Boivin M.J., Ruel T.D., Boal H.E., Bangirana P., Cao H., Eller L.A., Charlebois E., Havlir D.V., Kamya M.R., Achan J., Akello C., Wong J.K.
International Neurologic and Psychiatric Epidemiology Program, Michigan State University, East Lansing, MI, United States; Division of Infectious Disease, Department of Pediatrics, University of California, San Francisco, San Francisco, CA, United States; Department of Pediatrics, University of Washington Seattle Children's Hospital, Seattle, WA, United States; Department of Psychiatry, Makerere University School of Medicine, Kampala, Uganda; California Department of Public Health, Viral and Rickettsial Disease Laboratory, Richmond, CA, United States; Makerere University-Walter Reed Program, Kampala, Uganda; Department of Medicine, University of California, San Francisco, San Francisco, United States; Department of Medicine, University of California, San Francisco, San Francisco General Hospital, San Francisco, CA, United States; Department of Medicine, Makerere University School of Medicine, Kampala, Uganda; Department of Paediatrics and Child Health, Makerere University School of Medicine, Kampala, Uganda; Section of Infectious Diseases, Department of Medicine, University of California, San Francisco, San Francisco, CA, United States
Boivin, M.J., International Neurologic and Psychiatric Epidemiology Program, Michigan State University, East Lansing, MI, United States; Ruel, T.D., Division of Infectious Disease, Department of Pediatrics, University of California, San Francisco, San Francisco, CA, United States; Boal, H.E., Department of Pediatrics, University of Washington Seattle Children's Hospital, Seattle, WA, United States; Bangirana, P., Department of Psychiatry, Makerere University School of Medicine, Kampala, Uganda; Cao, H., California Department of Public Health, Viral and Rickettsial Disease Laboratory, Richmond, CA, United States; Eller, L.A., Makerere University-Walter Reed Program, Kampala, Uganda; Charlebois, E., Department of Medicine, University of California, San Francisco, San Francisco, United States; Havlir, D.V., Department of Medicine, University of California, San Francisco, San Francisco General Hospital, San Francisco, CA, United States; Kamya, M.R., Department of Medicine, Makerere University School of Medicine, Kampala, Uganda; Achan, J., Department of Paediatrics and Child Health, Makerere University School of Medicine, Kampala, Uganda; Akello, C., Department of Medicine, Makerere University School of Medicine, Kampala, Uganda; Wong, J.K., Section of Infectious Diseases, Department of Medicine, University of California, San Francisco, San Francisco, CA, United States
Background: HIV-subtype D is associated with more rapid disease progression and higher rates of dementia in Ugandan adults compared with HIV-subtype A. There are no data comparing neuropsychological function by HIV subtype in Ugandan children. Design: One hundred and two HIV-infected antiretroviral therapy (ART) naive Ugandan children 6-12 years old (mean 8.9) completed the Kaufman Assessment Battery for Children, second edition (KABC-2), the Test of Variables of Attention (TOVA), and the Bruininks-Oseretsky Test for Motor Proficiency, second edition (BOT-2). Using a PCR-based multiregion assay with probe hybridization in five different regions (gag, pol, vpu, env, gp-41), HIV subtype was defined by hybridization in env and by total using two or more regions. Analysis of covariance was used for multivariate comparison. Results: The env subtype was determined in 54 (37 A, 16 D, 1 C) children. Subtype A and D groups were comparable by demographics, CD4 status, and WHO stage. Subtype A infections had higher log viral loads (median 5.0 vs. 4.6, P = 0.02). Children with A performed more poorly than those with D on all measures, especially on KABC-2 Sequential Processing (memory) (P = 0.01), Simultaneous Processing (visual-spatial analysis) (P = 0.005), Learning (P = 0.02), and TOVA visual attention (P = 0.04). When adjusted for viral load, Sequential and Simultaneous Processing remained significantly different. Results were similar comparing by total HIV subtype. Conclusion: HIV subtype A children demonstrated poorer neurocognitive performance than those with HIV subtype D. Subtype-specific neurocognitive deficits may reflect age-related differences in the neuropathogenesis of HIV. This may have important implications for when to initiate ART and the selection of drugs with greater central nervous system penetration. © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins.