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

Feline immunodeficiency virus (FIV), formerly called feline T-lymphotropic lentivirus, causes an immune deficiency in cats that is very similar to the acquired immune deficiency syndrome in humans (N. C. Pedersen, E. M. Ho, M. L. Brown, and J. K. Yamamoto, Science 235:790-793, 1987). We have examined the reverse transcriptase of this virus to determine whether it is similar enough to the reverse transcriptase of the human immunodeficiency virus type 1 (HIV-1) to enable its use as a model for chemotherapy for acquired immune deficiency syndrome. The FIV reverse transcriptase is similar to that of HIV-1 in sensitivity to the noncompetitive inhibitor phosphonoformate (Ki, 0.3 microM) and relative insensitivity to phosphonoacetate. This enzyme was also sensitive to two competitive inhibitors, the 5'-triphosphates of 2', 3'-dideoxythymidine (Ki, 3.4 nM) and 3'-azido-3'-deoxythymidine (AZT; Ki, 6.2 nM). The ratios of Ki/Km for these two competitive inhibitors are similar to the ratios calculated from previously reported data for the HIV-1 enzyme assayed under identical conditions. In contrast, the FIV enzyme is different from the reverse transcriptase of avian myeloblastosis virus in sensitivity to those inhibitors. The replication of FIV in Crandell feline kidney cells was inhibited by AZT; virus production was inhibited more than 95% by 1.0 microM AZT.
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PMID:Feline immunodeficiency virus, a model for reverse transcriptase-targeted chemotherapy for acquired immune deficiency syndrome. 247 68

Placental isoferritins (PLF), known to be immunosuppressive in Hodgkin's disease and other states, were found to be increased in sera of subjects infected with HIV. We assayed for PLF using a 'sandwich' antigen capture enzyme-linked immunosorbent assay (ELISA) employing two monoclonal antibodies. Individuals with lymphadenopathy, with or without symptoms suggestive of AIDS-related complex, had the highest serum levels, which declined with progressive immunodeficiency. Total (normal) ferritins, in contrast, increased progressively with stage of disease. PLF was found on a subset of CD8 lymphocytes and appeared to block detection of the CD8 antigen by specific monoclonal antibodies. Elution of PLF by incubation with levamisole, but not by culture medium alone, led to the unblocking of the CD8 determinant on these cells. Profiles of isoferritins in HIV infection may provide clues to prognosis. PLF, a physiologic down-regulator of hematopoiesis and cellular immunity, could play a role in the progressive immune deficiency, marrow suppression and HIV expression that lead to AIDS.
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PMID:Isoferritins in HIV infection: relation to clinical stage, CD8 lymphocyte binding and the pathogenesis of AIDS. 249 6

CD4 + T-helper lymphocytes are the main target cells in HIV infection. Since CD4 molecules are not restricted to T-cells but also found on monocytes, macrophages, follicular dendritic cells, Langerhans cells, and microglial brain cells, these cells might be affected, too, by HIV. HIV binds via the gp 120 envelope protein to the 67 KD CD4 membrane protein. Patients with HIV infection show distinct autoimmunological reactions against the cells of their immune system. Autoantibodies directed against CD4 cells seem to be responsible for the extent of the immune deficiency and are, therefore, of prognostic value. Aside from CD4+ cell depletion, the functional impairment of the T-cell system plays an important part in the progress of the disease. Patients with depressed gamma-interferon production after stimulation with antigens are at a risk for AIDS-related opportunistic infections. Polyclonal production of immunoglobulins and impaired stimulation of B-cells are characteristic for B-cell dysfunction. NK-cell dysfunction depends on reduced production of IL-2 and altered gamma-interferon production of T-cells infected with HIV.
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PMID:[Impairment of the immune system by HIV infection]. 252 49

