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Background: Salvador is the city with the highest number of HTLV-1 infected individuals in Brazil, yet the main route of HTLV-1 transmission is unknown. Objective: To investigate the association of syphilis infection as a proxy for sexual transmission of HTLV-1 infection in the general population of this city. Methods: A cross sectional population-based study was conducted with 3,451 serum samples obtained by a representative simple random sampling. Data on gender, age, income, and years of education were collected by questionnaire and the presence of HTLV, HIV and Treponema pallidum infection was determined by serology. Logistic regression analysis was used to evaluate the independent effect of the potential explanatory variables to HTLV-1 infection and Odds Ratios (OR) and 95% CI were calculated. Results: The majority of studied individuals were female (56.4%), had less than 7 years of education (55.3%) and earned two or less minimum wages (52.0%). The overall prevalence of HTLV-1 was 1.48% (51/3,451; 95% CI: 1.10%– 1.94%), which increased with age. Only three persons younger than 17 (3/958; 0.31%; CI 95% 0.06–0.91) years were infected by HTLV-1. Among the 45 syphilis positives, 12 (26.7%) were HTLV positive, while among 21 HIV positives, only one (4.8%) was HTLV positive. HTLV-1 infection was found to be associated with syphilis infection (ORADJUSTED 36.77; 95% CI 14.96–90.41). Conclusion: The data presented herein indicate that horizontal transmission between adults is the main route of HTLV-1 infection in the general population of Salvador and that this is likely to occur through sexual contact. [ABSTRACT FROM AUTHOR]

Aims To assess the association between hepatitis C virus ( HCV) infection and overall and liver-related death in human immunodeficiency virus ( HIV)-infected patients with alcohol problems. Design We analyzed data from a cohort of HIV-infected adults with current or past alcohol problems enrolled between 2001 and 2003, searching for causes of death until 2010 using the National Death Index. Setting and participants Participants were HIV-infected adults with current or past alcohol problems, recruited in Boston, MA from HIV clinics at two hospitals, homeless shelters, drug treatment programs, subject referrals, flyers and another cohort study with comparable recruitment sites. Measurements The primary and secondary outcomes were all-cause and liver-related mortality, respectively. The main independent variable was hepatitis C virus ( HCV) RNA status (positive versus negative). Mortality rates and Kaplan- Meier survival curves were calculated by HCV status for both overall and liver-related mortality. Cox proportional hazards models were used to assess the association between HCV infection and overall and liver-related death, adjusting for alcohol and drug use over time. Findings A total of 397 adults (50% HCV-infected) were included. As of 31 December 2009, 83 cohort participants had died (60 HCV-infected, 23 HCV-uninfected; log-rank test P < 0.001), and 26 of those deaths were liver-related (21 HCV-infected, five HCV-uninfected; log-rank test P < 0.001). All-cause and liver-related mortality rates were 4.68 and 1.64 deaths per 100 person-years for HCV-infected patients and 1.65 and 0.36 per 100 person-years for those without HCV, respectively. In the fully adjusted Cox model, HCV infection was associated with both overall [hazard ratio ( HR) = 2.55, 95% confidence interval ( CI) = 1.50-4.33, P < 0.01], and liver-related mortality ( HR = 3.24, 95% CI = 1.18-8.94, P = 0.02]. Conclusion Hepatitis C virus infection is associated independently with all-cause and liver-related mortality in human immunodeficiency virus-infected patients with alcohol problems, even when accounting for alcohol and other drug use. [ABSTRACT FROM AUTHOR]

