Introduction: Prior studies assessing sex differences correlated with the levels of human immunodeficiency virus (HIV) RNA and absolute CD4 cell count in adults and children, treated

Previous studies of our team have shown that Romanian teenagers horizontally infected with HIV in early childhood, have a high prevalence of HBV co-infection (78.3% being anti-HBc positive vs. 21.8% of age-matched HIVnegative controls). Our aim was to investigate the frequency of mutations and variables potentially associated with an increased risk of liver disease evolution in HIV/ HBV co-infected individuals receiving 2NRTI + 1PI boosted with ritonavir. MethodsWe investigated 38 HIV+ adolescents (mean age 13.8 ± 1.3 years) with constant detectable HBV viral load, of whom 92.3% were chronic HBsAg carriers, 61.53% were HBeAg+, and 68.2% had lamivudine (LAM) in their regimen. HBV genotype was determined using commercial Line Probe Assay (Innogenetics) and sequencing of the HIV pol gene was carried out using Trugene genotyping kits (Bayer Diagnostics Inc.); for HIV subtyping the nucleotide sequences were submitted to the Stanford database.

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Objective: HIV can affect CNS in early stages of disease and determine neurological impairment. HBV DNA was found in CSF of HIV co-infected patients, but little is known about the neurotropic character of this virus. Here we assessed the degree of association between HBV infection and neurological impairment in a large cohort of long-term survivors, HIV-infected patients that experienced multiple therapeutic schemes over time. Methods: A total of 462 HIV-1-infected patients were retrospectively followed up for 10 years for HBV infection and neurological impairment. The patients were tested for immune (flow cytometry) and virological parameters of HIV infection (Roche Amplicor, version 1.5/ COBAS AmpliPrep/COBAS TaqMan HIV-1 test) and for HBV infection markers (HBsAg, anti HBc: Murex Biotech ELISA tests). Many of these patients have experienced between one and six regimens such as: 2 NRTIs, 3 NRTIs, 2 NRTIs+1 NNRTI, 1 NRTI+1 NNRTI+1 PI, 2 NRTIs+2 PIs. Results: After 10 years 29.87% of the patients presented neurological impairment. Out of them 56.52% were HBV-infected. The prevalence of HIV encephalopathy (HE) in our studied cohort was 22.7% and 50.4% of these patients were HBV-infected. The median HIV diagnosis age was 7 and the median age of HE diagnosis was 10. In order to establish a possible correlation between HBV infection and HE we first reviewed and excluded the main risk factors associated with HE at the moment of diagnosis: low weight, anemia, constitutional symptoms, low CD4+count, high plasma HIV-RNA load. No patient was infected with HCV. The groups of patients that presented HE and HBsAg and HE without HBsAg were balanced regarding sex, number of deceased patients, number of class C3 patients, but the patients in first group presented lower CD4 values at HE diagnosis vs patients from second group 2: 44.5 vs 95 cells/µL, p=0.3; lower nadir CD4 count: 38 vs 51 cell/µL, p=0.1; and slightly higher HIV viral load: 5.2 vs 5 log10 copies/mL, p = 0.2. There were only 53 patients that presented at the same time HE and HBV infection and the majority, 78.69%, were first infected with HBV. Conclusions: In our studied cohort HBV infection was associated with HE but further studies are needed to prove HBV neurotropic potential. Absolute CD4 nadir count and class C3 are proved to be strong predictors of HE in HIV-infected patients even after several changes in antiretroviral therapy schemes