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)

Earlier studies have supported a significant role for cocaine in the susceptibility to and the progression of human immunodeficiency virus type 1 (HIV-1) infection. Recently, several unique HIV-1 entry coreceptors (e.g., CCR5 and CCR3) and a trio of HIV-1-specific suppressor chemokines, namely, RANTES (regulated-upon-activation T expressed and secreted), macrophage inflammatory protein 1alpha (MIP-1alpha) and MIP-1beta, were identified. Although cocaine has been linked to the immunopathogenesis of HIV-1 infection, the corresponding cellular and molecular mechanism(s) have not been well defined. We hypothesize that cocaine mediates these pathologic effects through the downregulation of HIV-1-suppressing chemokines and/or upregulating HIV-1 entry coreceptors in HIV-1-infected subjects, resulting in disease progression to AIDS. Our results show that cocaine selectively downregulates endogenous MIP-1beta secretion by normal peripheral blood mononuclear cells (PBMC), while cocaine did not affect the MIP-1beta production by PBMC from AIDS patients. Cocaine also selectively suppresses lipopolysaccharide-induced MIP-1beta production by PBMC from HIV-infected patients. Further, cocaine significantly downregulates endogenous MIP-1beta gene expression, while it upregulates HIV-1 entry coreceptor CCR5 by normal PBMC. These studies suggests a role for cocaine as a cofactor in the pathogenesis of HIV infection and support the premise that cocaine increases susceptibility to and progression of HIV-1 infection by inhibiting the synthesis of HIV-1 protective chemokines and/or upregulating the HIV-1 entry coreceptor, CCR5.
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PMID:Cocaine differentially modulates chemokine production by mononuclear cells from normal donors and human immunodeficiency virus type 1-infected patients. 1061 85

California's Senate approved legislation authorizing experimental needle-exchange programs in four cities: San Francisco, Los Angeles, San Jose, and Long Beach. Officials in these cities will decide whether their city will participate. The proposed legislation cited several studies showing that HIV transmission rates declined in cities that have such programs. The project is seen as critical because changing patterns of injection-drug use indicate that cocaine is replacing heroin as the injection-drug user's drug of choice. Cocaine users inject more frequently than heroin users, increasing the risk of HIV infection.
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PMID:Needle-exchange bill passes California senate by one vote. 1136 9

Drug abuse is a growing problem in industrialized countries, opening the way to new diseases of the respiratory tract. It has been demonstrated that regular inhalation of cannabis has the same consequences as tobacco smoking. The same cannot be said for other drugs. Cocaine, amphetamines or crack expose the patient to particular toxic effects: in addition to barotrauma related to the administration route, syndromes of acute respiratory distress have been described. These result either from bronchial reactions, asthma exacerbation or eosinophil bronchopneumonia, or alveolar involvement: intra-alveolar bleeding, pulmonary edema or organized pneumonia. Respiratory complications induced by opiates, often used in injections, are related to central alveolar hypoventilation and/or the development of injury from pulmonary edema or pneumonia. The pathophysiology of these lesions is not perfectly understood. Besides these specific conditions, infection is a major problem in drug abusers, irrespective of the drug: bacterial pneumonia, tuberculosis, HIV infection are much more frequent in this high-risk group. Finally repeated intravenous injections of various drugs designed for oral intake can lead to severe complications such as pulmonary hypertension or toxic interstitial lung disease. Summarizing, respiratory diseases in drug abuses can take on a wide range of quite complex presentations. Occasional or regular use of illicit drugs can lead, not exceptionally, to severe respiratory complications requiring rapid management. Knowledge of the principal complications and the appropriate diagnostic procedures is indispensable.
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PMID:[Bronchopulmonary disease in drug abusers]. 1159 52

A study was conducted to ascertain correlates of HIV high risk behaviors and attitudes toward HIV. A questionnaire was administered to 103 men living in a modified therapeutic community (TC) for homeless, chemically addicted and mentally ill men. The psychiatric diagnoses of the sample population included psychotic disorders (48%), depressive disorders (36%), and bipolar disorders (16%). Forty-two percent reported that their primary substance of abuse was cocaine and another 40% named alcohol as the substance to which they were most addicted. Two logistic regression analyses were conducted, one with needle sharing as the outcome measure and one with endorsement of the need for lifestyle changes to reduce risk of HIV transmission. Cocaine users were 3.4 times more likely to have shared needles than the rest of the sample. Patients who had a history of sexually transmitted diseases (STDs) were 17 times more likely to endorse the need for lifestyle changes. The level of HIV transmission knowledge was unrelated to HIV risk behaviors or attitudes.
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PMID:Correlates of HIV transmission risk factors and considerations for interventions in homeless, chemically addicted and mentally ill patients. 1209

