Short communication: impact of hepatitis C viral clearance on CD4+ T-lymphocyte course in HIV/HCV-coinfected patients treated with pegylated interferon plus ribavirin

The long-term impact of pegylated-interferon plus ribavirin (Peg-IFN-RBV) treatment outcome on CD4 T cell course in patients coinfected with human immunodeficiency virus (HIV) and hepatitis C virus (HCV) is unknown. The aim of this study was to investigate the impact of HCV-RNA clearance by standard anti-HCV therapy on long-term CD4 cells recovery in HIV/HCV patients on successful combined antiretroviral therapy (cART). We retrospectively enrolled HIV/HCV-coinfected patients on stable cART, treated with Peg-IFN-RBV between 2005 and 2009. CD4(+) T cell counts were registered at baseline (pre-Peg-IFN-RBV), after 6, 12, and 24 months of follow-up from therapy discontinuation. Multiple linear regression analysis was performed to identify independent predictors of CD4(+) T cell change following the anti-HCV treatment outcome. Of the 116 patients enrolled, 54 (46.6%) reached a sustained virological response (SVR) and 62 (53.4%) did not. Throughout a median follow-up of 24 months, the SVR group showed a mean annual increase in CD4(+) T cell from baseline of 84 cells/μl at 1 year and of a further 38 cells/μl within the second year (p=0.01, 0.001, respectively). A nonsignificant mean increase of 77 cells/μl occurred in the non-SVR group within month 24 (p=0.06). Variables associated with greater CD4 gains were higher nadir and lower pre-interferon CD4 counts, and lower body mass index (BMI). The achievement of SVR was not significantly associated with the change in CD4(+) count. The clearance of HCV replication did not affect the CD4(+) changes after Peg-IFN-RBV therapy in coinfected patients on efficient cART. Liver fibrosis and higher BMI were negative determinants of immune recovery.     

Cognitive and affective disorders associated to HIV infection in the HAART era: findings from the NeuroICONA study. Cognitive impairment and depression in HIV/AIDS. The NeuroICONA study

OBJECTIVE: To assess the natural story of HIV-associated affective and cognitive disorders and the relationship with clinical, pharmacological, immunological and behavioural factors. METHOD: A total of 395 HIV-positive patients, naive to Highly Active Antirectroviral therapy (HAART), with no severe psychiatric disorders have been enrolled in the Neuro-ICONA Study. All participants were administered a comprehensive data collection instrument including an addiction behaviour survey, a medical problem list, a psychiatric assessment, a validated neuropsychological test battery. RESULTS: The global prevalence of cognitive impairment and of prominent depressive symptomatology were 17.9 and 15.5%, respectively. A significant difference in the prevalence of prominent depressive symptomatology was observed between patients in HAART and those not taking HAART(14.1 vs. 23.8%; P = 0.05). CONCLUSION: Depressive and cognitive disorders affect a substantial proportion of HIV-seropositive subjects. The prevalence of prominent depressive symptomatology appears to significantly vary in relationship to the therapeutic protocol.     

Yersinia pseudotuberculosis septicemia and HIV

Two cases of community-acquired septicemia caused by serotype-O1 Yersinia pseudotuberculosis were diagnosed in middle-aged, HIV-positive, immunodeficient patients during an 8-month period. Bacterial isolates were genetically indistinguishable, but no epidemiologic link between the 2 patients was established. HIV-related immunosuppression should be regarded as a risk factor for Y. pseudotuberculosis septicemia.     

Human immunodeficiency virus infection and acquired immunodeficiency syndrome dementia complex: role of cells of monocyte-macrophage lineage

The entry of human immunodeficiency virus (HIV) into the central nervous system (CNS) causes both the establishment of a lifelong viral reservoir in the brain and symptoms of neurological dysfunction that have an AIDS dementia complex (ADC) clinical appearance. Neurological dysfunction in ADC patients still remains an unresolved problem. However, ADC pathogenesis may be a multistep process that starts with HIV invasion of CNS by crossing the blood-brain barrier (BBB). It progresses by developing a chronic inflammatory status that can cause dysfunction in neurons and astrocytes that result in apoptotic death. Monocytes-macrophages (M/M) may play an important role by concealing the HIV transfer across the BBB. Furthermore, HIV-infected M/M could produce and release neurotoxic factors. In this review the main mediators and cells involved in pathogenesis and development of ADC are highlighted. A better understanding of the mechanisms involved in this process may help in a successful therapeutic approach to the neuropathogenesis of HIV infection.