secreting patient cells reacted with the gp160 envelope glycoprotein of HIV-1 (a 737-fold increase over background), while 1-9% reacted with p24 (140-fold over background). In addition to this HIV-specific B cell activation, the number of lymphocytes reactive with nonviral antigens such as DNA, myosin, actin, trinitrophenylated keyhole limpet hemocyanin, and ovalbumin was increased by a mean of 17.9-fold. Evidence suggests that the latter changes reflect an HIV-induced polyclonal B cell activation unrelated to the production of anti-HIV antibodies. For example, the proportion of IgG anti-gp160- and anti-p24-secreting lymphocytes declined in patients with advanced disease, whereas the number of B cells producing antibodies to non-HIV antigens rose. Moreover, CD4 cell count and T4/T8 ratio showed a significant inverse correlation with the degree of polyclonal activation but not with anti-HIV responsiveness. These observations demonstrate that both quantitative and qualitative changes in B cell activation accompany (and may be predictive of) disease progression in HIV-infected individuals.
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PMID:Human immunodeficiency virus infection induces both polyclonal and virus-specific B cell activation. 173 46

Twenty-eight paired blood and semen samples obtained from human immunodeficiency virus type 1 (HIV-1) seropositive men at various stages of disease progression were evaluated for titer and immunoglobulin (Ig) class by an enzyme-linked immunosorbent assay (ELISA). Blood antibody titers ranged from 40,000 to 4,000,000 with a median of 40,000. Semen titers ranged from 400 to 40,000 with a median of 400. HIV-1 antibody titers in matched semen and blood samples showed a strong positive correlation (r = 0.963). The ratio of semen:blood titers ranged from 1:1000 to 1:10 with a median of 1:100. There was no correlation between blood or semen antibody titer and stage of disease of the patients. However, there was a trend toward higher (greater than or equal to 4000) semen antibody titers in men with evidence of genital tract inflammation greater than 10(6) white blood cells/ml semen; 3/5 versus 5/23, p greater than 0.1 Fisher exact test). All HIV-1 antibodies detected were of the IgG class; no IgA or IgM class antibodies of titers greater than or equal to 40 were found in either blood or semen. Thirteen paired blood and semen samples from individual patients were analyzed for antibody specificity by Western blot. In some cases antibody profiles in semen were different from those in blood; strong antibody reactivity against the gp160 viral coat antigen band was consistently detected in semen and blood, whereas the prevalence of detectable antibody reactivity against the p55 and p17 HIV-1 antigen bands was significantly reduced in semen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A comparison of HIV-1 antibody classes, titers, and specificities in paired semen and blood samples from HIV-1 seropositive men. 173 88

Researchers wanted to determine whether they could do a more specific ELISA HIV test directed at IgA rather than IgG antibodies. So they 1st used streptococcal protein G to remove IgG from serum samples of 10 follow up patients from Guadeloupe who previously tested positive via ELISA for HIV-1/2 IgG and HTLV-I IgG. They did this to test sera for IgA. The protein G treatment resulted in a 99.9% reduction in the IgG concentration (12.21.7 mg/ml to .007-.017 mg/ml). After IgG depletion, the researchers noted no ELISA positive samples for HIV-1/2 or HTLV-I IgG. In fact, all the values were well below the cutoff levels. This result indicated that streptococcal protein G treatment followed by IgA ELISA is more specific than testing for IgG. The sera of 8 patients tested negative for HIV-1/2 IgA, but all tested positive for HTLV-1 IgA. This result showed that IgA may be more useful than IgG for also confirming retroviral infections. The sera of 2 patients were 44% and 27% above the cutoff level indicating that these patients had HIV-1/2 IgA antibodies. The researchers observed that protein G treatment suppressed all HIV-1/2 and HTLV-I IgG Western blot reactivity which confirmed the effectiveness of protein G treatment. Further the HIV IgG bands in the 8 false positive sera did not materialize at all suggesting that the IgG reactivity observed was most likely nonspecific. These results indicated that nonspecific HIV-1/2 IgG caused the false positive HIV-1/2 IgG ELISA results. In conclusion, in Caribbean countries where HTLV-1 infection can be as high as 13%, the more specific HIV IgA ELISA test should be used since its use saves time and money. Further it can do generalized testing for HTLV antibodies.
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PMID:IgA testing for diagnosis of retroviral infections in the Caribbean. 174 65

