Effects of cocaine and HIV on decision-making abilities.

Our study aimed to understand the impact of cocaine dependence on high-risk decision-making abilities in individuals with the human immunodeficiency virus (HIV) and individuals with cocaine dependence. We recruited 99 participants (27 HIV/Cocaine, 20 HIV Only, 26 Cocaine Only, and 26 Healthy Controls). The Iowa Gambling Task (IGT) was applied to assess decision-making abilities. Independent and interactive effects of HIV status and cocaine dependence were examined using 2 × 2 factorial ANCOVA with premorbid IQ (WRAT-4: WR) as the covariate. We found cocaine dependence had a significant adverse effect on overall IGT performance (p = 0.015). We also found individuals who were HIV-positive tended to have less total money at the end of the game than individuals who were HIV-negative (p = 0.032), suggesting individuals living with HIV had less focus on long-term gains and more focus on short-term gains. Our findings highlight the significant impact of cocaine dependence on decision-making abilities and the difficulty individuals with HIV have in adequately weighing the cost and benefits of their decisions and making appropriate changes for the future.

Male HIV-1 transgenic rats show reduced cocaine-maintained lever-pressing compared to F344 wildtype rats despite similar baseline locomotion.

The HIV-1 transgenic (Tg) rat model is valuable for understanding HIV-associated neurocognitive disorders (HAND) and accompanying substance use and misuse. Tg and F344/NHsd wildtype (WT) rats were allowed to self-administer intrajugular cocaine. For the first 7 sessions, neither genotype self-administered cocaine (0.1 mg/kg/infusion) on a fixed ratio 1 schedule. We thus implemented a lever-cocaine "autoshaping" session followed by a series of manipulations changing dose and reinforcement schedule. Tg rats self-administered much less cocaine than WT rats throughout the study. Of 8 Tg rats, 5 modestly increased self-administration from sessions 36-50. Of those, only 3 showed a lever discrimination. Of 10 WT rats, 8 acquired robust self-administration by session 19; all WT rats self-administered cocaine by the end of the study. WT and Tg rats had similar baseline locomotor activity in the self-administration chamber suggesting that the low levels of cocaine intake in the Tg rats did not reflect a nonspecific motor impairment in this rat strain. Concomitant measurement of activity with self-administration revealed activity increases that followed increased cocaine intake. That relation held in Tg rats. Therefore, the present study provides evidence that HIV-1 Tg rats are less sensitive to the reinforcing effects of cocaine than their F344 WT counterparts.

The effects of cocaine on HIV transcription.

Illicit drug users are a high-risk population for infection with the human immunodeficiency virus (HIV). A strong correlation exists between prohibited drug use and an increased rate of HIV transmission. Cocaine stands out as one of the most frequently abused illicit drugs, and its use is correlated with HIV infection and disease progression. The central nervous system (CNS) is a common target for both drugs of abuse and HIV, and cocaine intake further accelerates neuronal injury in HIV patients. Although the high incidence of HIV infection in illicit drug abusers is primarily due to high-risk activities such as needle sharing and unprotected sex, several studies have demonstrated that cocaine enhances the rate of HIV gene expression and replication by activating various signal transduction pathways and downstream transcription factors. In order to generate mature HIV genomic transcript, HIV gene expression has to pass through both the initiation and elongation phases of transcription, which requires discrete transcription factors. In this review, we will provide a detailed analysis of the molecular mechanisms that regulate HIV transcription and discuss how cocaine modulates those mechanisms to upregulate HIV transcription and eventually HIV replication.

Platelet Activation in Human Immunodeficiency Virus Type-1 Patients Is Not Altered with Cocaine Abuse.

Recent work has indicated that platelets, which are anucleate blood cells, significantly contribute to inflammatory disorders. Importantly, platelets also likely contribute to various inflammatory secondary disorders that are increasingly associated with Human Immunodeficiency Virus Type-1 (HIV) infection including neurological impairments and cardiovascular complications. Indeed, HIV infection is often associated with increased levels of platelet activators. Additionally, cocaine, a drug commonly abused by HIV-infected individuals, leads to increased platelet activation in humans. Considering that orchestrated signaling mechanisms are essential for platelet activation, and that nuclear factor-kappa B (NF-κB) inhibitors can alter platelet function, the role of NF-κB signaling in platelet activation during HIV infection warrants further investigation. Here we tested the hypothesis that inhibitory kappa B kinase complex (IKK) activation would be central for platelet activation induced by HIV and cocaine. Whole blood from HIV-positive and HIV-negative individuals, with or without cocaine abuse was used to assess platelet activation via flow cytometry whereas IKK activation was analyzed by performing immunoblotting and in vitro kinase assays. We demonstrate that increased platelet activation in HIV patients, as measured by CD62P expression, is not altered with reported cocaine use. Furthermore, cocaine and HIV do not activate platelets in whole blood when treated ex vivo. Finally, HIV-induced platelet activation does not involve the NF-κB signaling intermediate, IKKß. Platelet activation in HIV patients is not altered with cocaine abuse. These results support the notion that non-IKK targeting approaches will be better suited for the treatment of HIV-associated inflammatory disorders.

A pilot feasibility and acceptability study of yoga/meditation on the quality of life and markers of stress in persons living with HIV who also use crack cocaine.

BACKGROUND: Persons living with HIV (PLWH) who also use crack cocaine may have stressful, chaotic lives and typically do not engage in standard medical care that addresses a multitude of extenuating life circumstances. Yoga/meditation (YM) improves quality of life (QOL) and biomarkers of stress, but the effect of this intervention is almost unknown in PLWH, particularly those who use crack cocaine. OBJECTIVES: This pilot study sought to compare the feasibility and acceptability of 60-minute, twice-per-week sessions of YM for 2 months with those of no-contact control and to evaluate the effects of the intervention on QOL (according to the Short Form-36, Perceived Stress Scale [PSS], and Impact of Events Scale [IES]) and salivary cortisol and dehydroepiandrosterone sulfate (DHEA-S) among PLWH who use crack cocaine. DESIGN: Participants were randomly assigned to YM or no-contact control and were assessed at baseline, 2 months after the intervention, and 4 months' follow-up. RESULTS: The YM program was acceptable and feasible, with high overall attendance (89%) and individual participation in yoga sessions (83%). YM participants showed modest improvements on QOL. The PSS total score and the IES intrusion score improved significantly 2 months after the intervention, but cortisol and DHEA-S did not change. CONCLUSIONS: This pilot study showed a high level of feasibility and acceptability and modest effects on measures of QOL among PLWH who use crack cocaine. The results suggest utility of YM as a simple, safe, and inexpensive format to improve QOL in a population that has many medical difficulties and extenuating stressors.

Cocaine alters cytokine profiles in HIV-1-infected African American individuals in the DrexelMed HIV/AIDS genetic analysis cohort.

BACKGROUND: This study evaluated the relationship between illicit drug use and HIV-1 disease severity in HIV-1-infected patients enrolled in the DREXELMED HIV/AIDS Genetic Analysis Cohort. Because cocaine is known to have immunomodulatory effects, the cytokine profiles of preferential nonusers, cocaine users, and multidrug users were analyzed to understand the effects of cocaine on cytokine modulation and HIV-1 disease severity. METHODS: Patients within the cohort were assessed approximately every 6 months for HIV-1 clinical markers and for history of illicit drug, alcohol, and tobacco use. The Luminex human cytokine 30-plex panel was used for cytokine quantitation. Analysis was performed using a newly developed biostatistical model. RESULTS: Substance abuse was common within the cohort. Using the drug screens at the time of each visit, the subjects in the cohort were categorized as preferential nonusers, cocaine users, or multidrug users. The overall health of the nonuser population was better than that of the cocaine users, with peak and current viral loads in nonusers substantially lower than those in cocaine and multidrug users. Among the 30 cytokines investigated, differential levels were established within the 3 populations. The T-helper 2 cytokines, interleukin-4 and -10, known to play a critical role during HIV-1 infection, were positively associated with increasing cocaine use. Clinical parameters such as latest viral load, CD4 T-cell counts, and CD4:CD8 ratio were also significantly associated with cocaine use, depending on the statistical model used. CONCLUSIONS: Based on these assessments, cocaine use seems to be associated with more severe HIV-1 disease.

