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)

The clinical manifestations and some immunological parameters (CD4 lymphocytes, CD4/CD8 ratio, IgM, IgA, IgG levels, skin test) were examined in 226 adult patients (148 males and 78 females) infected with HIV. These included 58 (26%) asymptomatic patients with seropositive test, 109 (48%) with the only clinical manifestation generalized lymphadenopathy; 54 (24%) with AIDS-related infections, 5 (2%) with AIDS. A subsequent follow-up of 3 months to 3 years demonstrated that AIDS developed in 7 patients, 9 died. The period of infection with HIV and death ranged from 1.5 to 9 years. The signs of cell immunodeficiency were found in 70% of the examinees. Recommendations are given on the classification of HIV infection.
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PMID:[Clinical manifestations and the problems of classification of HIV infection]. 128 10

Substance P (sP) and Somatostatin (SOM), so as other neuropeptides can modulate neurologic and immunologic functions. sP has been described to enhance both in vitro and in vivo immunoglobulin synthesis. On the contrary, SOM has an inhibitory effect on the same activity. The modulating effect is more evident on IgA isotype. Hypergammaglobulinemia and in particular high levels of IgA is a common finding in pediatric AIDS and an imbalance among regulatory effects of neuropeptides might be suggested. In order to evaluate the plasma levels of sP in pediatric AIDS we studied 15 children with HIV infection (status P2), 10 seronegative children born to HIV positive mothers and 10 healthy children of the same age. All the HIV positive children had high plasma levels of IgG and IgA. The plasma level of sP was extremely higher in HIV positive children while no significant difference was found between seronegative children born to HIV positive mothers and healthy children. SOM was decreased in HIV positive children when compared to control groups but a significant difference was not reached. It might be supposed that HIV infection, through a dysregulation among neuropeptides interferes on immune functions and in particular on IgA synthesis. On the other hand it might be suggested that the imbalance between sP and SOM depends on the viral infection of immune cells since it has been demonstrated that SOM and other neuropeptide are synthesized by lymphoid tissue. Further studied relevance of neuropeptide disorders in pediatric AIDS.
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PMID:[Changed levels of substance P and somatostatin in HIV-positive children]. 128 55

Serum antibody responses were studied in detail in four vaccinia-naive volunteers in a phase I trial evaluating primary vaccination with a recombinant vaccinia virus expressing the HIV-1 gp160 envelope glycoprotein (HIVAC-1e, Oncogen/Bristol-Myers Squibb), followed by booster immunization with baculovirus-derived rgp160 (VaxSyn, MicroGeneSys). Prior to boosting, low-titer Fc receptor (FcR)-mediated, antibody-dependent enhancing (ADE) activity was detected in two of four volunteers but no IgM, IgG, IgA, neutralizing activity, or complement-mediated ADE activity was detected. Two weeks after boosting, all four volunteers developed HIV-1-specific IgG with titers of 1:160 to 1:640 by immunofluorescence assay. IgG1 was present in sera from each individual, while IgG2 and IgG3 were present in sera from two individuals, and IgG4 was present in serum from one individual. IgM and IgA were undetectable in all sera. Only one volunteer had IgG to the heterologous HIV-1 isolates, RF, MN, and SF2, after boosting. Serum from this volunteer neutralized the vaccine strain, LAV/IIIB, but not the heterologous strains, RF, MN, and SF2. Antibodies from the remaining volunteers had no neutralizing activity. The neutralizing serum had a positive reaction in a peptide-based ELISA utilizing a peptide corresponding to the principal neutralizing domain of the third hypervariable region (i.e., V3 loop) of the envelope glycoprotein. Neutralizing activity was partially removed by adsorption to this peptide, suggesting that it contained a type-specific neutralizing vaccine epitope. A low titer (1:40 to 1:80) of complement-mediated ADE activity to HIV-1 IIIB was present in sera from three vaccinees after boosting. FcR-ADE activity for HIV-1 SF2 and SF-128A were present in sera from two of these three vaccinees. None of the volunteers developed antisyncytial antibodies. These results indicate that inoculation with recombinant vaccinia followed by rgp160 boosting is the most effective strategy to date for inducing serum antibodies to the envelope glycoproteins of HIV-1, but further study is needed to optimize the functionality and cross-reactivity of these responses.
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PMID:Serum antibodies to HIV-1 in recombinant vaccinia virus recipients boosted with purified recombinant gp160. NIAID AIDS Vaccine Clinical Trials Network. 128 35