Background The effect of alcohol on liver disease in HIV infection has not been well characterized. Methods We performed a cross-sectional multivariable analysis of the association between lifetime alcohol use and liver fibrosis in a longitudinal cohort of HIV-infected patients with alcohol problems. Liver fibrosis was estimated with 2 noninvasive indices, ' FIB-4,' which includes platelets, liver enzymes, and age; and aspartate aminotransferase/platelet ratio index (' APRI'), which includes platelets and liver enzymes. FIB-4 <1.45 and APRI <0.5 defined the absence of liver fibrosis. FIB-4 >3.25 and APRI >1.5 defined advanced liver fibrosis. The main independent variable was lifetime alcohol consumption (<150 kg, 150 to 600 kg, >600 kg). Results Subjects ( n = 308) were 73% men, mean age 43 years, 49% with hepatitis C virus ( HCV) infection, 60% on antiretroviral therapy, 49% with an HIV RNA load <1,000 copies/ml, and 18.7% with a CD4 count <200 cells/mm3. Forty-five percent had lifetime alcohol consumption >600 kg, 32.7% 150 to 600 kg, and 22.3% <150 kg; 33% had current heavy alcohol use, and 69% had >9 years of heavy episodic drinking. Sixty-one percent had absence of liver fibrosis and 10% had advanced liver fibrosis based on FIB-4. In logistic regression analyses, controlling for age, gender, HCV infection, and CD4 count, no association was detected between lifetime alcohol consumption and the absence of liver fibrosis ( FIB-4 <1.45) (adjusted odds ratio [ AOR] = 1.12 [95% CI: 0.25 to 2.52] for 150 to 600 kg vs. <150 kg; AOR = 1.11 [95% CI: 0.52 to 2.36] for >600 kg vs. <150 kg; global p = 0.95). Additionally, no association was detected between lifetime alcohol use and advanced liver fibrosis ( FIB-4 >3.25). Results were similar using APRI, and among those with and without HCV infection. Conclusions In this cohort of HIV-infected patients with alcohol problems, we found no significant association between lifetime alcohol consumption and the absence of liver fibrosis or the presence of advanced liver fibrosis, suggesting that alcohol may be less important than other known factors that promote liver fibrosis in this population. [ABSTRACT FROM AUTHOR]

Aims To examine the impact of alcohol use on depressive symptoms in human immunodeficiency virus (HIV)-infected patients. Design Data were collected at 6-month intervals and analyzed to evaluate the association between alcohol dependence and consumption on depressive symptoms using longitudinal mixed-effects regression models controlling for specified covariates. Measurements The two independent variables were current alcohol dependence assessed using the Composite International Diagnostic Interview (CIDI) and past month consumption (heavy versus not heavy drinking) using a validated calendar-based method. The primary outcome was depressive symptoms as measured by the Center for Epidemiologic Studies Depression Scale (CES-D). Participants HIV-infected adults with current or past alcohol problems. Findings Alcohol dependence and heavy alcohol use were significantly associated with higher CES-D scores in unadjusted models. In adjusted analyses, the association of current alcohol dependence persisted [mean difference in CES-D was 3.49 for dependence versus non-dependence; 95% confidence interval (CI): 1.76–5.22]; however, the effect of heavy drinking was no longer statistically significant (mean difference in CES-D was 1.04 for heavy versus not heavy drinking; 95% CI: −0.24–2.32). Conclusions Alcohol use is associated with more depressive symptoms in HIV-infected patients with alcohol problems. This association remains significant after adjusting for potential confounders only when alcohol use meets the criteria for alcohol dependence. [ABSTRACT FROM AUTHOR]

Background: Coinfection of human immunodeficiency virus (HIV) and hepatitis C virus (HCV) is a substantial medical and public health concern due to its increasing prevalence and complex patient management. Alcohol use may worsen HCV-related liver disease and interfere with adherence to antiretroviral therapy (ART) and medical care. We therefore studied the association between HCV infection and markers of HIV disease progression in adults with alcohol problems. Methods: This is a longitudinal study of 396 HIV-infected persons with alcohol problems, 199 (50%) of whom were coinfected with HCV (positive HCV RNA test). CD4 cell counts and HIV RNA levels were assessed at baseline and then every 6 months for up to 42 months. Hepatitis C virus RNA status was determined at study enrollment. We examined the relationship between HCV infection and laboratory markers of HIV progression (CD4 cell count and log10 HIV RNA) by fitting multivariable longitudinal regression models for each outcome. Results: Among subjects who were adherent to ART, the presence of HCV infection was associated with a lower CD4 cell count (adjusted mean difference −46.0 cells/ μL, p=0.03). There was no association observed between HCV infection and CD4 cell count among those not adherent to ART or those not taking ART. No significant association was observed between HCV infection and HIV RNA regardless of ART status. Conclusions: Hepatitis C virus infection has an adverse effect on CD4 cell count in patients with alcohol problems who are adherent to ART. Addressing HCV coinfection among these patients may confer additional immunologic benefit for this patient population. [ABSTRACT FROM AUTHOR]

Background. Ongoing substance use is a potential confounder for immunological studies on hepatitis C virus (HCV), but there is little in the literature regarding the effects of injection drug use (IDU) or alcohol on HCV-specific immune responses. We wanted to determine whether IDU or alcohol affected immune responses in HCV-infected and human immunodeficiency virus (HIV)/HCV coinfected subjects. Methods. Eight-four subjects with HIV/HCV and 57 with HCV were classified as either injection drug users, drinkers, or nonusers based on questionnaire results. Immune responses were studied with enzyme-linked immunosorbent spot assay for interferon (IFN)-γ, interleukin (IL)-10, and tumor necrosis factor (TNF)-α against HCV proteins Core, NS3, and NS5 and recall antigens. Results. Subjects with HIV/HCV, in aggregate, had significantly lower HCV-specific IFN-g and TNF-aresponses than subjects with HCV. However, HIV/HCV injection drug users had HCV specific IFN-γ and IL-10 responses that were similar to those of HCV injection drug users and were significantly higher than in nonusers with HIV/HCV. Conversely, subjects who drank alcohol had similar immune responses to those who were abstinent, among both subjects with HIV/HCV and subjects with HCV. Conclusions. Studies that examine IFN-γ or IL-10 immune responses in HIV/HCV-coinfected or HCV-infected persons need to consider current IDU. Alcohol, at levels consumed in this cohort, does not appear to have as much of an effect on antigen-specific immune responses. [ABSTRACT FROM AUTHOR]

Background: Alcohol use and human immune deficiency virus (HIV) infection are both associated with accelerated progression of hepatitis C virus (HCV) disease and reduced response rates to interferon therapy. In this study, we assessed the prevalence of barriers to interferon treatment in a population of HIV/HCV-coinfected patients with current or past alcohol problems and the extent to which they received treatment to address the barriers. Methods: This is a cross-sectional, descriptive analysis of baseline data from a prospective study assessing the impact of HCV and alcohol use on HIV disease progression. Using consensus guidelines, subjects were categorized as having absolute, relative, or no contraindications to interferon therapy for HCV. Absolute contraindications to treatment included heavy alcohol use, decompensated liver disease, CD4 cell count <100 cells/ μL, recent needle sharing, and suicidal ideation. Relative contraindications included moderate alcohol use, recent injection drug use, depressive symptoms, and CD4 cell count from 100 to 199 cells/ μL. Results: Of 401 HIV-infected subjects, 200 were HCV RNA-positive. Fifty-three percent had an absolute contraindication to interferon therapy, 35% a relative but no absolute contraindication, and only 12% had no contraindication. Of those with an absolute contraindication, 61% reported heavy drinking and the majority (88%) had multiple contraindications. These contraindications were present despite the fact that over 50% were in receipt of substance abuse and mental health treatment. Conclusions: Continued alcohol and drug use as well as depressive symptoms are the major barriers to interferon therapy in HCV/HIV-coinfected subjects and these barriers persist despite high treatment rates for these problems. Therefore, more intensive treatments of alcohol, drug, and mental health issues are needed to improve HCV treatment eligibility in HCV/HIV-coinfected persons. [ABSTRACT FROM AUTHOR]

The article reports on the HIV infection that does not affect the performance of noninvasive markers of fibrosis for the diagnosis of Hepatitis C virus related in liver disease. The diagnostic performance of the evaluated noninvasive markers of liver fibrosis is equivalent in HCV/HIV-coinfected and HCV-infected subjects.