Predictive factors of herpes zoster HIV-infected patients: another adverse effect of crack cocaine.

A retrospective cohort study was conducted on 1541 HIV-infected patients to determine variables associated with the incidence of herpes zoster. A single failure Cox model showed that herpes zoster incidence increased following the first 6 months of antiretroviral treatment adjusted hazard ratio (AHR)=5 (95%CI=2.6-9.2), P<0.001; in the >60 years age group AHR=2 (95%CI=1-4), P=0.04; in patients in the top CD8 quartile AHR=2.1 (95%CI=1.3-3.6), P<0.001; and in patients previously reported to use crack cocaine AHR=5.9, (95%CI=1.4-25), P=0.02. Herpes zoster incidence increased in patients with CD4 counts<500 per mm(3) and gradually declined since 1992-1996, with AHR=0.3 (95%CI=0.2-0.5), P<0.001 for the 1997-2002 period and AHR=0.24 (95%CI=0.14-0.4), P<0.001 for the 2002-2008 period. Contrary to what has been described elsewhere, there was no specific effect of protease inhibitors on herpes zoster incidence. The present study is the first to suggest that crack cocaine is associated with an increased incidence of herpes zoster. The neurological or immunological effects of crack are discussed.

Cocaine and HIV-1 interplay in CNS: cellular and molecular mechanisms.

Although antiretrovirals are the mainstay of therapy against HIV infection, neurological complications associated with the virus continue to hamper quality of life of the infected individuals. Drugs of abuse in the infected individuals further fuel the epidemic. Epidemiological studies have demonstrated that abuse of cocaine resulted in acceleration of HIV infection and the progression of NeuroAIDS. Cocaine has not only been shown to play a crucial role in promoting virus replication, but also has diverse but often deleterious effects on various cell types of the CNS. In the neuronal system, cocaine exposure results in neuronal toxicity and also potentiates gp120-induced neurotoxicity. In the astroglia and microglia, cocaine exposure leads to up-regulation of pro-inflammatory mediators such as cytokines and chemokines. These in turn, can lead to neuroinflammation and transmission of toxic responses to the neurons. Additionally, cocaine exposure can also lead to leakiness of the blood-brain barrier that manifests as enhanced transmigraiton of leukocytes/monocytes into the CNS. Both in vitro and in vivo studies have provided valuable tools in exploring the role of cocaine in mediating HIV-associated neuropathogenesis. This review summarizes previous studies on the mechanism(s) underlying the interplay of cocaine and HIV as it relates to the CNS.

Patterns of heroin and cocaine injection and plasma HIV-1 RNA suppression among a long-term cohort of injection drug users.

BACKGROUND: Previous studies suggest that active drug use may compromise HIV treatment among HIV-positive injection drug users (IDU). However, little is known about the differential impacts of cocaine injection, heroin injection, and combined cocaine and heroin injection on plasma HIV-1 RNA suppression. METHODS: Data were derived from a longstanding open prospective cohort of HIV-positive IDU in Vancouver, Canada. Kaplan-Meier methods and Cox proportional hazards regression were used to examine the impacts of different drug use patterns on rates of plasma HIV-1 RNA suppression. RESULTS: Between May 1996 and April 2008, 267 antiretroviral (ART) naïve participants were seen for a median follow-up duration of 50.6 months after initiating ART. The incidence density of HIV-1 RNA suppression was 65.2 (95%CI: 57.0-74.2) per 100 person-years. In Kaplan-Meier analyses, compared to those who abstained from injecting, individuals injecting heroin, cocaine, or combined heroin/cocaine at baseline were significantly less likely to achieve viral suppression (all p<0.01). However, none of the drug use categories remained associated with a reduced rate of viral suppression when considered as time-updated variables (all p>0.05). CONCLUSIONS: Active injecting at the time of ART initiation was associated with lower plasma HIV-1 RNA suppression rates; however, there was no difference in suppression rates when drug use patterns were examined over time. These findings imply that adherence interventions for active injectors should optimally be applied at the time of ART initiation.

