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

Eleven (50%) of 22 HIV-seropositive patients suffering from congenital coagulation defects and followed at the Hemophilia Center of Padua met the eligibility criteria for zidovudine (AZT) therapy. A 3-year clinical and laboratory follow up is described. Mean length of AZT treatment was 14.3 +/- 11 months. Three patients were enrolled at the latest stages (CDC stage IV) of HIV disease. They showed no clinical improvement after AZT administration and died with AIDS. One CDC stage III patient died from a high-grade non-Hodgkin's lymphoma (NHL) which suddenly developed 3 months after starting AZT. Seven patients began antiretroviral treatment when they were mild or asymptomatic for HIV infection (CDC stage II and III). None developed any sign of HIV disease progression on the basis of CDC criteria. Moreover, AZT administration induced an improvement of the humoral markers related to HIV disease, as CD4 T-lymphocyte count, serum beta 2-microglobulin (B2M) and, although only for few months, neopterin (Np) levels. A mild thrombocytopenia due to HIV infection was detected in 5 patients. In all cases AZT treatment was effective in increasing and/or normalizing the platelet count. Reduced daily dose AZT (600-500 mg/day) appeared to be well tolerated and of minimal toxicity as compared to the higher dose (1200 mg/day). In our study, the zidovudine-induced bone marrow suppression, namely severe anemia or pancytopenia, was the major side-effect limiting tolerance of the higher dose AZT.
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PMID:Report on a 3-year follow-up zidovudine (AZT) treatment in a group of HIV-positive patients with congenital clotting disorders. 795 71

Genetic variation of human immunodeficiency virus (HIV) over time is an important consideration in long-term antiretroviral therapy, in all likelihood affecting the course of HIV disease and its response to antiretroviral therapy. Viral replication persists throughout HIV disease, and viral burden is correlated with disease stage. CD4+ T-helper cells, a prime target for HIV, appear responsible for direct cellular and humoral responses to infection. HIV can be divided into three groups: nonsyncytium-inducing (NSI) isolates with low replicative capacity; high-replicative-capacity NSI isolates; and high-replicative-capacity, syncytium-inducing (SI) isolates. The SI phenotype also is associated with T-helper-cell tropism, rapid CD4+ cell count decline, and rapid HIV disease progression. In some HIV-infected individuals, SI variants evolve from NSI variants at approximate mean CD4+ cell counts of 400 to 500 cells/microliters. Appearance of SI variants may be a useful prognostic marker for decline in cell counts and more rapid progression to AIDS. However, SI variants are not required for HIV disease progression. Only about one-half of AIDS patients harbor SI variants, indicating that HIV that remains NSI can cause AIDS and death. Zidovudine resistance has been found (in ACTG 116B/117) to be an independent predictor of HIV disease progression. Zidovudine resistance and SI phenotype together are closely associated with rapid HIV disease progression.
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PMID:Pathogenicity and diversity of HIV and implications for clinical management: a review. 796 48

The relationships among nutritional status, infectious disease, and the immune system suggest that nutrition may be a cofactor in human immunodeficiency virus (HIV) progression. We examined nutrition as a cofactor in HIV disease by reviewing the current literature on the interactions of nutrition, infectious disease processes, and immune system dysfunction. Studies demonstrate that poor nutritional status and infection affect the immune system and interact with each other. This relationship leads to the development of opportunistic infections and malignancies, which may result in a diagnosis of acquired immunodeficiency syndrome. Moreover, evidence from our review indicates that nutritional status may play a role in HIV disease progression. We recommend that clinical trials be conducted to evaluate general malnutrition and the efficacy of supplementation with specific nutrients at various stages of HIV disease.
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PMID:Nutrition: a cofactor in HIV disease. 807 83

Human immunodeficiency virus (HIV) interacts with the immune system throughout the course of infection. For most of the disease process, HIV activates the immune system, and the degree of activation can be assessed by measuring serum levels of molecules such as beta 2-microglobulin and neopterin, as well as other serum and cell surface phenotype markers. The levels of some of these markers correlate with clinical progression of HIV disease, and these markers may be useful as surrogate markers for development of clinical AIDS. Because the likelihood and timing of development of clinical AIDS following seroconversion, for any particular individual, are not readily predictable, the use of nonclinical disease markers has become critically important to patient management. Surrogate markers of HIV infection are, by definition, measurable traits that correlate with disease progression. An ideal marker should identify patients at highest risk of disease progression, provide information on how long an individual has been infected, help in staging HIV disease, predict development of opportunistic infections associated with AIDS, monitor the therapeutic efficacy of immunomodulating or antiviral treatments, and the easily quantifiable, reliable, clinically available, and affordable. This review examines the current state of knowledge and the role of surrogate markers in the natural history and treatment of HIV infection. The clinical usefulness of each marker is assessed with respect to the criteria outlined for the ideal surrogate marker for HIV disease progression.
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PMID:Markers predicting progression of human immunodeficiency virus-related disease. 811 88

