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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have recently demonstrated that human immunodeficiency virus type 1 (HIV-1) recombinant envelope glycoprotein precursor gp160 (rgp160) behaves as a mannosyl/N-acetylglucosaminyl (GlcNAc) binding protein. If such a carbohydrate-binding property were of biological relevance it should be shared by other related primate immunodeficiency viruses such as HIV-2. The present study confirms this hypothesis and extends these findings by showing that HIV-2 recombinant gp140 (rgp140) specifically interacts with three affinity matrices substituted by synthetic or natural carbohydrate structures: D-mannose-divinylsulphone-agarose, para-aminophenyl-beta-D-GlcNAc-agarose and the natural glycoprotein, bovine fetuin, also coupled to agarose. Binding of rpg140 to the matrices was inhibited by alpha-D-Man17-BSA (where BSA is bovine serum albumin), beta-D-GlcNAc47-BSA and fetuin, and by glycopeptides derived from pronase-treated porcine thyroglobulin. Glycopeptides obtained after endoglycosidase H treatment of thyroglobulin had a limited inhibitory effect, whereas beta-D-Gal17-BSA and beta-D-glucan had no effect. These results indicate that, like HIV-1 envelope glycoprotein, HIV-2 rgp140 interacts with high-mannose and with the mannosyl core of complex-type N-linked glycans, as well as with the N-acetylglucosaminyl core of oligosaccharidic structures.
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PMID:Mannosyl/N-acetyl-beta-D-glucosaminyl binding properties of the envelope glycoprotein of human immunodeficiency virus type 2. 128 Oct 21

New Zealand rabbits were used to demonstrate the in vitro and in vivo transfer of reactivity, including immunological memory, to a synthetic peptide corresponding to residues 586-606 of the gp-160 protein of human immunodeficiency virus (HIV-1). The transfer were mediated by immune poly (A)+ RNA from lymphoid organs (spleen and mesenteric nodules) harvested after immunization of a sheep with the peptide (8 subcutaneous injections plus glucan and complete Freund's adjuvant using a total of 1750 micrograms peptide). Immunological reactivity was detected by the leukocyte adherence inhibition (LAI) test for cellular immunity. A dose of 150 micrograms poly(A)- RNA ml-1 10(7) leukocytes-1 or 2.0 micrograms poly(A)+ RNA ml-1 10(7) leukocytes-1 was used for in vitro transfer. For in vivo transfer the recipient rabbits received 3,000 micrograms poly(A)- RNA or 20 micrograms poly(A)+ RNA. The mean non-adherence index (NAI) obtained in vitro was 10 +/- 7 for leukocytes treated with poly(A)-RNA and 60 +/- 10 leukocytes treated with poly(A)+ RNA. The poly(A)+ RNA fraction induced a primary-like response and memory cells in vivo. The poly(A)-RNA fraction had no effect. Since sheep are refractory to, and rabbits are sensitive to HIV-1, we suggest the use of this animal model for testing the immunomodulating effect of anti-HIV-1 immune poly(A)+ RNA.
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PMID:Immunological memory for HIV-1 induced in rabbits by immune poly(A)+ RNA. 172 53

A sulfate (GE-3-S) prepared by chlorosulfonic acid treatment of GE-3, a partially acetylated beta(1----6) glucan of the lichen Umbilicaria esculenta, inhibited the cytopathic effect of human immunodeficiency virus (HIV) and suppressed the HIV-antigen expression in Molt-4 (clone 8) cells. GE-3-S also suppressed the giant cell formation of HIV-infected Molt-4 cells, and inhibited HIV-induced plaque formation by 50% at the dose of 19.5 micrograms/ml and completely at 250 micrograms/ml in MT4 cells. GE-3-S had no direct effect on the reverse transcriptase of HIV.
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PMID:Inhibitory effect of a lichen polysaccharide sulfate, GE-3-S, on the replication of human immunodeficiency virus (HIV) in vitro. 257 16

