HIV Co-infected Individuals Research Articles

Prevalence of GB virus type C in urban Americans infected with human immunodeficiency virus type 1

GBV-C virus infection has been linked to improved clinical outcome in HIV-1 co-infected individuals. The epidemiology of GBV-C has, thus far, been limited to the gay male, HIV+ population. Here we describe the prevalence of antibodies against GBV-C envelope glycoprotein E2 and GBV-C viremia in an HIV+ inner city population. This study group is predominantly African-American; 41% of the participants are women. The major risk factor for HIV infection is intravenous drug use. Overall, 56% of the study population had evidence of current or past infection with GBV-C. GBV-C exposure was not associated with hepatitis C virus infection. The group of participants, who had GBV-C viremia and anti-E2 antibodies, had high percentage of patients with an undetectable HIV-1 viral load. These data provide increased insight into the prevalence of GBV-C co-infection in the HIV epidemic in this understudied population.

571 Gene expression profiles in HCV/HIV coinfection: Class prediction analyses prior to treatment predicts outcome of HCV therapy among HIV co-infected individuals

571 Gene expression profiles in HCV/HIV coinfection: Class prediction analyses prior to treatment predicts outcome of HCV therapy among HIV co-infected individuals

Serious ophthalmic pathology compromising vision in HCV/HIV co-infected patients treated with peginterferon alpha-2b and ribavirin.

To characterize the ocular changes associated with peginterferon alpha 2b (peg-IFN alpha-2b) and ribavirin therapy for chronic hepatitis C infection in HIV co-infected individuals. A prospective, open-label trial treating HIV/hepatitis C (HCV) co-infected individuals with peg-IFN alpha-2b and ribavirin at the Warren Grant Magnusson Clinical Center, National Institutes of Health, Bethesda, Maryland, USA. Twenty-three patients with a high mean CD4+ T-cell count were treated with peg-IFN alpha-2b and ribavirin and followed for 40 to 88 weeks. Ophthalmologic evaluations including visual acuity, visual field testing, color vision examination and indirect ophthalmoscopy were performed at baseline and every 3 months. Eight of the 23 patients (35%) developed ophthalmologic pathology, including cotton wool spots, cataracts, and two patients developed decreased color vision. These two patients regained their color vision, one after cessation of anti-HCV therapy. Although retinal pathologies have been reported in patients treated with interferon-alpha, they have not been reported during peg-IFN alpha-2b therapy nor in HIV/HCV co-infected patients. The incidence of serious ocular pathology associated with anti-HCV therapy may be very high and is probably associated with peg-IFN alpha-2b. Increased monitoring of patients treated with peg-IFN alpha-2b for retinal and visual changes is warranted.

Haemolytic anaemia after nucleotide antiretroviral treatment discontinuation in a chronic hepatitis B-virus co-infected AIDS patient

Haemolytic anaemia after nucleotide antiretroviral treatment discontinuation in a chronic hepatitis B-virus co-infected AIDS patient

Human immunodeficiency virus facilitates infection/replication of hepatitis C virus in native human macrophages

AbstractHepatitis C virus (HCV) was found to replicate in monocytes/macrophages particularly in patients with human immunodeficiency virus type 1 (HIV-1) infection. This study was undertaken to determine whether HIV facilitates HCV infection of native human macrophages in vitro. Monocytes/macrophages were collected from healthy donors, infected with HIV M-tropic molecular clone, and then exposed to HCV-positive sera. Presence of positive and negative HCV RNA strands was determined with a novel strand-specific quantitative real-time reverse transcription–polymerase chain reaction (RT-PCR). Preceding as well as near-simultaneous infection with HIV made the macrophages more susceptible to infection with HCV; in particular, an HCV RNA–negative strand was detectable almost exclusively in the setting of concomitant HIV infection. Furthermore, HCV RNAload correlated with HIV replication level in the early stage of infection. The ratio of positive to negative strand in macrophages was lower than in control liver samples. HIV infection was also found to facilitate HCV replication in a Daudi B-cell line with engineered CD4 expression. It seems that HIV infection can facilitate replication of HCV in monocytes/macrophages either by rendering cells more susceptible to HCV infection or by increasing HCV replication. This could explain the presence of extrahepatic HCV replication in HIV-coinfected individuals.

