Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021051 (immunodeficiency)
 71,517 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of inoculation of LP-BM5 murine leukemia retrovirus and chronic ethanol (5% v/v) ingestion on immunomodulation and Cryptosporidium parvum infection in C57BL/6 female mice were evaluated. The intestinal mucosae of retrovirally immunosuppressed animals were heavily colonized by Cryptosporidium parasites, and oocysts shedding in the feces persisted throughout the duration of the study. Mortality was exacerbated by murine retrovirus infection alone and exacerbated with concomitant chronic alcohol feeding (42.8 and 69.4%). Chronic ethanol ingestion decreased production of interferon-gamma and soluble interleukin-2 receptor released in supernatants of splenocytes when stimulated with concanavalin A, compared with the control group. Decreased production of interferon-gamma and interleukin-2 receptor was further exacerbated due to retrovirus infection. Tumor necrosis factor production by splenocytes stimulated with lipopolysaccharide, however, was significantly increased because of retrovirus infection. LP-BM5 retrovirus infection alone as well as with concomitant ethanol feeding altered cytokine production, which might have led to immunodeficiency. These changes may help explain the enhanced persistence of Cryptosporidiosis.
Alcohol Clin Exp Res 1993 Jun
PMID:Alcohol and murine acquired immunodeficiency syndrome suppression of resistance to Cryptosporidium parvum infection during modulation of cytokine production. 833 81

Hyperimmune gamma-globulins have proven efficacious in the prevention and treatment of viral infections, including those caused by hepatitis A and B viruses, cytomegalovirus, parvovirus. Interest in the prevention and/or treatment of infections caused by human immunodeficiency virus (HIV) has led to clinical trials with anti-HIV immune plasma and purified immune globulin prepared from donors who are actively infected with HIV. The handling and fractionation of this or other infectious plasma requires the construction and operation of virus containment facilities designed to protect fractionation employees and the immediate environment. This requirement would be reduced substantially by applying virucidal procedures prior to or during plasma pooling. We have shown that heating plasma at 56 degrees C for 1 h followed by treatment with 1% tri(n-butyl) phosphate (TNBP) and 1% Triton X-100 for 4 h at 30 degrees C resulted in the inactivation of > or = 10(12.1) tissue culture infectious doses (TCID50) of HIV. With this treatment, the recovery of IgG was 87 +/- 3%. Fractionation of treated plasma by cold ethanol precipitation proceeded normally, and overall recovery, purity, and potency against selected viral markers were unaffected. The additional treatment of plasma with 15 g/l Aerosil for 4 h at 45 degrees C removed 10(4.5) TCID50 of HIV but resulted in substantial IgG losses both prior to and following fractionation. We conclude that potentially infectious plasma can be treated at 56 degrees C for 1 h and by TNBP/Triton X-100 at 30 degrees C for 4 h prior to fractionation. These steps appear sufficient to assure safety and to permit routine fractionation of plasma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enhancement in the safety of immune globulins prepared from high-risk plasma. 839 Jul 65

A marine microalga, Cochlodinium polykrikoides, produces extracellular sulfated polysaccharides. Isolation and purification of the polysaccharides were accomplished by precipitation with ethanol and Cetavlon, followed by DEAE-cellulose column chromatography (polysaccharides A1 and A2). These polysaccharides, which were homogeneous when analysed by both ultracentrifugal and electrophoretic methods, were composed of mannose, galactose, glucose and uronic acid, together with sulfate groups (S = 7-8% w/w). Both A1 and A2 inhibited the cytopathic effect of influenza virus types A and B in MDCK cells, that of respiratory syncytial virus types A and B in HEp-2 cells, that of human immunodeficiency virus type 1 in MT-4 cells; and, except A1 for herpes simplex virus type 1 and A2 for parainfluenza virus type 2 in HMV-2 cells, the cochlodinium polysaccharides showed no antiviral activity against parainfluenza virus types 2 and 3, measles virus, mumps virus or herpes simplex virus type 1 in HMV-2 cells. No cytotoxicity for host cells was observed with these polysaccharides at a concentration of 100 micrograms ml-1. Inhibitory effects on various viruses were achieved at concentrations that were not markedly inhibitory to the blood coagulation process.
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PMID:In vitro antiviral activities of sulfated polysaccharides from a marine microalga (Cochlodinium polykrikoides) against human immunodeficiency virus and other enveloped viruses. 858 94

Previous studies have shown that alcohol ingestion significantly increases human immunodeficiency virus type 1 (HIV-1) replication in peripheral blood mononuclear cells (PBMC) isolated and infected with HIV-1 in vitro. Whether the increased replication of HIV-1 observed after alcohol ingestion was due to unknown factors released from the gastrointestinal tract during alcohol ingestion or to certain metabolites produced by intestinal flora that degraded alcohol was investigated. In addition, cellular mechanisms involved in the increased replication of HIV-1 after alcohol exposure were evaluated. Twelve healthy HIV-1-seronegative subjects abstained from alcoholic beverages for >10 days. Nine were infused with 500 mg/kg ethanol (7.5% at 20 ml/kg/h) in saline, whereas 3 were infused with saline alone. Compared with saline-infused subjects, ethanol-infused subjects' PBMC exhibited significantly increased replication of HIV-1 when infected in vitro, which was associated with increased inhibition of CD8+ T lymphocytes' function by alcohol.
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PMID:Increased human immunodeficiency virus type 1 replication in human peripheral blood mononuclear cells induced by ethanol: potential immunopathogenic mechanisms. 862 16

The human immunodeficiency virus (HIV) infection rate was examined in a selected cohort of healthy clients of an inner-city alcohol treatment center from 1990 through 1993. These subjects were also participating in a research protocol (n = 258) designed to assess immunity and HIV risk behaviors in inner city alcohol-dependent persons. Healthy alcohol-abusing heterosexual clients (165) had HIV testing conducted in an inner-city ambulatory alcohol treatment center between September 1990 and December 1993. Respondents were 93.9% African-American and 3.6% Hispanic; 72.1% were male. Anonymous HIV-1 antibody testing was conducted retrospectively for an additional 80 subjects who participated in the research protocol during the same interval, but for whom HIV-1 antibody testing was not conducted clinically at the time. HIV infection rate among the clinic-tested subjects (n = 165) was 4.4% for individuals who were exclusively alcohol-dependent, 1.4% for non-injecting drug use (IDU) mixed substance abusers, and 46.8% for clients with a history of IDU. Rates did not differ among cohorts tested in different years. Among non-injecting drug users tested in the clinic, all infected respondents (n = 3) were women (p = 0.03). Among those tested anonymously (n = 80), however, infection rate for exclusively alcohol-dependent persons was 16.7%, non-IDU mixed abusers 11.1%, and injecting drug users 48.3%, with seropositive males as well as females in each group. HIV infection rates for the pooled samples (n = 245) were 8.7% for exclusively alcohol-dependent persons, 5.1% for mixed abusers, and 54.5% for injecting drug users. Among non-injecting drug users, exclusively alcohol-dependent women had a significantly higher (p < 0.01) infection rate (20.0%) than the remaining females and males. Infection rates among exclusively alcohol-dependent males, male and female polysubstance non-IDU abusers, and injecting drug users were comparable with that seen in an earlier screening in the same clinic in 1989, with apparently little diffusion of infection from the IDU population to other substance abusers. An exception seemed to be exclusively alcohol-dependent females, who show substantially elevated rates. Age, housing, and other social differences may help segregated substance-abusing populations in the relatively small Newark metropolitan area, although not protecting exclusively alcohol-dependent females.
Alcohol Clin Exp Res 1996 Feb
PMID:Human immunodeficiency virus-type 1 infection in an inner-city alcohol treatment program. 865 66

Human immunodeficiency virus (HIV-1) was inactivated by either cupric or ferric ions when the virus was free in solution and also 3 hr after cell infection. Fifty percent inactivation of cell-free HIV was achieved with Cu(II) at a concentration between 0.16 and 1.6 mM, or by 1.8 to 18 mM Fe(III). Thus, the dose to inactivate 50% of infectious HIV (D50) by Cu(II) or Fe(III) is higher than that reported for glutaraldehyde (0.1 mM); between the D50 reported for sodium hypochlorite (1.3 mM) and sodium hydroxide (11.5 mM), and significantly lower than that required for HIV inactivation by ethanol (360 mM). Treatment of infected cells for 30 min at 20 degrees C with 6 mM Cu(II) or Fe(III) completely inhibited the formation of syncytia and the synthesis of virus-specific p24 antigen in HIV-infected cells, while still preserving cell viability. The virucidal properties of cupric and ferric ions could be exploited for the development of novel virucidal formulations efficient against HIV.
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PMID:Cupric and ferric ions inactivate HIV. 890 94