In previous studies, we have reported that opsonized candida species are ingested by monocytes and monocyte-derived macrophages (MDM), but uptake of unopsonized candida is mediated only by MDM, primarily through the mannose receptor (MR). This study examines the effects of recombinant IFN-gamma on the uptake and killing of unopsonized C. albicans by MDM. We report here that MDM treated with IFN-gamma developed an increase in their capacity to ingest and kill unopsonized C. albicans and to release O2- upon stimulation with candida. Mannan (0.1 to 5 mg/ml) inhibited uptake of candida in a dose-dependent manner, but glucan (5 mg/ml) did not. These data suggest that mannose receptors may be involved in the increased phagocytosis and killing of unopsonized candida by human macrophages treated with IFN-gamma.
Immunodeficiency 1993
PMID:Enhancement of macrophage candidacidal activity by interferon-gamma. 816 96

Sulfated derivatives of paramylon, a water-insoluble (1-3)-beta-D-glucan from Euglena gracilis, significantly inhibited the cytopathic effect of human immunodeficiency virus (HIV-1, HIV-2) and the expression of HIV antigen in cultured MT-4, MOLT-4 cells and human peripheral blood mononuclear cells. Native paramylon, N,N-dimethylaminoethyl paramylon, N,N-diethylaminoethyl paramylon, 2-hydroxy-3-trimethylammoniopropyl paramylon chloride, and carboxymethyl paramylon had little or no anti-HIV activity. The anti-HIV activity of the sulfated paramylon derivatives depended on the number of sulfate groups, and the molecular weight. Paramylon sulfate significantly inhibited HIV-1 binding to MT-4 cells. The anti-coagulant activity of the sulfated paramylon derivatives also depended on the number of sulfate groups, but was generally lower than that of dextran sulfate. The results point to the potential of paramylon sulfate in the treatment of HIV infection.
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PMID:Anti-HIV (human immunodeficiency virus) activity of sulfated paramylon. 831 20

Cryptococcus neoformans-induced tumor necrosis factor alpha (TNF-alpha) production may lead to increased human immunodeficiency virus replication in patients with AIDS. In order to identify cryptococcal components that are predominantly responsible for stimulating TNF production, various concentrations of glucuronoxylomannan (GXM), galactoxylomannan (GalXM), mannoproteins (MP), and alpha(1-3) [corrected] glucan were added to whole-blood cultures. All of the cryptococcal components tested, as well as whole heat-killed cryptococci, were capable of inducing TNF-alpha release in a dose-dependent manner. MP were significantly more potent than any of the other cryptococcal components tested or heat-killed cryptococci in stimulating TNF-alpha production (P < 0.05). GXM, in contrast, was significantly less potent in this activity than either GalXM or MP (P < 0.05). As little as 0.5 microg of MP per ml was sufficient to produce moderate but significant elevations of TNF-alpha release. Maximal MP-induced TNF-alpha levels were similar to those induced by Salmonella enteritidis lipopolysaccharide, our positive control. Further experiments using isolated leukocytes suggested that monocytes were the cell population mainly responsible for TNF-alpha production, although the participation of other cell types could not be excluded. The presence of complement-sufficient plasma was a necessary requirement for TNF-alpha induction by GXM, GalXM, and low doses of MP. High MP concentrations (100 microg/ml) were also capable of stimulating TNF-alpha production in the absence of plasma. These data indicate that soluble products released by C. neoformans are capable of inducing TNF-alpha secretion in human leukocytes. This may be clinically relevant, since high concentrations of such products are frequently found in the body fluids of AIDS patients infected with C. neoformans.
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PMID:Tumor necrosis factor-inducing activities of Cryptococcus neoformans components. 894 66