Latent classes of heroin and cocaine users predict unique HIV/HCV risk factors.

BACKGROUND: Patterns of heroin and cocaine use vary and may be associated with unique risk factors for bloodborne infections. METHODS: Latent class analysis identified sub-populations of 552 heroin and cocaine users in Baltimore, Maryland. Using latent class regression, these classes were analyzed for associations with demographic characteristics, risky behaviors, Hepatitis C, and HIV. RESULTS: Three classes were found: Crack/Nasal-Heroin users (43.5%), Polysubstance users (34.8%), and Heroin Injectors (21.8%). Compared to Polysubstance users, Crack/Nasal-Heroin users were almost 7 times more likely to identify as Black (OR=6.97, 95% CI=4.35-11.2). Sharing needles was over 2.5 times more likely among Polysubstance users than among Heroin Injectors (OR=2.66, 95% CI=1.49-4.75). Crack/Nasal-Heroin users were 2.5 times more likely than Polysubstance users to exchange drugs for sex (OR=2.50, 95% CI=1.22-5.13). Crack/Nasal-Heroin users were less likely than Heroin Injectors to have Hepatitis C (OR=0.10, 95% CI=0.06-0.18), but no significant differences were found for HIV. CONCLUSIONS: Subpopulations of cocaine and heroin users differed in demographic classifications, HIV-risk behaviors, and Hepatitis C infection. All subpopulations included substantial numbers of HIV-positive individuals. Findings provide further evidence that non-injection drug users face significant infectious disease risk.

Cocaine and HIV-1 interplay: molecular mechanisms of action and addiction.

Human immunodeficiency virus (HIV) infection is now being driven by drug-abusing populations. Epidemiological studies on drug abusers with AIDS link abuse of cocaine, even more than other drugs, to increased incidence of HIV seroprevalence and progression to AIDS. Both cell culture and animal studies demonstrate that cocaine can both potentiate HIV replication and can potentiate HIV proteins to cause enhanced glial cell activation, neurotoxicity, and breakdown of the blood-brain barrier. Based on the ability of both HIV proteins and cocaine to modulate NMDA receptor on neurons, NMDA receptors have been suggested as a common link underlying the crosstalk between drug addiction and HIV infection. While the role of dopamine system as a major target of cocaine cannot be overlooked, recent studies on the role of sigma receptors in mediating the effects of cocaine in both cell and organ systems warrants a deeper understanding of their functional role in the field. In this review, recent findings on the interplay of HIV infection and cocaine abuse and their possible implications in mode of action and/or addiction will be discussed.

Epidemiological survey of hepatitis C virus infection in a cohort of patients from a ser.T in naples, Italy.

