Serum cortisol predicts death and critical disease independently of CRB-65 score in community-acquired pneumonia: a prospective observational cohort study

Background

Co-infection with hepatitis C (HCV) is very common in human immunodeficiency virus 1 (HIV-1) infected patients. Although HIV co-infection clearly accelerates progression of HCV-related fibrosis and liver disease, controversy remains as to the impact of HCV on HIV disease progression in co-infected patients. HIV can cause immune dysfunction, in which the regulatory function of T helper (Th) cells is very essential. Moreover, cytokines derived from Th cells play a prominent role in viral infection. Investigating the functional changes of Th1 and Th2 cells in cytokine level can improve the understanding of the effect of co-infected HCV on HIV infection.

Methods

In this study, we measured the baseline Th1/Th2 cytokine concentration in sera by using flow cytometry in HIV/HCV co-infection, HIV mono-infection, HCV mono-infection, and healthy control group, as well as the dynamic changes of these cytokine levels after receiving highly active antiretroviral therapy (HAART).

Results

The ratio of Th1 and Th2 cytokine concentration in HIV/HCV co-infection was higher than HCV mono-infection and healthy control group, while lower than HIV mono-infection group. After HAART was initiated, the Th1/Th2 ratio of HIV/HCV co-infection group decreased to the same level of healthy control, while HIV mono-infection group was still higher than the control group.

Conclusions

There was no significant evidence showing co-infected with HCV had negative effect on HIV related diseases. However, co-infected with HCV can decrease Th1/Th2 ratio by affecting Th1 cytokine level, especially the secretion of IFN-??. With the initiation of HAART, Th1 and Th2 cytokine levels were progressively reduced. HIV was the main stimulating factor of T cells in HIV/HCV co-infection group.     

Impact of chronic hepatitis C infection on outcomes of patients with an advanced stage of HIV-1 infection in an area of low prevalence of co-infection

To ascertain whether hepatitis C (HCV) co-infection affects the progression of HIV infection, we initiated an eight-year prospective observational study at a university hospital in Taiwan where seroprevalences of HCV antibody and HIV antibody were low. Fifty-three (12.0%) consecutive non-haemophiliac HIV1-infected patients with HCV co-infection and 387 (88.0%) patients without HCV and hepatitis B co-infection were enrolled between June 1994 and June 2002 and observed until December 2002. Outcomes evaluated included the risk for acute hepatitis, hepatic decompensation, HIV disease progression and mortality, and changes of CD4+ count and plasma viral load (PVL) after initiation of highly active antiretroviral therapy (HAART) at the end of the study. The baseline CD4+ count, PVL and proportion of patients with AIDS-defining opportunistic illnesses (OI) at study entry were similar between patients with HCV co-infection and those without co-infection, but HCV-co-infected patients were older (39 versus 35 years, P = 0.01) and had a higher proportion of intravenous drug use (17.0% versus 0.8%, P < 0.001). After a total observation duration of 1137 patient-years (PY) (median, 791 days; range, 3-3053 days), the incidence of acute hepatitis in HCV-co-infected patients was 13.89 per 100 PY (95% confidence interval [CI], 13.31-14.49) and that in patients without co-infection was 6.39 per 100 PY (95% CI, 6.24-6.55 per 100 PY), with an adjusted odds ratio (OR) of 2.769 (95% CI, 1.652-4.640). At the end of the study, CD4+ count increased by 137 x 10(6) and 157 x 10(6)/L in patients with and without HCV co-infection, respectively, (P = 0.47). The proportions of achieving undetectable PVL (<400 copies/mL) after HAART was similar (76.7% versus 74.9%, P = 0.79). The adjusted OR for development of new AIDS-defining OI was 1.826 (95% CI, 0.738-4.522) in HCV-co-infected patients as compared with HCV- uninfected patients. The adjusted hazards ratio for death of HCV-co-infected patients when compared with those without co-infection was 0.781 (95% CI, 0.426-1.432). Our findings suggested that HCV co-infection was associated with a significantly higher risk for acute hepatitis in HIV-infected patients receiving antiretroviral therapy, but it had no adverse impact on virological, immunological and clinical responses to HAART and survival when compared with patients without HCV and HBV co-infection.     