Management of hepatitis B and C in HIV co-infected patients.

Morbidity and mortality from co-morbid hepatitis B (HBV) and hepatitis C (HCV) infection in HIV co-infected patients are increasing; hence, the management of HIV and HBV or HCV co-infected individuals is now one of the most challenging clinical management issues. Less than 10% of all HIV-infected patients show markers of chronic HBV infection. Hepatitis B in HIV co-infected patients is characterized by high levels of HBV replication and a high risk for cirrhosis. Treatment of HBV with lamivudine (3TC) remains the best treatment option at this time. Initial results of studies of adefovir or tenofovir, however, demonstrate good antiretroviral efficacy, even in patients with 3TC-resistant HBV. In Europe, it is estimated that approximately 30% of HIV-infected individuals are co-infected with HCV. HIV accelerates HCV liver disease especially when HIV-associated immune deficiency progresses. Within 10-15 years of initial HCV infection, 15-25% of patients who are co-infected with HIV develop cirrhosis compared with 2-6% of patients without HIV infection. With the introduction of pegylated interferon in combination with ribavirin, promising treatment options have become available for HIV/HCV co-infected patients leading to early virological response rates of approximately 50%. The high number of HIV/HCV and HIV/HBV co-infections, as well as the much more unfavorable course of HBV and HCV in these patients, underlines the need to establish treatment strategies for HBV and HCV in HIV co-infected individuals.

Serologic Diagnosis of Tuberculosis Using a Simple Commercial Multiantigen Assay

Seven primary health clinics and a pulmonary disease specialty clinic in Rio de Janeiro City, Brazil. To evaluate a commercial immunochromatographic test kit (ICT Tuberculosis; AMRAD-ICT; Sidney, Australia) employing five recombinant Mycobacterium tuberculosis proteins for the detection of pulmonary tuberculosis (TB). Serology test results were compared with duplicate sputum microscopy and culture in 277 patients with symptomatic pulmonary disease (243 with pulmonary TB and 34 with nontuberculous disease). An additional 110 healthy control subjects were also tested. The serology test was simple and rapid to perform and detected 64.2% of smear-positive and 46.3% of smear-negative TB patients overall. HIV co-infection was present in 15.3% of TB patients, and serology was much less sensitive (overall 27.6%) in this small group, as was microscopy (13.8%). Specificity of the serology test was 100% in healthy control subjects and 85.2% in the small number of control patients with pulmonary disease, including those with prior TB. Combined with microscopy, serology detected 72.8% of TB patients. Depending on the population studied, multiantigen serologic tests for TB may be as sensitive as microscopy, but detect a different and overlapping subset of patients. The use of multiple antigens in this kit increased test sensitivity without significant loss of specificity. Bacille Calmette-Guérin vaccination and tuberculin sensitivity did not affect serology results. Estimating specificity in clinical use will require testing a much larger cohort of symptomatic patients with nontuberculous disease. The TB diagnostic performance of this group of antigens in HIV co-infected individuals was poor.

In vitro production of type 1 and type 2 cytokines by peripheral blood mononuclear cells from subjects coinfected with human immunodeficiency virus and Leishmania infantum.

To explore the type 1 and type 2 cytokine profile in cases coinfected with human immunodeficiency virus (HIV) and Leishmania infantum, production of interleukin-4 (IL-4), interleukin-10 (IL-10), interferon-gamma (IFN-gamma), and interleukin-2 receptor (IL-2R) was investigated in mitogen-stimulated and unstimulated peripheral blood mononuclear cell cultures from eight HIV/Leishmania coinfected subjects matched with eight anti-HIV-positive subjects with no evidence of Leishmania coinfection. Levels of IL-4 and IL-2R increased significantly from the baseline levels in the peripheral blood mononuclear cell supernatants of HIV/Leishmania coinfected subjects following stimulation with phytohemoagglutin, whereas the postchallenge concentration of IFN-gamma was significantly increased in the HIV-infected group. The levels of IL-4 and IL-10 were significantly higher in the HIV/Leishmania group throughout evaluation. Post-stimulation IFN-gamma production was significantly higher in the HIV-positive group in comparison with that of the HIV-Leishmania coinfected subjects. These observations support the notion that a Th2 cytokine response is present during a Leishmania infection, even among HIV-coinfected individuals.