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)

Sixty percent of HIV-infected children malabsorbed carbohydrate (lactose or D-xylose). Surprisingly, however, carbohydrate malabsorption was not predictive of growth failure. Although HIV infection, in the absence of detectable enteric infection, may result in small intestinal injury, additional factors may also be responsible for growth failure in HIV-infected children.
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PMID:Is malabsorption an important cause of growth failure in HIV-infected children? 177 Oct 35

Case management strategies for the nutritional support of patients infected with the human immunodeficiency virus (HIV) are evolving as the disease becomes less rapidly fatal and more chronic. Nutritional status changes in advanced HIV infection are similar in many respects to protein-calorie malnutrition. Current clinical effort and research focuses on the beneficial effects of preserving lean body mass and keeping asymptomatic patients in good nutritional status by preventing micronutrient deficiencies and by treating preexisting nutritional problems rather than attempting to intervene late in the disease's course, after secondary malnutrition has already developed. Nutrition support and intervention trials only late in the disease process have not been promising in reversing weight loss once it has occurred. Special diets, such as lactose- or gluten-free diets, may be helpful in some cases as asymptomatic treatment of some opportunistic infections, and such measures may slow additional losses. However, secretory diarrhea, which often seems to be inherent to the disease itself, is not ameliorated by such measures. Current research is focusing on the potential role of glutamine in slowing malabsorption and on combinations of diet and drug treatments. Asymptomatic patients are now the focus of concern. Preserving good nutritional status by attention to preventing weight loss and loss of lean body mass and assuring food safety are primary. Symptomatic patients require specific assistance depending on the presence of opportunistic infections and the drugs required. Specific nutrition support measures depend on whether or not the gut is functional.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nutrition support of HIV+ patients. 185 4

The nutritional needs of children with human immunodeficiency virus infection are poorly understood. Twenty-eight children with vertically transmitted human immunodeficiency virus infection were evaluated for carbohydrate malabsorption using lactose hydrogen breath tests and d-xylose absorption studies. Lactose malabsorption was a common finding in human immunodeficiency virus-infected children and occurred in 8 of 20 patients who had no identifiable enteric pathogen. Lactose malabsorption occurred at an earlier age in human immunodeficiency virus-infected children than in an age-matched group of 45 symptomatic control children (P = 0.02). However, lactose malabsorption was not associated with higher rates of diarrhea or growth failure. Abnormalities in d-xylose absorption were not significantly associated with either diarrhea or growth failure. However, 39% of d-xylose studies (9 of 23) showed abnormal results and were significantly associated with enteric infections (P = 0.004). Abnormalities in small-bowel morphology were found in 4 of 9 children with growth failure, 3 of whom had an enteric infection and low d-xylose absorption. Lactose hydrogen breath testing and d-xylose testing showed carbohydrate malabsorption in 61% of children (17 of 28). This study demonstrates that human immunodeficiency virus-infected children are at risk for malabsorptive disorders, which are not always related to clinical symptoms. We speculate that human immunodeficiency virus may be directly involved in the development of lactose malabsorption. Carbohydrate malabsorption in human immunodeficiency virus-infected children may not be the only factor responsible for growth failure.
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PMID:Malnutrition and carbohydrate malabsorption in children with vertically transmitted human immunodeficiency virus 1 infection. 201 74

Various sulfated cerebroside analogs, which are mimicks of cerebroside, have been prepared from per-O-acetylated D-glucose, per-O-acetylated D-galactose, and per-O-acetylated D-lactose with ethyleneglycol dodecyl ether, 3-docosyloxy-1-propanol, 2-hydroxymethyl-1,3-O-dimyristyl-1,3-propanediol, and L-serine diamide derivatives as ceramide moieties. The synthesized sulfated glycolipids showed anti-HIV-1 activities.
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PMID:Synthesis of sulfated cerebroside analogs having mimicks of ceramide and their anti-human immunodeficiency virus type 1 activities. 760 Jun 12