The alloantigen responses of hemophilic patients was evaluated using a unidirectional mixed lymphocyte culture (MLC). The results of this study indicate that both the ability of peripheral blood mononuclear cells (PBMC) to proliferate in response to alloantigens and the capacity to stimulate the MLC are impaired in hemophilic patients infected with the human immune deficiency virus (HIV). These defects cannot be overcome by addition of exogenous interleukin-2 (IL-2) and are not related to the absence of IL-2 receptors (IL-2R). Lack of response was evident in PBMC from HIV+ patients with a high proportion of IL-2R+ cells. The number of IL-2 cells was similar in HIV+ and HIV- individuals, and higher than that of normal controls. Impaired MLC proliferation was not related to the occurrence of clinical symptoms. Apparently, MLC is a useful procedure for distinguishing the cell mediated immunity defects associated with HIV infection and unrelated to replacement therapy in hemophilia patients.
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PMID:Impaired response to alloantigens in HIV positive hemophilic patients. 253 Nov 12

The testing for human immune deficiency virus type 2 (HIV-2) antibodies of 794 sera collected in July-August 1985 in the 4 regions of Korhogo, Bondoukou, Man, and Bouake in Ivory Coast and the collection and testing for HIV-1 and HIV-2 antibodies of 1126 sera collected in July-August 1987 in the same regions and age groups showed a remarkable stability in the prevalence of infection by these 2 retroviruses (0.7 and 0.4% in 1985 vs 0.9 and 0.2% in 1987, respectively for HIV-1 and HIV-2) in rural areas. In contrast, the increase in prevalence of both HIV-1 (from 1-1.9%) and HIV-2 (from 0.8-1.3%) from 1985-87 in the urban population was accompanied by a sharp increase during these 2 years in the number of AIDS cases in regional hospitals. (author's modified).
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PMID:Compared prevalence of infections by HIV-1 and HIV-2 during a 2-year period in suburban and rural areas of Ivory Coast. 253 99

Animal models of AIDS are essential for understanding the pathogenesis of retrovirus-induced immune deficiency and encephalopathy and for development and testing of new therapies and vaccines. AIDS and related disorders are etiologically linked to members of the lentivirus subfamily of retroviruses; these lymphocytopathic lentiviruses are designated human immuno-deficiency virus type 1 (HIV-1) and human immuno-deficiency virus type 2 (HIV-2). The only animals susceptible to experimental HIV-1 infection are the chimpanzee, gibbon ape, and rabbit but AIDS-like disease has not yet been reported in these species. Macaques can be persistently infected with some strains of HIV-2 but no AIDS-like disease has resulted. It is not yet clear how suitable HIV-infected SCID-hu mice will be as a model for AIDS. Several subfamilies of naturally occurring cytopathic retroviruses cause immune suppression, including fatal immunodeficiency syndromes in chickens, mice, cats, and monkeys. Domestic cats suffer immunosuppression from both an onco-virus, feline leukemia virus, and a member of the lentivirus subfamily, feline immunodeficiency virus (FIV). Asian macaques are susceptible to fatal simian AIDS from a type D retrovirus, indigenous in macaques, and from a lentivirus, simian immunodeficiency virus (SIV), which is indigenous to healthy African monkeys. SIV is the animal lentivirus most closely related to HIV. Of these animal models, the lentivirus infections of cats (FIV) and macaques (SIV) appear to bear the closest similarity in their pathogenesis to HIV infection and AIDS. This review will summarize these various animal model systems for AIDS and illustrate their usefulness for antiviral therapy and vaccinology.
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PMID:Animal models of AIDS. 255 12

Human herpesvirus-6 (HHV-6), formerly known as human B-lymphotropic virus (HBLV), was first isolated in 1986 from patients with lymphoproliferative disorders and AIDS. Antibody prevalence against HHV-6 varies between about 60-80% indicating a widespread latent infection. Although HHV-6 infects in vivo primarily T-lymphocytes, it is associated with similar diseases as in infection with Epstein-Barr virus (EBV), a clearly B-lymphotropic virus. Reactivation of latent HHV-6 infection in patients with subnormal host defense may cause persistent active infection with so-called postinfectious chronic fatigue syndrome (PICFS) or may contribute to other pathologies such as immune deficiency itself, autoimmune disorders or progressive lymphoproliferation. Coinfection of CD4 cells by HHV-6 and human immunodeficiency virus (HIV 1) in AIDS patients can aggravate HIV-induced acquired immune deficiency. These characteristics of the only recently detected new virus justify further intense investigation.
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PMID:What's new in human herpesvirus-6? Clinical immunopathology of the HHV-6 infection. 255 96