HIV and hepatitis C virus co-infection

Since the decline in HIV-related morbidity and mortality after introduction of highly active antiretroviral therapy (HAART) in 1996, liver disease caused by chronic infection with hepatitis C virus (HCV) has become an increasingly important cause of morbidity and mortality among HIV-infected patients infected parenterally with HCV in more developed countries. A third of HIV-infected individuals in Europe and the USA have HCV co-infection. HIV accelerates HCV liver disease especially when HIV-associated immunodeficiency progresses. With the introduction of pegylated interferon in combination with ribavirin, greatly improved treatment options for patients with HIV and HCV co-infection have become available and have led to sustained virological response rates of up to 40%. Furthermore, recent cohort analyses have shown that immune reconstitution induced by HAART can improve the course of hepatitis C leading to a decline in liver-related mortality. However, patients with HCV co-infection are at increased risk of hepatotoxicity from HAART. Owing to the high rates of HIV and HCV co-infection worldwide, new improved treatment strategies and guidelines for the management of co-infection remain a major future goal.     

The influence of hepatitis C virus-human immunodeficiency virus co-infection on the appearance of liver enzyme elevation in people on high activity antiretroviral treatment

BACKGROUND: Liver enzyme elevation (LEE) as a consequence of HAART is a problem among patients with HIV-HCV co-infection. METHODS: In this retrospective study, 145 patients with HIV who were on HAART and who developed LEE grades 3 and 4 of the World Health Organization (WHO) were followed up. Basal ALT, alcohol consumption, and HCV and HBV co-infection were recorded. Comparisons were made between patients with and without HCV co-infection. RESULTS: Three patients without co-infection presented LEE grade 3 versus 38 with co-infection (104 episodes). An increase in basal ALT (RR: 1.01) and HCV co-infection (RR: 6.6) were the variables associated with LEE grade 3. The number of days that HAART had to be withdrawn due to LEE was 58.15 and 4.85 in subjects with and without co-infection, respectively (p=0.024). CONCLUSION: Patients with HCV-HIV co-infection have more episodes of LEE and must go longer without HAART than people without co-infection.     

Highly active antiretroviral therapy and allogeneic CD34(+) peripheral blood progenitor cells transplantation in an HIV/HCV coinfected patient with acute myeloid leukemia

OBJECTIVE: To evaluate the safety, feasibility, and efficacy of allogeneic stem cell transplantation (SCT) for acute myelogenous leukemia (AML) in a young female coinfected by HIV and HCV undergoing highly active antiretroviral therapy (HAART). PATIENTS AND METHODS: A 33-year-old female HIV(+), HCV(+) in complete remission after standard chemotherapy was submitted to CD34(+) selected allogeneic transplantation from her HLA-identical HIV(-) brother after myeloablative regimen. HAART was started before transplantation, achieving a reduction of HIV load to undetectable levels. GVHD prophylaxis was carried out with cyclosporine A alone. RESULTS: The patient achieved prompt and durable engraftment with acute GVHD grade II easily managed with steroids; CMV prophylaxis was prolonged, no clinically relevant infectious complications developed early after transplantation and during follow-up. HIV viremia was controlled by HAART although medication adherence was reduced early after transplantation and required drug adjustment. There was a gradual recovery of immune cells with normal CD4-cell count 39 months after engraftment, a significantly higher level than before transplantation. At 39 months post-transplantation follow-up the patient is alive and in continuous complete remission with undetectable levels of plasma HIV RNA on HAART. CONCLUSION: The introduction of HAART has recently changed the paradigm of AIDS, allowing the control of HIV replication, the reduction of opportunistic infections, and the overall improvement of survival. One may therefore reconsider the current exclusion of patients with AIDS and a concomitant lethal malignancy from programs of high-dose chemotherapy and stem cell transplantation, as suggested by this report.     