Viral infections such as with the human immunodeficiency virus (HIV) present difficult challenges for the development of effective antiviral therapies. These viruses depend on the host cell machinery for their existence, and interference with these processes typically interferes with other important host physiology. HIV presents other challenges as well because of its inherent pathogenic destruction of the immune system. It is the goal of HIV therapeutics to attempt to cure HIV infection, or if that is not possible, to stop HIV disease progression while preserving a high quality of life for HIV-infected individuals. This may be achieved through an effective combination of interference with the viral life cycle and the pathogenic processes, and by slowing or reversing the immunologic dysfunction that leads to the complications of HIV infection. Unprecedented progress has been made in understanding the virus and HIV disease pathogenesis. This knowledge has led to the identification of viral features that have become targets for therapeutic intervention. This article reviews the most important priorities of HIV treatment research for adult HIV-infected patients for the immediate future. These priorities include the following: development of new antiretroviral compounds and their application as both monotherapies and in combination therapy approaches; immune-based therapeutic approaches; and research and treatment for acute or primary HIV infections.
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PMID:Treatment research priorities for human immunodeficiency virus infection. 817 14

To examine the effects of Mycobacterium tuberculosis on human immunodeficiency virus type 1 (HIV-1) expression, the monocytoid cell line U1 containing integrated provirus was incubated with the H37Ra strain of M. tuberculosis. This resulted in heightened expression of virus in supernatant that was partially inhibited by antibody to tumor necrosis factor-alpha (TNF-alpha). Purified protein derivative (PPD) prepared from M. tuberculosis also could activate HIV expression, and this was less affected by anti-TNF antibody. PPD could activate the HIV promoter in both U937, the monocytoid cell line from which U1 was derived, and Jurkat, a CD4+ lymphoid line. Activation was abolished by mutations in the nuclear factor (NF)-kB binding domains. Jurkat cells transfected with a plasmid construct linking 8 NF-kB binding domains to the chloramphenicol acetyltransferase (CAT) gene showed increased activity of the reporter gene after activation with PPD. Transcriptional activation of HIV expression by mycobacteria and mycobacterial products may enhance propagation of HIV in monocytoid and lymphoid cells. This may result in accelerated HIV disease progression in persons coinfected with M. tuberculosis.
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PMID:Mycobacterium tuberculosis and its purified protein derivative activate expression of the human immunodeficiency virus. 820 50

The authors provide a brief review of laboratory methods used to diagnose infection, monitor HIV disease progression, and monitor response to treatment in the HIV-infected person. Included are descriptions of the characteristics of the HIV virus, and the immune damage that results from HIV infection. The authors describe the antibody tests, tests of the virus, "surrogate markers" of disease progression, and immune parameters. Nurses' understanding of these tests will facilitate effective patient monitoring and education.
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PMID:Laboratory methods for diagnosing and monitoring HIV infection. 836 97

Serum beta-2 microglobulin (beta 2-M) has prognostic value similar to lymphocyte profiles for predicting disease progression in those infected with the human immunodeficiency virus (HIV). However, the relationship between beta 2-M and HIV disease progression among inhabitants of countries with endemic tropical diseases has not been evaluated. To determine the relationship between serum beta 2-M levels and HIV infection and disease status in an African population, serum beta 2-M levels were measured in 369 patients attending a sexually transmitted disease (STD) clinic in Nairobi, Kenya. Mean serum beta 2-M was significantly higher in HIV seropositive than in HIV seronegative individuals. Among HIV infected patients, higher mean beta 2-M levels were observed in those with HIV associated symptoms or laboratory markers of advanced HIV disease. Significant inverse correlations between beta 2-M and the percentage of CD4 lymphocytes or CD4/CD8 ratio were found. These findings suggest that beta 2-M measurements may have prognostic value for HIV infected populations in developing countries.
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PMID:Beta-2 microglobulin as a marker of HIV disease status in Nairobi, Kenya. 842 3