Newborn rabbits were inoculated with bovine leukaemia virus (BLV). The majority of infected rabbits produced antiviral antibodies. All the seroconverted animals developed symptoms resembling AIDS and died several months after inoculation. The course of experimental infection of rabbits with BLV resembled in many respects the broad spectrum of clinical disorders associated with AIDS induced by HIV. Antibody response to virus proteins was followed by immune deficiency and signs of neuropathy, and the animals subsequently died of opportunistic infections. Virus transmission from infected babies to the mothers by contact was also observed. In some cases the virus was salvaged from lymphocytes of rabbits with the immune deficiency syndrome. The virus-specific sequences were found to be integrated at random in the DNA of haematopoietic cells and of some organs. Slight expression of viral RNAs in lymphocytes was found. Experimental infection of rabbits with BLV can be used in experiments to understand AIDS induction.
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PMID:Induction of immune deficiency syndrome in rabbits by bovine leukaemia virus. 255 51

Acquired immune deficiency syndrome (AIDS) is a disease caused by the human immunodeficiency virus (HIV) in which cellular immune functions are severely impaired. Acute infection and subsequent destruction of helper T cells, although occurring readily in cell cultures, do not appear to be the only mechanisms mediating helper T cell loss. Other mechanisms that may account for the loss of helper T cells include: T cell syncytia formation, decreased T cell production, and autoimmune-related destruction of helper T cells. Immune abnormalities seen early in the course of HIV infection include immune hyperactivation and autoimmune phenomena suggestive of immune dysregulation rather than immune deficiency. Many changes in immune function are, in fact, seen in HIV-seropositive patients who possess a normal number of helper T cells. Mechanisms (other than the loss of helper T cells) that may contribute to the immune abnormalities seen in these patients include noninfectious effects of HIV and HIV proteins, effects of HIV on non-T cells, autoimmune-related manifestations of HIV infection, and HIV-induced activation of normal immunosuppressive circuits.
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PMID:AIDS: a syndrome of immune dysregulation, dysfunction, and deficiency. 256 47

The pathogenesis of cellular immune deficiency following human immunodeficiency virus (HIV) infection could result from quantitative and/or qualitative dysfunction of the CD4+ lymphocyte population. To better characterize the T-cell response to soluble antigen with HIV infection, we have isolated peripheral blood lymphocytes and purified populations of CD4+ lymphocytes from healthy HIV antibody-positive subjects, patients with acquired immunodeficiency syndrome (AIDS)-related complex (ARC), and healthy HIV antibody-negative controls. T-lymphocyte function was determined by proliferative response to lectin (phytohemagglutinin), phorbol 12-myristate 13-acetate (PMA), calcium ionophore, purified recombinant HIV envelope gp120, tetanus toxoid antigen, and tetanus toxoid antigen in the presence of recombinant gp120 or purified recombinant soluble CD4. PBLs and CD4+ lymphocytes from asymptomatic HIV-infected subjects responded equally well to lectin, PMA, and/or calcium ionophore and to tetanus toxoid as cells from uninfected control subjects. The cells that proliferated in response to a soluble antigenic stimulus did not respond to gp120. Cells from subjects with ARC had a selective antigen recognition defect independent of the number of CD4+ lymphocytes. Recombinant gp120 inhibited CD4+ lymphocyte proliferation to antigenic stimulus by 30-40%. Recombinant soluble CD4, a proposed therapeutic for HIV, had no effect on T-cell response to antigen. A selective antigen recognition response was not compromised early in HIV infection but was compromised in subjects with ARC. Inhibition of proliferation to tetanus toxoid by gp120 suggests that HIV may affect major histocompatibility complex II restricted antigen recognition independent of CD4+ cell loss.
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PMID:CD4+ lymphocyte function with early human immunodeficiency virus infection. 256 77


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