人类免疫缺陷病毒感染者混合感染丙型和乙型肝炎病毒后对高效抗逆转录病毒治疗疗效的影响

目的 观察HIV感染者合并HCV和HBV感染后对高效抗逆转录病毒治疗(HAART)疗效的影响.方法 对某地区HIV、HCV共感染患者166例(HIV+HCV组),HIV、HCV和HBV混合感染患者23例(H1V+HCV+HBV组)及单纯HIV感染者178例,给予1年的HAART治疗,观察3组患者病毒学反应、免疫学反应和肝功能动态变化.以流式细胞仪检测外周血CD4+T淋巴细胞;实时PCR定量检测HCV、HIV和HBV病毒载量.结果 单纯HIV感染组、HIV+HCV+HBV组和HIV+HCV组经HAART 1年后,HIV病毒载量分别由治疗前(6.78±1.08)、(6.23±1.34)、(6.54±1.23)lg拷贝/ml下降至(0.53±0.15)、(0.67±0.16)、(0.43±0.11)lg拷贝/ml(P值均＜0.001).CD4+T淋巴细胞计数分别由治疗前的(197±127)、(184±113)、(213±143)个/μl上升至(382±74)、(383±70)、(378±76)个/μl(P值均＜0.001).3组之间各时间点CD4+T淋巴细胞、HIV病毒载量差异无统计学意义.3组患者ALT、AST、总胆红素治疗前后无显著变化,相同时间点组间比较差异无统计学意义.HAART前后,HCV病毒载量差异无统计学意义.结论 HIV感染者混合感染HBV和(或)HCV,不影响HAART的疗效;HAART对HCV复制无抑制作用.     

Hepatitis C and HIV co—infection：a review

Co-infection with hepatitis C virus and human immunodeficiency virus is common in certain populations. Among HCV (+) persons, 10 % are also HIV (+), and among HIV (+) persons, 25 % are also HCV (+). Many studies have shown that in intravenous drug users, co-infection prevalence can be as high as 90-95 %. There is increasing evidence supporting the concept that people infected with HIV have a much more rapid course of their hepatitis C infection. Treatment of co-infection is often challenging because highly active anti-retroviral therapy (HAART) therapy is frequently hepatotoxic, especially in the presence of HCV. The purpose of this review is to describe the effects that HIV has on hepatitis C, the effects that hepatitis C has on HIV, and the treatment options in this challenging population.     

Natural history of anemia associated with interferon/ribavirin therapy for patients with HIV/HCV coinfection

The natural history of anemia related to interferon/ribavirin (IFN/RBV) treatment in patients with human immunodeficiency virus/hepatitis C virus (HIV/HCV) coinfection is not completely understood. The current 8-week, multicenter, observational study characterized anemia over the course of HCV treatment in patients with HIV/HCV coinfection. Eligible HIV/HCV coinfected patients were receiving care in community-based and academic institutions and were on stable antiretroviral therapy and initiating IFN/RBV therapy. Hb, sEPO, reticulocytes, transfusions, laboratory values (e.g., total bilirubin), and IFN and RBV dosages were monitored weekly. Ninety-one patients were analyzed (mean age, 46 years; 71% on HAART) and 53 patients completed the study. Mean Hb decreased significantly (5.0 g/dl) within 1 week of initiating IFN/RBV therapy (p = 0.0002); Hb nadir occurred at a median of 37 days. Maximum Hb decreases of > or =2.0 g/dl occurred in 56 (62%) patients and > or =3.0 g/dl occurred in 45 (49%) patients. Reticulocyte count increased within the first 2 weeks and sEPO peaked at week 3. Mean increase from baseline to week 2 in reticulocyte count and sEPO, respectively, was 1.3% (n = 74) and 45.0 mIU/ml (n = 80) (p < 0.0001 for each parameter), and from baseline to week 8 was 0.9% (n = 48) and 41.0 mIU/ml (n = 52) (p < or = 0.0001 for each parameter). Adverse events (AEs) were the most common reason for study discontinuation (66% of discontinuing patients). Among the 25 patients who discontinued due to AEs, 84% discontinued due to anemia (n = 21). Significant decreases in Hb were observed in HIV/HCV-coinfected patients within 1 week of initiating IFN/RBV therapy. sEPO and reticulocyte increases were blunted in response to anemia; Hb levels did not return to baseline values and anemia was a frequent reason for discontinuing the study.     