In December 2002, the author conducted a comprehensive review of indicators of use of illicit substances in the San Francisco Bay Area. Cocaine use prevalence appears to be rising again, after a significant decline in the late 1990s. The shift away from smoking crack and toward snorting powder cocaine persists. The former predominance of Blacks among users continues to ebb. Heroin use indicators consistently show a peak in 1999, followed by a significant decline. The average age of users keeps increasing. Local street prices of heroin have risen considerably since 2001. Marijuana indicators suggest a continued increase in prevalence. Methamphetamine indicators are mixed. Usage is still widespread, and risky injection practices among gay/bisexual men remain a major factor for HIV incidence. Incidence of new HIV infection declined between 1997 and 2001 for heterosexual drug injectors, but increased for gay male and transsexual injectors.
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PMID:Patterns and trends of drug use in the San Francisco Bay Area. 1282 55

Cardiac dysfunction in AIDS is an important problem. Cocaine is an epidemic associated with sudden death, cardiac dysfunction, and congestive heart failure. Cocaine use and HIV infection frequently coexist in the same patient, yet the combined impact of both is poorly understood. The present study uses cocaine treatment of an established murine AIDS transgenic model (NL4-3Delta gag/pol; TG) to define the combined effects of AIDS and cocaine on cardiac pathophysiology. To determine the effects of cocaine and HIV-1 proteins on mortality, wild-type and NL4-3Delta gag/pol mice received saline or cocaine via continuous infusion by Alzet osmotic pumps for 28 days (chronic). Acute cocaine administration (10 days; 40 mg/kg/day) was used to study the nonlethal effects of cocaine in TGs. Echocardiograms and single time point electrocardiograms were performed at the termination of each experiment. Hearts were removed and examined histopathologically. Chronic cocaine treatment (80 mg/kg/day; 28 days) markedly decreased median survival in both wild-type and TG; however, TG survival was significantly more decreased. In acute studies, TG echocardiographic changes included increased left ventricular mass and increased left ventricular fractional shortening compared with all cohorts. Electrocardiographic changes were absent among the groups. Histopathologically, perivascular fibrosis and interstitial fibrosis were evident in cocaine-treated TG. Data suggest that additive cardiac insults (from AIDS and cocaine) result in combined deleterious effects.
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PMID:Cocaine increases mortality and cardiac mass in a murine transgenic model of acquired immune deficiency syndrome. 1286 Oct 38

Evidence derived fromin vitro experiments would suggest that cocaine exposure may hasten the progression of HIV disease among infected individuals. Epidemiologic support for this association is equivocal at best. We examined the relationship between cocaine use and decline in CD4 cell counts over a 6-month period in a cohort of 81 heterosexually active men and women who were infected with HIV. Overall, cocaine users were 1.4 times (90% CI=1.0-2.1) more likely to experience a decline in CD4 count than were non-cocaine users. Cocaine users with a baseline CD4 count of greater than 500 cells/mm(3) were at 1.6 times (90% CI=1.2-2.3) greater risk for a CD4 decline than non-cocaine users at this baseline CD4 level. Concurrent treatment with an antiretroviral agent [AZT] modified the strength of this association, as evidenced by a cumulative incidence ratio (CIR) of 0.4 (90% CI=0.1-1.3) among AZT users and a CIR=2.2 (90% CI=1.5-3.2) among those not undergoing AZT treatment. The results of this study raise concerns about the negative effects of cocaine on people living with HIV infection, particularly those not receiving antiretroviral therapy who entered our study with a relatively intact immune system.
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PMID:Cocaine use and HIV disease progression among heterosexuals. 1507 25