We employed the Rauscher murine leukemia virus (RMuLV) as a murine retrovirus model of AIDS, to test biological response modifiers (BRM) and antiviral agents for potential therapeutic activity against the human immunodeficiency virus (HIV). We examined the relationship between the augmentation of natural killer (NK) cell activity and antiviral efficacy of a series of BRM, most of which are known inducers of interferon, in this model. Poly [I,C]-LC, MVE-2, and CL 246,738, but not Ampligen, soluble glucan, or 7-thia-8-oxoguanosine, consistently produced antiviral activity. In addition, the combination of suboptimal doses of oral 3'-azido-3'-deoxythymidine (AZT) (in drinking water) and poly [I,C]-LC produced a synergistic antiviral effect. With all the BRM tested, a consistent pattern emerged, namely that antiviral activity always correlated with the augmentation of splenic NK cell activity in infected animals. For instance, poly [I,C]-LC boosted NK activity much more in infected mice treated therapeutically (treatment initiated after infection) than prophylactically (treatment initiated before infection), and it had greater antiviral activity therapeutically than prophylactically. For the BRM tested, antiviral activity did not occur without augmentation of NK activity in infected mice. In contrast, augmentation of NK activity in uninfected mice bore no relationship to antiviral activity. Furthermore, elimination of NK cells by treating mice with anti-asialo GM1 abolished the antiviral activity of poly [I,C]-LC. Although splenic NK activity was ablated by anti-asialo GM1, serum interferon levels were not affected by this treatment. These results point to a causal connection between the augmentation of NK cell activity and the antiviral efficacy of these BRM in this murine AIDS model. NK cells thus appear to play a key role in resistance to this retrovirus, as has been suggested for HIV.
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PMID:Antiviral activity of biological response modifiers in a murine model of AIDS. Requirement for augmentation of natural killer cell activity and synergy with oral AZT. 908 7

In order to ascertain if Cryptococcus neoformans components can induce interleukin-6 (IL-6) production, we stimulated human whole blood with purified capsular products. Their potencies in stimulating IL-6 release were mannoproteins > galactoxylomannan = glucuronoxylomannan > alpha(1-3)glucan. IL-6 production was tumor necrosis factor alpha independent and required the presence of monocytes and plasma. Since IL-6 can stimulate replication of the human immunodeficiency virus in monocytic cells, these findings may be clinically relevant.
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PMID:Interleukin-6 production by human monocytes stimulated with Cryptococcus neoformans components. 916 90

Induction of mucosal immunity to the human immunodeficiency virus (HIV) envelope (env; gp160) glycoprotein has been demonstrated with orally administered recombinant vaccinia virus (rVV) vectors and poly(DL-lactide-co-glycolide) (PLG)-encapsulated plasmid DNA expressing gp160. In this study, we investigated the effect of an oral DNA-prime/rVV-boost vaccine regimen in conjunction with adjuvants on the level of gp160-specific cellular and humoral responses in BALB/c mice. We demonstrated that DNA priming followed by a booster with rVV expressing gp160 (vPE16) significantly augmented env-specific immunity in systemic and mucosal tissues of the immunized mice. Association of vPE16 with liposomes and coadministration of liposome-associated beta-glucan lentinan or IL-2/Ig-encoded plasmid DNA-encapsulated in PLG microparticles triggered the optimal cell-mediated immune (CMI) responses. Lentinan was found to increase env-specific type 1 cytokine production and cytotoxic T-lymphocyte (CTL) activities but had no effect on humoral responses. On the other hand, IL-2/Ig-mediated increases in both type 1 and 2 activities were associated with higher levels of env-specific CTL and antibody responses. Results of these studies demonstrated the effectiveness of oral vaccines with DNA and rVV vectors in conjunction with immunomodulators in inducing specific immune responses in systemic and mucosal tissues.
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PMID:Immunization strategies to augment oral vaccination with DNA and viral vectors expressing HIV envelope glycoprotein. 1181 48

Echinocandins are a novel class of antifungal drugs that target beta (1, 3)-D-glucan synthesis. Animal studies have shown that these agents have activity against Pneumocystis jiroveci infection; however, clinical data are lacking. We reviewed all cases of proven P. jiroveci pneumonia (PCP) in non-human immunodeficiency virus-infected patients at our hospital over a 5 year period (2001-2005). Two patients received conventional PCP treatment and concomitant use of echinocandins for presumed invasive aspergillus. In both cases, PCP progressed, and the patient died. The use of echinocandins in the prevention or treatment of PCP cannot be recommended without evidence to support their effectiveness.
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PMID:Progression of Pneumocystis jiroveci pneumonia in patients receiving echinocandin therapy. 1702 29


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