We estimate that only one-third of patients coinfected with hepatitis C virus (HCV) and human immunodeficiency virus (HIV) are eligible for therapy for HCV with interferon (IFN) and ribavirin, and, of those who are eligible, two-thirds decline treatment. To date we have initiated treatment with IFN and ribavirin for 8% of coinfected patients evaluated, and <1% of patients have had a sustained virological response. During this process, we have identified many problems that significantly limit our ability to initiate and complete treatment with IFN in this population and have categorized these difficulties into 4 main challenges. They include access to care, contraindications or barriers to treatment, patients' reluctance to start treatment with IFN, and the low tolerability of treatment. If patients coinfected with HCV and HIV are to be treated for hepatitis C in greater numbers, these issues will need to be addressed. [ABSTRACT FROM AUTHOR]

Background. Human immunodeficiency virus (HIV) coinfection accelerates liver disease progression in individuals with chronic hepatitis C. We evaluated the associations of CD4, HIV RNA, and antiretroviral therapy (ART)-induced CD4 recovery with liver diagnoses in a prospective cohort of injecting drug users (IDUs). Methods. We evaluated 383 coinfected IDUs in the Boston area, prospectively observed for a median of 1.8 years. Liver disease progression included the first occurrence of hepatocellular carcinoma, variceal bleeding, ascites, encephalopathy, or death due to hepatic failure. Multivariable-adjusted extended Cox models were specified to estimate hazard ratios (HRs) for comparisons of CD4, change in CD4 (from nadir), and HIV RNA with respect to liver disease progression events. Results. Twenty-four persons experienced a liver disease progression event over 1155 person-years (2.1 per 100 person-years), including 20 deaths attributed to end-stage liver disease (1.7 per 100 person-years). CD4 at baseline and over follow-up strongly predicted liver disease progression (baseline CD4 <200 vs ≥200: HR = 5.23, 95% confidence interval [CI], 2.30–11.92; time-updated CD4 <200 vs ≥200: HR = 11.79, 95% CI, 4.47–31.07). Nadir CD4 was also a strong indicator (<100 vs ≥100: HR = 3.52, 95% CI, 1.54–8.06). A lack of CD4 recovery (failure to increase 100 cells over nadir) among ART initiators was associated with increased risk (HR = 7.69; 95% CI, 2.60–22.69). Human immunodeficiency virus RNA was not significantly associated with liver disease progression. Conclusions. Impaired immune function was highly predictive of liver disease progression in this cohort of IDUs, and a lack of CD4 recovery on ART was associated with increased risk of progression to HCV-associated liver disease.

Background: The impact of Hepatitis C virus (HCV) RNA levels on the evolution of chronic HCV infection-related liver damage is controversial. Heavy alcohol use is believed to have a deleterious impact on the course of HCV disease, but current knowledge about the possible effect of alcohol use on HCV RNA levels in HIV/HCV coinfected patients is limited. Methods: We examined 107 HIV/HCV-infected individuals with current or past unhealthy alcohol use to assess the association between alcohol consumption (any drinking vs. abstinent) and HCV RNA levels. Results: Participants were 75% male, with a mean age of 43 years, and 63% were on antiretroviral therapy. Mean (SD) log HIV RNA was 3.1 (1.4) and mean (SD) log HCV RNA was 6.1 (0.8). Past-month alcohol use was present in 38% of participants. In a multivariable linear regression analysis we found no significant differences in mean log HCV RNA levels between those reporting alcohol use and those who were abstinent [β (95%CI): −0.04 (−0.34, 0.26), p = 0.79)]. There was no significant association between any heavy drinking day and HCV RNA level (0.07, 95% CI: (−0.24, 0.38), p = 0.66). Conclusions: We did not detect significant associations between alcohol use and HCV RNA levels among HIV/HCV coinfected patients. [ABSTRACT FROM AUTHOR]