Hepatitis C virus infection, HIV co-infection, and associated risk among injecting drug users in Togliatti, Russia

The objective of this study was to estimate the prevalence of hepatitis C virus (HCV) infection and co-infection with HIV among injecting drug users (IDUs) in Togliatti City, Russia. Unlinked anonymous cross-sectional survey of IDUs recruited from community settings, with oral fluid sample collection for HCV and HIV antibody (anti-HCV, anti-HIV) testing, was carried out. The anti-HCV prevalence was 87% (357/411), anti-HIV prevalence 56% (234/418), and 93% (214/230) of HIV-positive IDUs were co-infected with HCV. Only 23% (94/411) of those HCV positive self-reported as such. In an adjusted model, increased odds of HCV positivity were associated with needle and syringe, as well as injecting paraphernalia sharing in the last four weeks. IDUs injecting more than once with the same needle also had raised odds. There were no marked associations between HCV positivity and the duration of injecting or age group. Almost all IDUs were HCV positive, and almost all HIV-positive IDUs were HCV co-infected. There is an urgent need to maximize syringe distribution coverage, develop health promotion targeting HCV prevention for IDUs, and improve access among IDUs to treatments for HIV and HCV infection.     

Immunologic dynamics in hemophiliac patients infected with hepatitis C virus and human immunodeficiency virus: influence of antiretroviral therapy

Infection with hepatitis C virus (HCV) or human immunodeficiency virus (HIV) or both is common in hemophiliac patients due to putative transmission through clotting factor concentrates. Recently, highly active antiretroviral therapy (HAART) has been found to markedly improve viremia and immunologic parameters in patients infected with HIV. This report considers interactions between these viral infections, the immune system, and antiretroviral therapy. A total of 130 male hemophiliac patients were grouped according to type of viremia (HCV, HIV, both, or neither). Along with 30 healthy men age-matched to viremic patients, these groups were compared with respect to viral load and immunologic parameters. Thirty-five patients treated as above for HIV were serially followed up. HCV infection was associated with reduced peripheral B-cell and CD4(+)-cell counts and with increased serum IgG and IgM levels, whereas HIV infection was associated with reduced peripheral CD4(+)-cell counts and increased serum IgG and IgA levels. In patients with both viruses, HCV and HIV RNA load correlated inversely with peripheral B-cell and CD4(+)-cell counts, respectively. HAART reduced levels of both viruses in the blood. Of the 25 patients with both viruses, HAART eliminated HCV in 2. In conclusion, immunologic dynamics differed between hemophiliac patients infected with HCV, HIV, or both. The relative dynamics of HCV viral load, peripheral B-cell count, and serum IgM level were similar to those of HIV viral load, CD4(+)-cell count, and serum IgA. (Blood. 2000;96:4293-4299)     