We report that cocaine may act as cofactor in HIV pathogenesis by increasing dendritic cell-specific C type ICAM-3-grabbing nonintegrin (DC-SIGN) expression on dendritic cells (DC). Our results show that cocaine-using, long-term nonprogressors and normal progressors of HIV infection manifest significantly higher levels of DC-SIGN compared with cocaine-nonusing long-term nonprogressors and normal progressors, respectively. Furthermore, in vitro HIV infection of MDC from normal subjects cultured with cocaine and/or HIV peptides up-regulated DC-SIGN, confirming our in vivo finding. Cocaine, in synergy with HIV peptides, also up-regulates DC-SIGN gene expression by MDC. Furthermore, the cocaine-induced effects were reversed by a D1 receptor antagonist demonstrating the specificity of the reaction. Our results indicate that cocaine exacerbates HIV infection by up-regulating DC-SIGN on DC and these effects are mediated via dysregulation of MAPKs. These data are the first evidence that cocaine up-regulates the expression of DC-SIGN on DC. A better understanding of the role of DC-SIGN in HIV infection may help to design novel therapeutic strategies against the progression of HIV disease in the drug-using population.
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PMID:Cocaine modulates dendritic cell-specific C type intercellular adhesion molecule-3-grabbing nonintegrin expression by dendritic cells in HIV-1 patients. 1590

Cocaine use is associated with injecting and sexual HIV risk behaviors. This study was a randomized controlled trial of behavioral interventions for cocaine dependence and HIV risk behaviors among dually (cocaine and heroin) dependent outpatients. Methadone maintenance was augmented with cognitive-behavioral therapy (CBT), contingency management (CM), both (CBT+CM), or neither. The study sample (n=81) was 52% female, 70% African American, and 37.9+/-7.0 years old. Proportions reporting HIV risk behaviors at intake were: 96.3% (78/81) injection drug use, 56.8% (46/81) sharing needles, 30.9% (25/81) unprotected sex, 28.4% (23/81) trading sex for money or drugs. Proportions who no longer reported behaviors at study exit were: 51.3% (40/78) injection drug use, 91.3% (42/46) sharing needles, 88% (22/25) unprotected sex, 91.3% (21/23) trading sex for money or drugs. Participants receiving CBT+CM were more likely to report cessation of unprotected sex relative to control (OR=5.44, 95% CI 1.14-26.0, p=0.034) but this effect was no longer significant after adjusting for drug-negative urines. These results suggest broad beneficial effects of methadone maintenance augmented with behavioral interventions for reducing HIV risk behaviors.
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PMID:Changes in HIV risk behaviors among patients receiving combined pharmacological and behavioral interventions for heroin and cocaine dependence. 1608 66

Cocaine is associated with an increased risk for, and progression of, clinical disease associated with human immunodeficiency virus (HIV) infection. A human xenograft model, in which human peripheral blood mononuclear cells were implanted into severe combined immunodeficiency mice (huPBL-SCID) and infected with a HIV reporter virus, was used to investigate the biological interactions between cocaine and HIV infection. Systemic administration of cocaine (5 mg/kg/d) significantly increased the percentage of HIV-infected PBL (two- to threefold) and viral load (100- to 300-fold) in huPBL-SCID mice. Despite the capacity for cocaine to increase corticosterone and adrenocorticotropic hormone levels in control mice, the hypothalamic-pituitary-adrenal axis was suppressed in HIV-infected animals, and corticosterone levels were further decreased when animals were exposed to HIV and cocaine. Activating huPBL in vitro in the presence of 10(-8) M cocaine increased expression of CC chemokine receptor 5 (CCR5) and CXC chemokine receptor 4 (CXCR4) coreceptors. Expression of CCR5 was also increased at early time-points in the huPBL-SCID model following systemic exposure to cocaine (54.1+/-9.4% increase over control, P<0.01). This effect preceded the boost in viral infection and waned as HIV infection progressed. Cocaine has been shown to mediate immunosuppressive effects by activating sigma-1 receptors in immune cells in vitro and in vivo. Consistent with these reports, a selective sigma-1 antagonist, BD1047, blocked the effects of cocaine on HIV replication in the huPBL-SCID mouse. Our results suggest that systemic exposure to cocaine can enhance HIV infection in vivo by activating sigma-1 receptors and by modulating the expression of HIV coreceptors.
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PMID:Cocaine and sigma-1 receptors modulate HIV infection, chemokine receptors, and the HPA axis in the huPBL-SCID model. 1620 38


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