B-cell dysfunction in HIV-infected children is reflected by hypergammaglobulinemia and high levels of serum IgA. Little is known about antibody specificity since only a small portion of serum IgA appears to be directed against HIV proteins. In the present study the specificity of IgA antibodies against food, inhalant, bacterial and fungi antigens were evaluated in a population of HIV infected children. ELISA method was used for antibody testing. Our results show that in 84.6% of patients IgA against at least one food antigen are present. IgA against inhalant allergens were present in most of HIV-infected children but in none of controls. As for anti-tetanus toxoid antigens and anti-fungi antigens, though present in higher percentage in patients, specific IgA were found also in healthy children. If a gastrointestinal dysfunction might be supposed as the cause of presence of anti-food antigen IgA, it is difficult to consider this factor as the cause of presence of specific IgA directed against different antigens. It is possible to postulate that an immunologic dysregulation based on an imbalance between Th1 and Th2 cells or on higher levels of IL-5 and/or IL-6 may lead to a misfunction of B cell and consequently to hypergammaglobulinemia with high IgA levels.
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PMID:[Specific IgA against multiple antigens as expression of immunologic deregulation in HIV-positive children]. 129 28

The present retrospective study compares the laboratory diagnosis of cytomegalic inclusion disease (CID) by the use of "shell vial culture" [i.e., immunoperoxidase staining of human cytomegalovirus (HCMV) early antigen in human fibroblasts 24 h postinoculation] to the results of serology (i.e. immunoglobulins IgG, IgM, and IgA HCMV antibody testing) in 21 infants with congenital or postnatally acquired HCMV infection, 5 patients with lymphoproliferative disorders, 35 human immunodeficiency virus (HIV)-seropositive patients who met the Centers for Disease Control (CDC) criteria for stages IVA and IVB of HIV infection, and 115 patients suffering from the acquired immunodeficiency syndrome, AIDS (stages IVC-IVE according to CDC criteria). HCMV infection was diagnosed by means of the shell vial culture inoculated with patient samples (e.g., urine, bronchoalveolar lavage, induced sputum, etc.) and serology in 163 (92.6%) and 65 (36.9%) patients, respectively. Viral shedding was detected by shell vial culture in 100% of the neonates, 80% of the patients suffering from lymphoproliferative disorders, 100% of the AIDS related complex (ARC) and 89.6% of the AIDS patients. In contrast, serologic testing for HCMV-specific antibodies was positive in only 28.6%, 42.9%, and 34.8% of the neonates, ARC, and AIDS patients, respectively. In lymphoma patients, serologic testing gave identical results (80%) to the shell vial culture technique. With the use of the shell vial procedure, active HCMV infection in immunocompromised subjects and neonates can be recognized more reliably than by serologic testing. Nevertheless, in a low percentage of patients (7.4%), virus isolation by the shell vial culture may fail to detect HCMV infection.
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PMID:Comparison of shell viral culture and serology for the diagnosis of human cytomegalovirus infection in neonates and immunocompromised subjects. 132 25

The IgE synthesis is tightly controlled by a complex network of T and B cells. Because human immunodeficiency virus (HIV) disease associates T cell activation and depletion, polyclonal B cell activation, atopic symptoms, drug hypersensitivity, and autoimmune activity, we have evaluated IgE, as well as IgA, IgG, and IgM, in 315 HIV-seropositive individuals with or without acquired immunodeficiency syndrome (AIDS) and compared the results to those of 100 HIV-seronegative subjects. IgE levels were higher in HIV-infected subjects as a whole, compared to levels in seronegative control subjects (p less than 0.05). This difference was particularly marked between patients with AIDS and control subjects (p less than 0.005). A strong relationship appeared between IgE and the immune status as assessed by CD4 cell counts (p less than 0.001 between IgE values in patients with CD4 less than 300 or greater than 300/microliters). In addition, we assessed the predictive value of IgE elevation over disease progression: in subjects with a CD4 count less than 300/microliters, the survival analysis disclosed a 24-month occurrence rate of AIDS of 83% in individuals with IgE greater than 150 KIU/L versus 44% in individuals with IgE less than 150 (p = 0.016). In subjects with an AIDS-related complex, IgE greater than 150 indicated a 100% rate of AIDS versus 9% in individuals with IgE less than 150 (p = 0.003). Thus, IgE levels appear to be a very discriminative marker between patients in late stages of HIV infection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Elevation of IgE in HIV-infected subjects: a marker of poor prognosis. 134 48