Rifampin, an agent known to decrease the half-life of methadone, and rifabutin are two rifamycins that are structurally similar and share mechanisms of action. Hence the possibility of a drug-drug interaction between rifabutin and methadone was evaluated in 24 methadone-maintained, former injecting drug users infected with the human immunodeficiency virus. The study was an open-label, drug-drug interaction and safety trial in which patients were followed for 15 days. Each patient received rifabutin 300 mg as a single dose concomitantly with their individualized methadone dosage. No significant differences in methadone peak plasma concentration, time to peak plasma concentration, area under the plasma concentration-time curve, systemic clearance or renal clearance was observed in the presence of rifabutin. Seventy-five percent of the patients reported at least one symptom of narcotic withdrawal during the study, however, these symptoms were mild. A relationship between the development of narcotic withdrawal and methadone systemic exposure could not be established. Concurrent administration of rifabutin and methadone appeared to be safe in human immunodeficiency virus-infected injecting drug users maintained on stable doses of methadone and is not expected to produce any significant changes in the pharmacokinetics of methadone in these patients.
Drug Alcohol Depend 1996 Dec 02
PMID:Lack of a pharmacologic interaction between rifabutin and methadone in HIV-infected former injecting drug users. 895 45

Human immunodeficiency virus-infected (HIV) patients frequently present left ventricular dysfunction. Its etiology is not elucidated but zidovudine has been postulated as a possible cause factor. This study is an attempt to clarify this issue by evaluating the effect of zidovudine therapy on left ventricular function in these patients. We prospectively studied by echocardiographic examination 11 consecutive HIV-infected patients who were assigned for zidovudine therapy. We excluded patients that had a history or a physical examination suggestive of ischemic, rheumatic, congenital, or hypertensive heart disease. Patients with diabetes mellitus, excessive ethanol intake and patients on potentially cardiodepressant drugs were also excluded. Echocardiographic examination was performed immediately before the initiation of zidovudine therapy and 1 and 3 months later. Left ventricular diameters, mass and fractional shortening showed no significant difference from baseline, at 1 or 3 months after the initiation of zidovudine therapy. Our results suggest that zidovudine therapy has no effect on left ventricular diameters, mass or fractional shortening during a short term.
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PMID:Zidovudine therapy and left ventricular function and mass in human immunodeficiency virus-infected patients. 896 Jun 21

Acquired immune deficiency syndrome (AIDS) is a clinical disorder caused by a human immunodeficiency virus (HIV), representing the end point in a progressive sequence of immunosuppressive changes. HIV, the key causative agent of AIDS, induces immunosuppression that render the body highly susceptible to opportunistic infections and neoplasm. However, the onset of clinical symptoms of AIDS (e.g., low CD4+ T cells count, opportunistic infections, and tumors) is quite variable among HIV+ individuals with a mean incubation times 3-10 years following seroconversion. Because of the deleterious effects of chronic alcohol (EtOH) consumption on cytokine release, immune response, host defense, nutritional status, and oxidative stress, it has been believed to be a possible cofactor that could enhance the host's susceptibility to HIV infection, and subsequently accelerate the development of AIDS. The purpose of this review is to present evidence of EtOH-induced cytokine dysregulation during murine AIDS. Our results done in murine AIDS indicate the EtOH consumption may accelerate the development of AIDS by disrupting cytokine production. These EtOH-induced abnormalities in cytokine release may promote a more rapid development of AIDS as a cofactor, which exacerbates the immune dysfunctions initiated by retrovirus infection.
Alcohol
PMID:Alcohol consumption alters cytokine release during murine AIDS. 908 16

Anti-human immunodeficiency virus (HIV)-bioassay-guided fractionation of aqueous extracts of the Caribbean sponge Niphates erecta led to isolation of a novel anti-HIV protein, named niphatevirin. The protein was purified to homogeneity by ethanol precipitation, ammonium sulfate precipitation, gel-permeation chromatography and concanavalin-A-Sepharose affinity chromatography. Niphatevirin potently inhibited the cytopathic effects of HIV-1 infection in cultured human lymphoblastoid (CEM-SS) cells; the effective concentration of drug that results in 50% protection of the cells through inhibition of cell lethality, cell-cell fusion and syncytium formation was approximately 10 nM. Delay of addition of niphatevirin to infected cultures by two hours markedly decreased (approximately 50%) cytoprotection; delay of addition by eight hours resulted in no antiviral activity. Niphatevirin bound to CD4 in a manner that prevented the binding of gp120, but did not directly bind gp120. Niphatevirin (6.5 microM) was inactive in both hemagglutination and hemolysis assays. Niphatevirin had a molecular mass of about 19 kDa by matrix-assisted laser-desorption ionization-time of flight (MALDI-TOF) mass spectrometry, and a native molecular mass of approximately 18 kDa by gel-filtration chromatography. The protein had an acidic isoelectric point of 4.2-4.6, and was shown by periodate acid Schiff's staining to be glycosylated.
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PMID:Isolation and characterization of niphatevirin, a human-immunodeficiency-virus-inhibitory glycoprotein from the marine sponge Niphates erecta. 912 23


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