Hepatitis C virus (HCV) has infected an estimated 170 million people worldwide, most of whom are chronically infected (60% to 80%). In Italy, the estimate of anti-HCV antibody (Ab) prevalence, in the general population of Northern Italy, is 3.2%; in Central and Southern Italy, it is 8.4% to 22.4%. Highest prevalence of infection (70% to 90%) is found among intravenous drug users. Our purpose is to monitor HCV infection among drug users treated in a Drug Addiction Centre (Ser.T) in Naples and to gain a better understanding of that relationship with the abused substance(s). Epidemiological data are shown for viral coinfections. Finally, the authors investigate access to specific HCV therapy in an Italian Ser.T. The study analyzed a group of 1753 consecutive subjects treated from 1988 to 2008 in the O.U. Ser.T D.S.31 (Gesù e Maria Hospital), ASL Napoli 1 Centre. HCV Abs were detected by enzyme immune assay method and confirmed by recombinant immunoblot assay III method. During the entire period, we performed real-time polymerase chain reaction at random for 312 patients. The incidence (per year) of HCV infection showed a rapid spread decrease from 49.5% in 2003 to 14.5% in 2008. The overall prevalence of HCV was 48.1%. We tested 312 randomly selected patients for viral replication. Our study showed active viral replication in 201 (64.4%) patients as follows: 97 of 201 (31.1%) resulted infected by genotype (gt) 1; 3 of 201 (1.0%) gt 2; 84 of 201 (26.9%) gt 3; and 4 of 201 (1.3%) gt 4. Coinfection data showed that HCV Ab prevalence was 58.5% (48 of 82) in hepatitis B virus chronically infected patients. Human immunodeficiency virus (HIV)/HCV coinfection resulted in 95.2% (80 of 84) HIV patients. The prevalence of HIV Abs in HCV-infected patients was 8.99% (80 of 889). Analysis of drug abuse showed high prevalence of opiate addicted, multiabusers, and with high-risk factors. Cocaine abuser prevalence was 14.4%, and incidence, during past 4 years of the study, rose to 42.6%. Alcohol abuser prevalence represented 5.8% of patients and incidence rose to 17.7% in final 4 years of the study. In those opiate addicted, HCV infection was 61.0% (805 of 1320). HCV infection in cocaine-addicted patients was 9.5% (24 of 253). In 78 delta-9-tetra-hydro-cannabinol addicted patients, 5.1% of tests were positive (4 of 78). In alcohol abusers, HCV infection was 9.8% (10 of 102). Access to HCV treatment in our cohort from 2000 to 2008 resulted low (15.4%). Enhancing the Ser.Ts efficiency can result in health and financial benefits.

Cocaine hijacks σ1 receptor to initiate induction of activated leukocyte cell adhesion molecule: implication for increased monocyte adhesion and migration in the CNS.

Human immunodeficiency virus (HIV)-associated increase in monocyte adhesion and trafficking is exacerbated by cocaine abuse. The underlying mechanisms involve cocaine-mediated upregulation of adhesion molecules with subsequent disruption of the blood-brain barrier (BBB). Recently, a novel activated leukocyte cell adhesion molecule (ALCAM) has been implicated in leukocyte transmigration across the endothelium. We now show that upregulation of ALCAM in the brain endothelium seen in HIV(+)/cocaine drug abusers paralleled increased CD68 immunostaining compared with HIV(+)/no cocaine or uninfected controls, suggesting the important role of ALCAM in promoting leukocyte infiltration across the BBB. Furthermore, ALCAM expression was increased in cocaine-treated mice with concomitant increase in monocyte adhesion and transmigration in vivo, which was ameliorated by pretreating with the neutralizing antibody to ALCAM, lending additional support to the role of ALCAM. This new concept was further confirmed by in vitro experiments. Cocaine-mediated induction of ALCAM in human brain microvascular endothelial cells through the translocation of σ receptor to the plasma membrane, followed by phosphorylation of PDGF-ß (platelet-derived growth factor-ß) receptor. Downstream activation of mitogen-activated protein kinases, Akt, and NF-κB (nuclear factor-κB) pathways resulted in induced expression of ALCAM. Functional implication of upregulated ALCAM was confirmed using cell adhesion and transmigration assays. Neutralizing antibody to ALCAM ameliorated this effect. Together, these findings implicate cocaine-mediated induction of ALCAM as a mediator of increased monocyte adhesion/transmigration into the CNS.

Cocaine reduces thymic endocrine function: another mechanism for accelerated HIV disease progression.