European patients with human immunodeficiency virus type 1 (HIV-1) infection have been reported to have lower titers of anti-p24 antibody than Central African HIV seropositive patients. Recently, black HIV positive patients in the United States were reported to be more likely to have detectable anti-p24 antibodies, less p24 antigenemia, and higher combined serum immunoglobulins than white HIV positive patients. We measured individual total serum immunoglobulins in 853 HIV positive patients (94% male; 58% white and 42% black) on their initial medical evaluation and compared them with CD4+ T-cell counts. Blacks had notably higher IgG levels (p = 0.001) across the entire spectrum of CD4+ T-cell counts. Serum IgM levels were slightly higher in blacks. IgA levels were not significantly different between the races, although the trend (p = 0.006) was toward higher levels in whites. We also measured these three serum immunoglobulins in 60 HIV seronegative, healthy blood donors (30 black and 30 white). In this control group, blacks had statistically higher IgG and IgA levels than whites. A review of the literature prior to the HIV/acquired immune deficiency syndrome epidemic also supports the view that racial differences in IgG levels are not specific for HIV infection. We speculate that racial differences in humoral immunity, independent of geography or strain of HIV, may account for differences in anti-HIV antibody levels and HIV antigenemia.
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PMID:Comparison by race of total serum IgG, IgA, and IgM with CD4+ T-cell counts in North American persons infected with the human immunodeficiency virus type 1. 134 87

Interaction between herpesviruses and human immunodeficiency virus (HIV)1 is postulated in the progression of HIV disease. In order to evaluate the specific antibody responses directed to Epstein-Barr virus (EBV) and cytomegalovirus (CMV) and to provide serological evidence suggesting reactivation of these viruses able to accelerate the immunodeficiency, we studied IgA and IgG titres to EBV and CMV in the serum of HIV positive patients in relation to the CD4 cell number. The titres of IgG antibodies to EBV and the prevalence of IgG to CMV were significantly higher in HIV positive patients compared to control high risk HIV negative subjects. In HIV infected patients, anti-VCA IgG antibodies increased and anti-EBNA IgG antibodies decreased progressively in relation to the decline of CD4 cell number whereas anti-CMV IgG antibodies did not varied significantly at the same time. Anti-VCA IgA and anti-EA IgG antibodies were found uncommonly and with low titres. IgA antibodies to EA and CMV were not detected in any patient. The variations in EBV antibody response that we describe in HIV infection were previously reported in other immunodeficiency states and could be distinctive of these diseases.
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PMID:Antibodies to Epstein-Barr virus and cytomegalovirus in relation to CD4 cell number in human immunodeficiency virus 1 infection. 134 40

Certain immunological parameters (i.e. low CD4+ T cell numbers, high serum soluble CD8) have been described as prognostic factors for the progression of human immunodeficiency virus (HIV) infection to later clinical stages. In the present study we have found in one hundred HIV-infected Spanish patients (81% drug abusers, 7% homosexuals, 6% heterosexuals, and 6% other or unknown risk groups) that CD11b+ peripheral blood mononuclear cells are increased in those with persistent lymphadenopathy as compared to other clinical stages (asymptomatic, AIDS-related complex and AIDS). Serum IgA was significantly increased in AIDS patients, and in patients at any other clinical stage who had concomitant infections (mainly mycobacterial and fungal). CD11b (an integrin with complement receptor functions) may thus be of clinical interest for the staging of HIV-infected patients, and reflect stage-selective immunological changes in mononuclear cell biology during HIV infection. High IgA on the other hand, would be a marker of concomitant infection as well as of disease progression. The results concern mostly drug addicts (the main risk group in Spain), but may apply to the other risk groups because no significant differences were detected between drug addicts (n = 81) and non-drug addicts (n = 19) for the studied variables (p greater than 0.05).
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PMID:CD11b-bearing mononuclear leucocytes and IgA levels in the staging of human immunodeficiency virus infection. 134 66

Infection by the human immunodeficiency virus is associated with polyclonal B cell activation and increased levels of serum IgA. In order to characterize the molecular species of serum IgA, we have measured total IgA, IgA1, and IgA2 in sera from 60 HIV-1-infected patients and 40 healthy controls. In addition, secretory IgA (S-IgA), secretory IgM (S-IgM), free immunoreactive secretory component (SC), and the distribution of monomeric and polymeric IgA were determined. The data confirm the elevation of total serum IgA levels in HIV-1-infected patients, and both IgA1 and IgA2 concentrations are elevated. Furthermore, the data show a substantial increase in serum levels of both monomeric and polymeric IgA. Serum S-IgA levels were significantly increased in CDC group II patients versus controls and more frequently elevated in CDC group IV patients. The highest S-IgA levels were found among patients with the lowest blood CD4+ cell counts. Serum S-IgA levels were not correlated with serum levels of either total IgA or polymeric IgA. Serum S-IgM levels were also increased in HIV-1-infected patients and positively correlated with serum S-IgA levels. Conversely, serum levels of free SC were not altered. An increase in serum S-IgA was not related to human hepatitis B virus infection and/or to hepatic dysfunction or to diarrhea or overt intestinal infection. The data indicate that secretory Ig (S-IgM and S-IgA), which are likely to be produced at mucosal sites, increase in the serum of HIV-1-infected patients.
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PMID:Secretory immunoglobulins in serum from human immunodeficiency virus (HIV)-infected patients. 135 13


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