We describe here a two-phase approach for the development of high-affinity human anti-HIV immunoglobulin Fab domains in a bacterial expression system. The first phase of this technique involves the generation of human hybridoma cell lines producing high-affinity antibodies (MAbs). Anti-HIV-1 human MAbs from peripheral blood lymphocytes (PBLs) were prepared from an HIV-1-seropositive patient and from an HIV-1-seronegative volunteer immunized with HIV-1 rgp160. One MAb (T15G1), derived from the blood of the seropositive donor, was specific for HIV-1 gp41, recognized gp41 on the surface of HIV-1-infected cells and bound this antigen with an apparent dissociation constant of 4 x 10(-10) M. A second MAb (M7B5), developed from the immunized volunteer, was specific for HIV-1 gp120 with a dissociation constant on the order of 8 x 10(-10) M, but was unable to recognize cell surface antigen. In the second phase of this technique the Fab domains of these two MAbs were molecularly cloned into a bacterial expression vector. mRNA was isolated from the M7B5 and T15G1 hybridoma cell lines and used as a template for the production of cDNA. The cDNA was amplified using the polymerase chain reaction (PCR) technique, and then fused, in frame, into a bacterial expression vector. The recombinant Fabs (rFabM7B5 and rFabT15G1) were expressed as dicistronic messages in bacteria using the IPTG-inducible lactose promoter (LacZ). DNA sequencing was used to define the gamma chain isotypes and the VH and VL chain gene usage. The binding specificities of rFabM7B5 and rFabT15G1 were indistinguishable from their respective intact MAbs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Two-phase approach for the expression of high-affinity human anti-human immunodeficiency virus immunoglobulin Fab domains in Escherichia coli. 776 38

The development of the Escherichia coli expression system, which was prepared by transferring the F' episome from strain 71/18 to a highly to a transformable F- strain HB101, is described. These new HB101 (F+) cells, which produced high levels of lac repressor, were capable of taking up lactose and grew under strict selection conditions. A relatively simple two-step purification of part of a protein (M(r) 27,000) encoded by the gag gene of HIV-1 in this expression system is described. The supernatant prepared by removal of cell debris was precipitated by 30% saturation of ammonium sulphate. The protein spectrum was characterized by gel electrophoresis, immunoblotting and ion-exchange titration curves. Optimum separation was achieved using a strong anion exchanger (Mono Q) at pH 8.0. The purified protein did not cross-react with antibodies to E. coli.
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PMID:Production and simple purification of a protein encoded by part of the gag gene of HIV-1 in the Escherichia coli HB101F+ expression system inducible by lactose and isopropyl-beta-D-thiogalactopyranoside. 795 23

Forty HIV-infected adult patients at different disease stages and 44 healthy volunteers were evaluated for lactose malabsorption using the hydrogen breath test after 20 g lactose ingestion. All subjects were previously tested for breath hydrogen (H2) excretion after 12 g lactulose ingestion. The presence of intestinal superinfections, gastrointestinal symptoms and the intensity of clinical intolerance after lactose load were accurately searched in each patient. The cumulative H2 excretion after lactulose did not significantly differ between the different groups studied. The prevalence of lactose malabsorption turned out to be significantly higher (P < 0.001) in HIV-infected patients (70%) than in controls (34%). Moreover, in patients in more advanced disease stages the degree of lactose malabsorption was significantly greater than in patients at earlier disease stages, who did not differ from healthy volunteers. Furthermore the degree of lactose intolerance was significantly greater (P < 0.001) in symptomatic patients than in those without intestinal symptoms and in healthy volunteers, while no significant difference was observed between these latter groups. The results here demonstrate the negative impact of HIV infection on lactose absorptive capacity in adult patients, particularly marked in more advanced stages of the disease, suggesting that, in addition to the presence of the virus alone, other factors may contribute to determine the enterokinetic alterations responsible for lactase deficiency.
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PMID:The impact of HIV infection on lactose absorptive capacity. 927 21