Thymulin is a thymic peptide important for the maturation and differentiation of immature thymocytes, which have been found to be depressed in patients with low-level CD4(+) cell recovery despite viral control. Substance use is associated with faster progression of HIV disease, which has been ascribed to poor adherence to antiretroviral medication. Recent findings of an association between cocaine use and decline in CD4(+) cell counts independent of antiretroviral adherence indicate alternative mechanisms for disease progression. We evaluated the relationship between thymulin activity, CD4(+) and CD8(+) cell counts and the CD4(+)/CD8(+) ratio, and the covariate effects of substance use cross-sectionally in 80 HIV(+) active substance users and over 12 months in 40 participants. Thymulin activity was analyzed in plasma using a modification of the sheep rosette bioassay. Thymulin activity was negatively associated with cocaine use (ß = -0.908,95% CI: -1.704, -0.112; p = 0.026). Compared to those who do not use cocaine, cocaine users were 37% less likely to have detectable thymulin activity (RR = 0.634, 95% CI: 0.406, 0.989 p = 0.045) and were 75 times more likely to show a decrease in thymulin activity (OR = 74.7, 95% CI: 1.59, 3519.74; p = 0.028) over time. CD4(+) cell count was positively associated with thymulin activity (ß = 0.127, 95% CI: 0.048,0.205; p = 0.002), detectable thymulin activity was 2.32 times more likely in those with a CD4 cell count ≥200 cells/µl (RR = 2.324, 95% CI: 1.196, 4.513, p = 0.013), and those with an increase in CD4 cell counts were more likely to show an increase in thymulin activity (OR = 1.02, 95% CI: 1.00, 1.034; p = 0.041) over time. Thymulin activity is predictive of HIV disease progression and is depressed in cocaine users independent of antiretroviral treatment (ART) and HIV viral load. Understanding the mechanisms for accelerated HIV disease progression provides opportunities to find alternative strategies to counteract immunosuppression.

Sexual behavior and HBV infection among noninjecting cocaine users (NICUs).

The aim is to estimate HBV prevalence and the associated risks among noninjecting cocaine users (NICUs). In 2002-2003, a total of 824 NICUs from Buenos Aires (Argentina) and Montevideo (Uruguay) were interviewed using a structured questionnaire. Serologic tests were carried out for Human Immunodeficiency Virus (HIV), hepatitis B (HBV), syphilis, and others. The population was divided into two serologic groups: HBV-infected and seronegative group. Univariate and binary logistic model were developed. The results seem to indicate that, among NICUs, HBV is transmitted through sexual contact. Prevention measures, including vaccine, are needed in order to control and minimize risks. The study's limitations are noted.

Risk behaviors for HCV- and HIV-seroprevalence among female crack users in Porto Alegre, Brazil.

Several studies have shown a high prevalence of HIV-seropositive status among crack users, though most refer to North American populations. Few studies evaluate HCV prevalence among female crack users. In addition, there is a particular lack of data about risk behaviors and HIV/HCV prevalence in this population around the world. In order to ascertain the HIV/HCV serostatus and associated risk behaviors for infection of female crack users of Porto Alegre, Brazil. A cross-sectional study of a convenience sample of 73 current female crack users was conducted. Subjects answered NIDA's Risk Behavior Assessment and an AIDS Information Questionnaire. In addition, blood was collected from subjects for HIV/HCV tests. The overall prevalence of HIV was 37.0%; HCV seroprevalence was 27.7%; of 15.1% the sample was co-infected with HIV and HCV. Four years of schooling or fewer (OR 4.72-CI 95%; 1.49-14.99) and having three or more HIV tests in one's lifetime (OR 4.26-CI 95% (1.29-14.04)) were associated with HIV infection (after multivariate logistic regression). The single greatest risk factor for HCV infection was having 4 years of schooling or fewer (OR 4.51-CI 95%; 1.18-17.27). We found a very high prevalence of HIV and HCV infection among female crack users, and low education was the most significant risk factor associated with both infections.

The human immunodeficiency virus-1-associated protein, Tat1-86, impairs dopamine transporters and interacts with cocaine to reduce nerve terminal function: a no-net-flux microdialysis study.