CD38, a molecule with multilineage distribution but unknown function, and the MHC class II molecule HLA-DR (DR) have markedly elevated levels of expression on CD8+ cells of HIV-infected people. This study investigated the expression of CD38 and DR Ag on circulating HIV-specific CD8+ CTL in HIV-seropositive subjects. Purified CD8+ lymphocytes from 22 participants in the University of California at Los Angeles Multicenter AIDS Cohort Study were screened for CTL activity against autologous EBV-immortalized lymphoblast targets infected with vaccinia vectors that carried HIVIIIB gag, pol, and env genes. Sixty-seven percent (14 of 21), 64% (14 of 22), and 9% (2 of 22), respectively, of the subjects had HIV-specific CD8+ CTL activity against gag, pol, and env proteins. CD8+ cells from 11 of the subjects who had high CTL activity were then FACS-separated using three-color immunofluorescence sorting. Circulating DR-CD38- CD8+ cells had little activity. Highly purified DR+CD38+ CD8+ cells had higher HIV-specific CTL activity than other CD8+ cells. DR+CD38- or DR-CD38+ CD8+ cells also mediated significant activity, but only about half as much on a per cell basis as DR+CD38+ CD8+ cells. This is the first report that the CD38 molecule is expressed in vivo on Ag-specific CD8+ CTL, and confirms previous reports that DR is expressed on these cells. Both asymptomatic HIV-seropositive subjects (144 +/- 132/mm3) and AIDS patients (253 +/- 178/mm3) had markedly elevated levels of DR+CD38+ CD8+ cells compared with the levels in HIV-seronegative controls (7 +/- 3/mm3). However, the level of anti-HIV CTL activity was not correlated with the level of DR+CD38+ CD8+ cells, indicating that enumeration of this lymphocyte population by flow cytometry most likely will not be a useful surrogate for measuring functional CTL activity. Low levels of HIV-specific CTL activity, especially against gag, were correlated with lower CD4+ cells numbers, suggesting that the loss of CD8+ T cell cytotoxic activity against HIV that has been reported to occur with advancing HIV disease progression may reflect in part the extent of CD4+ cell immunodeficiency in HIV-infected subjects.
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PMID:Circulating HIV-specific CD8+ cytotoxic T cells express CD38 and HLA-DR antigens. 845 74

In 1987, exploratory clinical studies were initiated to determine whether the development of AIDS in HIV-infected individuals might be delayed or prevented by immunization with an inactivated HIV preparation. Preclinical studies had shown the preparation to be safe and immunogenic. Twenty-three patients with biopsy-confirmed persistent generalized lymphadenopathy (CDC III) and two with asymptomatic HIV infection and CD4 lymphocyte counts between 135 and 769/mm3 were studied, of whom eight (32%) had additional HIV-related symptoms. Over a 3-year period, they received a median of eight open-label inoculations of 100 micrograms of inactivated gp 120-depleted HIV-1 Immunogen in incomplete Freund's adjuvant (IFA). Clinical, general laboratory, immunologic, and virologic parameters were followed for up to 6 years. No serious treatment-related adverse experiences were reported, nor was accelerated HIV disease progression seen. Twelve patients developed a delayed-type hypersensitivity response (HIV-DTH) to the immunogen and nine showed fourfold or greater increases in anti-p24 antibody titers. In the follow-up period, 10 of the 25 patients developed AIDS and one with Kaposi's sarcoma (KS) at baseline progressed. Of the 12 patients who became HIV-DTH-responsive, one developed an opportunistic infection (OI), occurring approximately 5 years from study onset, and subsequently died. One additional HIV-DTH responder developed KS. Of the 13 patients who remained HIV-DTH-nonresponsive, nine (69%) progressed to AIDS and seven of these have died. Differences were also observed in terms of HIV-DNA copy number, CD4 percentages, and anti-p24 antibody patterns between the HIV-DTH-responsive and -nonresponsive groups, suggesting a more favorable clinical course in the former. HIV-1 Immunogen in IFA appears to be safe and immunogenic. Further studies are indicated to determine clinical efficacy of the HIV Immunogen as well as the significance of the apparent correlation between HIV-DTH responsivity and a more favorable clinical course.
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PMID:Initial studies on active immunization of HIV-infected subjects using a gp120-depleted HIV-1 Immunogen: long-term follow-up. 860 Dec 21


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