Exogenous gangliosides affect the angiogenic activity of fibroblast growth factor-2 (FGF-2), but their mechanism of action has not been elucidated. Here, a possible direct interaction of sialo-glycolipids with FGF-2 has been investigated. Size exclusion chromatography demonstrates that native, but not heat-denatured, 125I-FGF-2 binds to micelles formed by gangliosides GT1b, GD1b, or GM1. Also, gangliosides protect native FGF-2 from trypsin digestion at micromolar concentrations, the order of relative potency being GT1b > GD1b > GM1 = GM2 = sulfatide > GM3 = galactosyl-ceramide, whereas asialo-GM1, neuraminic acid, and N-acetylneuramin-lactose were ineffective. Scatchard plot analysis of the binding data of fluorochrome-labeled GM1 to immobilized FGF-2 indicates that FGF-2/GM1 interaction occurs with a Kd equal to 6 microM. This interaction is inhibited by the sialic acid-binding peptide mastoparan and by the synthetic fragments FGF-2(112-129) and, to a lesser extent, FGF-2(130-155), whereas peptides FGF-2(10-33), FGF-2(39-59), FGF-2(86-96), and the basic peptide HIV-1 Tat(41-60) were ineffective. These data identify the COOH terminus of FGF-2 as a putative ganglioside-binding region. Exogenous gangliosides inhibit the binding of 125I-FGF-2 to high-affinity tyrosine-kinase FGF-receptors (FGFRs) of endothelial GM 7373 cells at micromolar concentrations. The order of relative potency was GT1b > GD1b > GM1 > sulfatide a = sialo-GM1. Accordingly, GT1b,GD1b, GM1, and GM2, but not GM3 and asialo-GM1, prevent the binding of 125I-FGF-2 to a soluble, recombinant form of extracellular FGFR-1. Conversely, the soluble receptor and free heparin inhibit the interaction of fluorochrome-labeled GM1 to immobilized FGF-2. In agreement with their FGFR antagonist activity, free gangliosides inhibit the mitogenic activity exerted by FGF-2 on endothelial cells in the same range of concentrations. Also in this case, GT1b was the most effective among the gangliosides tested while asialo-GM1, neuraminic acid, N-acetylneuramin-lactose, galactosyl-ceramide, and sulfatide were ineffective. In conclusion, the data demonstrate the capacity of exogenous gangliosides to interact with FGF-2. This interaction involves the COOH terminus of the FGF-2 molecule and depends on the structure of the oligosaccharide chain and on the presence of sialic acid residue(s) in the ganglioside molecule. Exogenous gangliosides act as FGF-2 antagonists when added to endothelial cell cultures. Since gangliosides are extensively shed by tumor cells and reach elevated levels in the serum of tumor-bearing patients, our data suggest that exogenous gangliosides may affect endothelial cell function by a direct interaction with FGF-2, thus modulating tumor neovascularization.
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PMID:Interaction of fibroblast growth factor-2 (FGF-2) with free gangliosides: biochemical characterization and biological consequences in endothelial cell cultures. 995 Jun 79

An isothermal microcalorimeter was utilized to characterize a model solid-state interaction. The degradation of the HIV protease inhibitor, DMP 450, in a binary mixture with hydrous lactose was followed in the presence of 5% additional water. Heat produced in the microcalorimeter sample vessel from either chemical or physical change is channeled through extremely sensitive thermopile blankets and is measured as it flows into infinite heat sinks. Solid-state 1:1 mixtures of DMP 450 and hydrous lactose each with 5% water added were analyzed in the microcalorimeter at 50, 60 and 65 degrees C. The resulting heat flow profiles were consistent with an autocatalytic rate law. An activation energy of 26.12 kcal mol(-1) for the DMP 450:lactose mixture was determined from the slope of the Arrhenius plot of the microcalorimetry heat flow maximum value versus the reciprocal of the absolute temperature. The activation energy determined by the traditional method with HPLC analysis was found to be in excellent agreement with the microcalorimetry value at 26.38 kcal mol(-1).
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PMID:Utility of microcalorimetry in the characterization of the browning reaction. 1070 46

Unwanted weight loss in people with HIV can be caused by one or more factors simultaneously. A two-pronged approach that addresses the factors causing weight loss and malnutrition, and maintaining or gaining weight is critical. Many opportunistic infections (OIs) can cause diarrhea, but both the drugs used to treat diarrhea and the infections themselves can contribute to weight loss. Lactose intolerance is a common cause of diarrhea in people living with HIV. Because some of the drugs used to treat HIV and OIs are packaged with lactose, it may be necessary to replace the enzymes needed to break down lactose. Appetite loss may also contribute to wasting, and the lack of nutrients from a lost appetite can tax the body and further aggravate the problem. Appetite stimulants, vitamin supplements, or weight gain products that promote the building of protein are possible treatment options. Lean body mass production may require the use of anabolic (protein building) steroids or testosterone replacement therapy. Another wasting intervention option involves recombinant human growth hormone (rHGH), however, unsubstantiated safety concerns have arisen on the use of rHGH, and may require increased monitoring. Finally, counteracting weight loss may require adjusting the elevated levels of an immune system chemical called tumor necrosis factor (TNF) with thalidomide. Because of thalidomide's association with birth defects, sexually active heterosexual women should be advised to use multiple contraceptive mechanisms.
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PMID:Weight loss update. 1136 68


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