Injection drug use accounts for approximately one-third of human immunodeficiency virus (HIV) infections in the United States. HIV-associated proteins have been shown to interact with various drugs of abuse to incite concerted neurotoxicity. One common area for their interaction is the nerve terminal, including dopamine transporter (DAT) systems. However, results regarding DAT function and regulation in HIV-infection, regardless of drug use, are mixed. Thus, the present experiments were designed to explicitly control Tat and cocaine administration in an in vivo rat model in order to reconcile differences that exist in the literature to date. We examined Tat plus cocaine-induced alterations using no-net-flux microdialysis, which is sensitive to alterations in DAT function, in order to test the potential for DAT as an early mediator of HIV-induced oxidative stress and neurodegeneration in vivo. Within 5 h of intra-accumbal administration of the HIV-associated protein, Tat, we noted a significant reduction in local DAT efficiency with little change in DA overflow/release dynamics. Further, at 48 h post-Tat administration, we demonstrated a concerted effect of the HIV-protein Tat with cocaine on both uptake and release function. Finally, we discuss the extent to which DAT dysfunction may be considered a predecessor to generalized nerve terminal dysfunction. Characterization of DAT dysfunction in vivo may provide an early pharmacotherapeutic target, which in turn may prevent or attenuate downstream mediators of neurotoxicity (i.e., reactive species) to dopamine systems occurring in neuro-AIDS.

Hospitalized HIV-infected patients in the era of highly active antiretroviral therapy.

We interviewed 1038 HIV-positive inpatients in public hospitals in Miami, Florida, and Atlanta, Georgia, to examine patient factors associated with use of HIV care, use of antiretroviral therapy, and unprotected sexual intercourse. Multivariate analyses and multiple logistic regression models showed that use of crack cocaine and heavy drinking were associated with never having had an HIV-care provider, high-risk sexual behavior, and not receiving antiretroviral therapy. Inpatient interventions that link and retain HIV-positive persons in primary care services could prevent HIV transmission and unnecessary hospitalizations.

HIV risks associated with incarceration among injection drug users: implications for prison-based public health strategies.

BACKGROUND: Recent policy announcements in Canada and the United States may potentially affect the risk environment for HIV transmission among incarcerated injection drug users (IDU). We sought to evaluate the potential impact of incarceration on HIV risk behaviour among the IDU enrolled in a prospective cohort study. METHODS: We examined patterns of incarceration among 1247 IDU participants enrolled in a 6-year prospective cohort study in Vancouver, Canada, and tested for potential associations between HIV risk behaviour and incarceration. Correlates of incarceration were identified using generalized estimating equations (GEE). RESULTS: At baseline, factors significantly associated with incarceration included daily injection heroin and injection cocaine use and inconsistent condom use with casual sexual partners. In a GEE analysis, factors independently associated with incarceration included: used syringe borrowing (adjusted odds ratio [AOR] = 1.36; [95% CI: 1.16-1.60]), used syringe lending (AOR = 1.31; [95% CI: 1.12-1.55]) and inconsistent condom use with casual sexual partners (AOR = 1.16; [1.02-1.33]). All variables P < 0.05. CONCLUSION: In our study, incarceration was independently associated with HIV transmission and acquisition behaviours. These findings suggest that increased rates of incarceration of IDU may be associated with increased HIV transmission among this group.

Hepatitis C virus transmission among oral crack users: viral detection on crack paraphernalia.

OBJECTIVE: Epidemiological studies present oral crack use as a potential independent risk factor for hepatitis C virus (HCV) status, yet actual HCV transmission pathways via crack use have not been evidenced. To this end, this exploratory study sought to detect HCV on crack-use paraphernalia used by street crack users. METHODS: Crack-use paraphernalia within 60 min of use was collected from 51 (N) street-crack users. HCV RNA detection was conducted through eluate sampling and manual RNA extraction. Participants provided a saliva sample to test for HCV antibody, and had a digital photograph taken of their oral cavities, to assess the presence of oral sores as a possible risk factor for oral HCV transmission. RESULTS: About 43.1% (n=22) of the study participants were HCV-antibody positive. One (2.0%) of the 51 pipes tested positive. A minority of the participants presented oral sores. The pipe on which HCV was detected was made from a glass stem; its owner was HCV-antibody positive, and there was full rater agreement on the presence of oral sores in the pipe owner's oral cavity. CONCLUSIONS: HCV transmission from an infected host onto paraphernalia as a precondition of HCV host-to-host transmission via shared crack paraphernalia use seems possible, with oral sores and paraphernalia condition constituting possible risk modifiers. Larger-scale studies with crack users are needed to corroborate our findings.