HIV/AIDS病人合并HCV感染对HAART不良反应的影响

目的研究合并丙型肝炎病毒(HCV)感染,对艾滋病病毒(HIV)/艾滋病(AIDS)病人接受高效抗反转录病毒治疗(HAART)后,不良反应发生的影响,为HIV/AIDS合并HCV感染的综合治疗提供依据。方法前瞻性观察167例合并HCV感染的HIV/AIDS患者(HIV/HCV组),接受HAART治疗2-5年出现不良反应的类型、频率、严重程度,以同期264例HIV/AIDS患者(HIV组)作为对照组。结果 167例合并HCV感染的HIV/AIDS患者中,163例(97.6%)出现疲乏症状,163例(97.6%)发生胃肠道反应,107例(64.1%)出现肝功能异常,98例(58.7%)出现血脂升高,83例(49.7%)出现药物性皮疹,56例(33.5%)出现腹泻,52例(31.1%)出现贫血。与HIV组相比,HIV/HCV组出现肝功能损害的频率较高(P<0.05),但严重程度无明显差异(P>0.05),其余不良反应发生的类型、频率及严重程度无显著性差异(P>0.05)。结论 HIV/AIDS病人在HAART过程中可发生多种不良反应,合并HCV感染时更容易发生肝功能损害,选择HAART方案时应尽量选择肝毒性少的药物。     

Prevalence of occult hepatitis B & C in HIV patients infected through sexual transmission.

BACKGROUND: Prevalence of Hepatitis B virus (HBV) and Hepatitis C virus (HCV) markers including active and occult infection has not been described in diverse cohorts among HIV-infected patients in India. Earlier studies have explained the role of HBV/HCV co-infection in cohorts of injection drug users (IDUs) but the sexual co-transmission of HBV/ HCV is not completely understood. OBJECTIVE: The objective of this study was to assess the prevalence of occult HBV & HCV infection in HIV positive sexually acquired transmission risk group. MATERIALS AND METHODS: 58 sexually acquired HIV positive patients were taken up for the study of occult HBV/HCV co-infection. Data on demographics, sexual behaviour, sexually transmitted diseases (STD), medical history, laboratory tests viz., serum ALT and CD4 count were recorded. HBV serology included HBsAg, anti HBs, IgG anti HBc and HBV DNA (PCR). HCV serology included anti HCV & HCV RNA (RT-PCR). RESULTS: Occult HBV infection (HBV DNA) was observed in 12.2% (7/58 with HBsAg -ve and IgG anti HBc +ve subjects) while an overall prevalence of HBV DNA was 13.7% (12% occult & 1.7% in HBsAg+ve patients). Out of 58 HIV positive patients 29.3% demonstrated reactivity for any marker of past or current HBV infection. (HBsAg 1.7%, anti HBs 10.3% anti HBc IgG 17.2%). 4/58 (6.8%) revealed anti HCV positivity along with HCV RNA positivity by RT-PCR while 6/58 (10.3%) individuals revealed an occult HCV infection (anti HCV negative). The overall HCV RNA prevalence was 17.2%. 2 out of 58 (3.4%) individuals were positive for occult infection of both HBV DNA & HCV RNA (Triple infection HIV/HBV/ HCV). The HBV/HCV co-infected group (n = 18) showed a significantly high ALT (114.3 + 12.3 U/I) & low CD4 count (202.5 + 33.7 cells/mm3). The percent prevalence of HBV/ HCV co-infection was higher in the illiterate group, in men less than 30 years of age, and in those who were married and exhibited polygamous activity. CONCLUSIONS: The study demonstrated that in HIV infected patients testing only serological viral markers like HBsAg, antiHBcIgG & anti HCV, fails to identify the true prevalence of co-infection with HBV & HCV. Qualitative PCR for HBV DNA & HCV RNA detects co-infection in patients who are negative for serological markers. Also, in subjects who had only a sexual risk factor for parenterally transmitted infections, HIV may enhance the sexual transmission of HBV and HCV.     

Is the increased risk of liver enzyme elevation in patients co-infected with HIV and hepatitis virus greater in those taking antiretroviral therapy?