Given the sexual transmission of HIV, the establishment of a genital mucosal immunity through secretory IgA may be necessary to achieve protection. We have investigated if repeated stimulations of oral mucosa with HIV-Immunosomes would lead to the production of secretory IgA in saliva and also, if such an oral immunization could prime the immune system to an early systemic immune response following a parenteral immunisation with a low dose of the antigen. HIV-1 gp 160-specific secretory IgA were detected in the saliva of all rabbits orally immunized with HIV-Immunosomes. As early as one week after the parenteral immunization, high titers of serum IgA, IgM and IgG were detected both in mice and rabbits that had been orally stimulated with the antigen. These antibodies could neutralize HIV infectivity in vitro. Animals that were immunized only parenterally showed a very weak humoral immune response.
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PMID:[Oral and parenteral immunization with HIV immunosome induce the secretion of IgA specific of HIV-1 in the salivary and the production of circulatory IgA in mice and rabbits]. 175 12

Hypergammaglobulinemia is one of the most consistent, and usually the first observable abnormality in infants vertically infected with HIV. We have analyzed serum interleukin (IL)-4, IL-6, tumor necrosis factor (TNF)-alpha, and immunoglobulin (Ig) concentrations in 23 HIV-infected and 21 uninfected children. IL-6 and TNF-alpha concentrations in HIV-infected children were significantly higher than those in uninfected children, and mutually correlated. No differences in serum IL-4 levels between infected and uninfected children were observed. There was a correlation between serum IL-6 and IgG and between IL-6 and IgA concentrations. Furthermore, during follow-up changes in IL-6 levels were usually accompanied by corresponding changes in IgG levels. Our data indicate an association between HIV, IL-6, TNF-alpha and hypergammaglobulinemia. Regardless of the source and initial stimulus, continued production of IL-6 and TNF-alpha may result in augmentation in an auto-feedback manner, accompanied by increases in Ig synthesis and, more importantly, HIV replication. Thus, elucidation of the mechanisms responsible for overproduction of these two cytokines in HIV-infected patients is not only interesting from a biologic point of view, but is likely to have important clinical implications as well.
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PMID:Serum interleukin-6 concentrations are elevated and associated with elevated tumor necrosis factor-alpha and immunoglobulin G and A concentrations in children with HIV infection. 176 80

The autopsy material of 15 children aged from 2 months to 3 years from the zonal group of increased risk of the ecologic pathology, acquired immunodeficiency and viral infections was assessed morphologically and clinically. Decreased number of T-cells (T4, T8), an increase of the level of serum IgA, IgE and immune complexes, HIV-antibodies (4 cases) were found in the patients. The method of the molecular hybridization by means of virus-specific 32P-DNA probes was used. Bronchopneumonia was the cause of death. Severe deficiency of the organs and cells of the immune system, alternative-proliferative lung inflammation, mainly in the form of pneumonitis and alveolitis, were found. The latter differed either individually or as a result of the predominant infectious agent (RNA- or DNA-viruses, pneumocysts, bacterial flora, fungi). Considerable immunity dysfunctions enhanced the intensity of the specific features in pneumonia morphology.
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PMID:[Intrauterine and postnatal pneumonia in acquired immunodeficiency of infants]. 180 64

We studied serological aspects of autoimmunity in patients with AIDS, AIDS-related complex (ARC) and in individuals at risk for AIDS. Immunoglobulin (Ig) M, IgG and IgA rheumatoid factors (RF) were quantified by enzyme-linked immunosorbent assay (ELISA), Ig by radial immunodiffusion, and circulating immune complexes (CIC) by the CIC-conglutinin and CIC-complement 1q (C1q) assays. Mean IgM RF levels were normal in AIDS patients, but those of ARC patients were higher and more frequent than the levels defined by agglutination methods. Similar observations were made for intravenous drug users (IVDU) and for both HIV-seropositive and HIV-seronegative homosexual men. Mean IgG RF levels were normal in AIDS and ARC patients but high in homosexual men and, to a lesser degree, in IVDU. IgA RF levels were high in many AIDS and ARC patients, in homosexual men, and in haemophiliac and control groups. The selective increase of the IgA isotype in AIDS was confirmed by the Ig results, which also showed an IgG increase in all groups. IgM were mainly high in people with ARC. CIC were detected in 68% of ARC patients by both methods, and in 55% of AIDS patients by CIC-Clq. A high incidence of positive samples in all at-risk populations, but particularly in seronegative individuals, was observed using CIC-conglutinin. CIC-C1q also revealed larger amounts of CIC in HIV-seronegative individuals, mainly in homosexual men. The study of these humoral aspects of autoimmunity provides useful information on the impairment of B-cells in patients with AIDS and ARC.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Rheumatoid factors and circulating immune complexes in HIV-infected individuals. 181 28


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