ObjectivesDifferent immune alterations have been described in HIV-infected patients with visceral leishmaniasis (VL). We aimed to identify the immunological factors involved in the lack of immunological recovery and VL relapses in HIV-infected patients with VL, by comparison with other HIV-infected patients. MethodsWe carried out a cross-sectional study of 55 patients receiving suppressive combination antiretroviral therapy (cART) for at least 1 year: nine with previous relapsing VL, 20 with an immunodiscordant response (IDR) to cART (CD4 count < 200 cells/μL) and no previous VL, and 26 with a concordant response (CR) to cART (CD4 count > 350 cells/μL) without VL. Immunosenescence was investigated by analysing CD57 + CD28− levels, immune activation by analysing CD38 + HLA-DR + levels, inflammation by analysing interleukin (IL)-6 levels, and microbial translocation by analysing lipopolysaccharide (LPS) and soluble CD14 (sCD14) levels. ResultsIn VL patients, the median time since VL diagnosis was 42 months, and all patients had had at least one relapse despite suppressive cART for a median time of 43 months. Patients with previously diagnosed VL had a higher CD8 T-cell activation level (P < 0.001) than those with IDR. Also, levels of IL-6, LPS and especially sCD14, associated with bacterial translocation and additional monocyte activation, were significantly increased in patients with previous VL compared with patients with IDR (P = 0.048, P = 0.049 and P < 0.001, respectively). In addition, patients with previous VL had higher levels of CD8 T-cell senescence. Notably, the levels of immune activation and inflammation in patients with previous VL were not related to the time of VL diagnosis, the number of VL relapses, or hepatitis C virus (HCV) coinfection. ConclusionsOur data demonstrate that VL patients had an even worse immunological status than patients with IDR, which was probably associated with increased microbial translocation and additional monocyte/macrophage activation. These data explain the observed lack of immunological recovery and the occurrence of VL relapses in HIV-infected patients with previous VL. Specifically, visceral leishmaniasis (VL) is an infectious disease caused mainly by Leishmania donovani and Leishmania infantum (Leishmania chagasi), intracellular protozoans that infect macrophage cell lineages from lymphoid organs. It is a common coinfection in HIV-1-infected individuals in the Mediterranean basin, including Spain, with a prevalence of up to 9%. VL/HIV-1 coinfection is characterized by significantly lower cure rates, higher drug toxicity, higher relapse rates, and higher mortality rates (nearly 50%) than those for non-HIV-1-infected individuals with VL [5,6].While cART has been shown to decrease the incidence of leishmaniasis in HIV-1-infected patients, it does not seem to prevent the appearance of frequent relapses in patients previously diagnosed and largely pretreated with antiretrovirals [7][8][9], demonstrating the persistence of the parasite in different cell lines. Moreover, ...

Patients' beliefs and satisfaction with therapy influence the durability of the first antiretroviral regimen. These patient-related factors modulate the impact of mild adverse events, and could explain differences in the rate of discontinuation.

Myeloradiculitis is a rare neurological complication of herpes simplex type 2 (HSV-2) infection, frequently associated with a fatal outcome. Among patients with HIV infection, HSV-2 myeloradiculitis has occasionally been reported, always associated with advanced immunosuppression and AIDS. We report a patient with HIV infection but no history of previous opportunistic infections, who developed sacral myeloradiculitis immediately after an episode of genital herpes. Magnetic resonance imaging with gadolinium showed necrotizing myelitis in the conus medullaris and enhancement of sacral roots. CD4 lymphocyte count was 530/mm3. Other possible causes of myeloradiculitis in HIV-infected patients were appropriately excluded. Acyclovir therapy resulted in partial clinical improvement. This report shows that myeloradiculitis as a complication of genital herpes may occur in the early stages of HIV infection and may have a favourable outcome with antiviral treatment.

ObjectivesTo determine the effect of food on the antiviral activity of enteric-coated (EC) capsules of didanosine (ddI). MethodsWe conducted a pilot, randomized, open-label study of 28-day ddI-EC capsules monotherapyadministered in a fasted state (group 1, n 5 11) or with food (group 2, n 5 10) to treatment-naïve chronically HIV-1-infected individuals. To assess the antiviral efficacy, HIV-1 RNA was determined at baseline, day 3, day 7 and weekly thereafter. The area under the HIV-1 RNA curve minus baseline weighted by time (AUCMB/day) was calculated. ResultsMean baseline HIV-1 RNA was 4.2 log 10 copies/mL in group 1 and 3.8 log 10 copies/mL in group 2. After 28 days, the mean HIV-1 RNA reduction was 0.99 log 10 copies/mL [95% confidence interval (CI) 0.45-1.53] for group 1 and 0.89 log 10 copies/mL (95% CI 0.38-1.40) for group 2. AUCMB/day values were 0.775 log 10 copies/mL (95% CI 0.33-1.22) and 0.774 log 10 copies/mL (95% CI 0.48-1.07), respectively, showing no difference in the rate of decrease of HIV-1 RNA (P 5 0.995). Mean ddI plasma levels at day 28 were 0.0234 mg/L for group 1 and 0.0227 mg/L for group 2 (P 5 0.96). ConclusionsIn this pilot study, the administration of food did not have any significant effect on the antiviral activity of ddI-EC capsules.

7‐11 November 2010, Tenth International Congress on Drug Therapy in HIV Infection, Glasgow, UK