OBJECTIVES: To investigate if the risk of liver enzyme elevation (LEE) in HIV/hepatitis B or C (HBV, HCV) co-infection is altered by HAART (two or more drugs). METHODS: Analysis comprised HIV-positive patients in the ICoNA study without acute hepatitis who had >or= 1 positive HCV antibody test and > 1 positive HBV surface antigen test. LEE was defined as > 5x baseline alanine aminotransferase (ALT) or > 3.5x baseline if the baseline was > 40 IU/l. Analysis used Poisson regression with generalized estimating equation correction to examine HBV or HCV co-infection, use of HAART, baseline ALT and demographics as LEE predictors. RESULTS: Of the 5272 patients, 47.6% were co-infected with HCV/HBV; 29.9% were female and 39% were intravenous drug users. There were 275 episodes of LEE during 18 259 person-years follow up. Taking HAART did not significantly increase risk of LEE [adjusted relative risk (RR), 1.19; 95% confidence interval (CI), 0.81-1.75; P = 0.37]. Co-infection increased the risk of LEE (adjusted RR, 5.07; 95% CI, 3.47-7.48; P < 0.001), with no significant differences if taking HAART (adjusted RR, 4.99; 95% CI, 3.38-7.37) or not (adjusted RR, 6.02; 95% CI, 2.02-17.98) (P = 0.74 for interaction). Females were at lower risk of LEE than males (adjusted RR, 0.59; 95% CI, 0.42-0.83; P = 0.02). CONCLUSIONS: HIV and HBV/HCV co-infection per se is associated with increased risk of LEE that is not modified by HAART. The recommendation for caution in HAART use in co-infected patients, simply based on a high rate of LEE in people on therapy, may be questionable.     

Therapy of chronic hepatitis C in the setting of HIV co-infection

Hepatitis C virus (HCV) and human immunodeficiency virus (HIV) infections are major health problems world-wide. As both viruses partially share routes of transmission, co-infection is common. This is especially the case in patients infected through intravenous drug use. It has been shown that HIV accelerates HCV progression to cirrhosis. The influence of HCV infection on the natural history of HIV disease remains highly controversial. It is also known that HCV co-infection increases the risk of hepatotoxicity of Highly Active Antiretroviral Therapy (HAART). These considerations as well as the improved survival of HIV patients due to HAART leads to increasing numbers of patients undergoing assessment and treatment of HCV infection. HCV treatment should be considered in stable HIV disease. Recent data indicate that HCV treatment schedules should be similar in co-infected and HCV mono-infected individuals, with pegylated interferon combined with ribavirin. For all treatment regimens published, coinfected patients had a lower sustained viral response rate compared to HCV mono-infected patients. Similar predictive factors determine the success rate. The effect of prolonging therapy to 12 months in genotype 2/3 and to 18 months in early viral responders with genotypes 1/4 needs to be assessed in further studies.     

Could anti-HCV treatment prevent recurrence of hepatocellular carcinoma in HIV-infected patients? Two case reports

Highly active antiretroviral therapy (HAART) has proven long-term efficacy in human immunodeficiency virus (HIV) infection. Combination therapy with pegylated interferon and ribavirin has become the standard of care in patients with both hepatitis C virus (HCV) chronic hepatitis and HIV/HCV co-infection. Data on the safety and efficacy of combination therapy in chronic hepatitis C patients with hepatocellular carcinoma (HCC) is scarce and even more so in HIV/HCV co-infected subjects. We report the successful administration of both HAART and anti-HCV therapies in two HIV/HCV co-infected patients after HCC eradication. These encouraging results might argue for the feasibility of an aggressive approach in the management of co-infected patients with HCC.     

Assessment of the Factors Involving in the Development of Hypothyroidism in HIV-infected Patients: A Case-Control Study

Abstract Objectives: Increased prevalence of thyroid dysfunction has been reported in HIV-infected patients, and recent studies have shown hypothyroidism as the most common thyroid function abnormality in this population, especially after treatment with antiretroviral drugs (HAART). The aim of this study is to assess risk factors of hypothyroidism in HIVinfected patients in Iran. Design: This case-control study was conducted among 15 hypothyroid (cases) and 70 euthyroid (control group) HIV-infected outpatients. Serum Free T4, Free T3, and TSH levels were measured, and data on age, sex, body mass index, opium addiction or injection of illicit drugs, duration of HIV infection and HAART, disease stage, CD4-cell count, opportunistic infection (OI) or malignancy, HCV co-infection, and drug use were collected. Results: We found no association between hypothyroidism in HIV-infected patients and any parameters measured, and P value was not significant for receipt of HAART (0.141), CD4-cell count (0.094), duration of HIV infection (0.474), duration of HAART (0.418), HCV co-infection (0.146), OI (0.566), or receipt of rifampin (0.816). Conclusion: In this study, age, sex, HAART, mean CD4- cell count, duration of HIV infection, HCV co-infection, and OI were not significant risk factors of hypothyroidism in HIV-infected patients. The occurrence of hypothyroidism may be related to other factors or HIV infection itself. Therefore, hypothyroidism should be considered in all HIV-infected patients.     

Impact of human immunodeficiency virus infection on the course of hepatitis C virus infection： A meta-analysis

AIM： TO analyze the influence of human immunodeficiency virus （HIV） infection on the course of hepatitis C virus （HCV） infection. METHODS： We performed a meta-analysis to quantify the effect of HIV co-infection on progressive liver disease in patients with HCV infection. Published studies in the English or Chinese-language medical literature involving cohorts of HIV-negative and -positive patients coinfected with HCV were obtained by searching the PUBMED, EMBASE and CBM. Data were extracted independently from relevant studies by 2 investigators and used in a fixed-effect meta analysis to determine the difference in the course of HCV infection in the 2 groups. RESULTS： Twenty-nine trails involving 16750 patients were identified including the outcome of histological fibrosis or cirrhosis or de-compensated liver disease or hepatocellular carcinoma or death. These studies yielded a combined adjusted odds ratio （OR） of 3.40 [95% confidence interval （CI） = 2.45 and 4.73]. Of note, studies that examined histological fibrosis/ cirrhosis, decompensated liver disease, hepatocellular carcinoma or death had a pooled OR of 1.47 （95% CI = 1.27 and 1.70）, 5.45 （95% CI = 2.54 and 11.71）, 0.76 （95% CI = 0.50 and 1.14）, and 3.60 （95% CI = 3.12 and 4.15）, respectively. CONCLUSION： Without highly active antiretroviral therapies （HAART）, HIV accelerates HCV disease progression, including death, histological fibrosis/ cirrhosis and decompensated liver disease. However, the rate of hepatocellular carcinoma is similar in persons who had HCV infection and were positive for HIV or negative for HIV.     

Neurocognitive functioning and HAART in HIV and hepatitis C virus co-infection

OBJECTIVES: This study examined the effects of HAART on neurocognitive functioning in persons with hepatitis C virus (HCV) and HIV co-infection. DESIGN: A prospective study examining neurocognitive performance before and after HAART initiation. METHOD: Participant groups included a mono-infected group (45 HIV+/HCV- participants) and a co-infected group (20 HIV+/HCV+ participants). A neuropsychological battery (attention/concentration, psychomotor speed, executive functioning, verbal memory, visual memory, fine motor, and gross motor functioning) was used to evaluate all participants. After 6 months of HAART, 31 HIV+ mono-infected and 13 HCV+/HIV+ co-infected participants were reevaluated. RESULTS: Neurocognitive functioning by domain revealed significantly worse performance in the co-infected group when compared to the monoinfected group on domains of visual memory and fine motor functioning. Assessment of neurocognitive functioning after antiretroviral therapy revealed that the co-infected group was no longer performing worse than the monoinfected group. CONCLUSIONS: The findings of the current study suggest that persons with HCV+/HIV+ co-infection may have greater neurocognitive declines than persons with HIV infection alone. HCV+/HIV+ co-infection may accelerate the progression of HIV related neurocognitive decline.