[1] Opportunistic Infections Project Team of the Collaboration of Bbservational HIV Epidemiological Research in Europe C01. CD4 cell count and the risk of AIDS or death in HIV-Infected adults on combination antiretroviral therapy with a suppressed viral load: a longitudinal cohort study from COHERE[J]. PLoS Med, 2012,9(3): e1001194.[2] Tan I L, Smith B R, Von Geldern G, et al. HIV-associated opportunistic infections of the CNS[J]. Lancet Neurol, 2012,11(7): 605-617.[3] Riveiro-Barciela M, Falcó V, Burgos J, et al. Neurological opportunistic infections and neurological immune reconstitution syndrome: impact of one decade of highly active antiretroviral treatment in a tertiary hospital[J]. HIV Med, 2013,14(1): 21-30.[4] Wei F, Wang X, Liu L, et al. Characterization of HIV type 1 env gene in cerebrospinal fluid and blood of infected Chinese patients[j]. AIDS Res Hum Retroviruses, 2011,27(7):793-796.[5] Liu L, ZhAO Q, Wei F, et al. Genetic analysis of HIV type 1 env gene in cerebrospinal fluid and plasma of infected Chinese paid blood donors[J]. AIDS Res Hum Retroviruses, 2012,28(1): 106-109.[6] Zhang Y, Qiao L, Ding W, et al. An initial screening for HIV-associated neurocognitive disorders of HIV-1 infected patients in China[J]. J Neurovirol, 2012,18(2): 120-126.[7] Zhang Y, Wang M, Li H, et al. Accumulation of nuclear and mitochondrial DNA damage in the frontal cortex cells of patients with HIV-associated neurocognitive disorders[J]. Brain Res, 2012,1458: 1-11.[8] Masur H, Kaplan J E. New guidelines for the management of HIV-related opportunistic infections[J]. JAMA, 2009,301(22): 2378-2380.[9] 宋凤丽,张玉林,乔录新,等.中国HIV-1感染人群神经认知损害初步筛查[J].首都医科大学学报,2012, 33(5):610-615.[10] Mocroft A J, Lundgren J D, d'Armino Monforte A, et al. Survival of AIDS patients according to type of AIDS-defining event. The AIDS in Europe Study Group[J]. Int J Epidemiol, 1997,26(2): 400-407.[11] Christo P P, Greco D B, Aleixo A W, et al. Factors influencing cerebrospinal fluid and plasma HIV-1 RNA detection rate in patients with and without opportunistic neurological disease during the HAART era[J]. BMC Infect Dis, 2007, 7: 147.[12] Christo P P, Greco D B, Aleixo A W, et al. HIV-1 RNA levels in cerebrospinal fluid and plasma and their correlation with opportunistic neurological diseases in a Brazilian AIDS reference hospital[J]. Arq Neuropsiquiatr, 2005,63(4): 907-913.[13] Martin C, Albert J, Hansson P, et al. Cerebrospinal fluid mononuclear cell counts influence CSF HIV-1 RNA levels[J]. J Acquir Immune Defic Syndr Hum Retrovirol, 1998,17(3): 214-219.[14] van Marle G, Power C. Human immunodeficiency virus type 1 genetic diversity in the nervous system: evolutionary epiphenomenon or disease determinant[J]. J Neurovirol, 2005, 11(2): 107-128.[15] Persidsky Y, Gendelman H E. Mononuclear phagocyte immunity and the neuropathogenesis of HIV-1 infection[J]. J Leukoc Biol, 2003,74(5): 691-701.[16] Wu D T, Woodman S E, Weiss J M, et al. Mechanisms of leukocyte trafficking into the CNS[J]. J Neurovirol, 2000, 6(Suppl 1): 82-85.[17] Gras G, Kaul M. Molecular mechanisms of neuroinvasion by monocytes-macrophages in HIV-1 infection[J]. Retrovirology, 2010,7: 30.[18] Wang H, Sun J, Goldstein H. Human immunodeficiency virus type 1 infection increases the in vivo capacity of peripheral monocytes to cross the blood-brain barrier into the brain and the in vivo sensitivity of the blood-brain barrier to disruption by lipopolysaccharide[J]. J Virol, 2008,82(15): 7591-7600.[19] Haughey N J, Mattson M P. Calcium dysregulation and neuronal apoptosis by the HIV-1 proteins Tat and gp120[J]. J Acquir Immune Defic Syndr, 2002, 31(Suppl 2): 55-61.[20] Wang Z, Pekarskaya O, Bencheikh M, et al. Reduced expression of glutamate transporter EAAT2 and impaired glutamate transport in human primary astrocytes exposed to HIV-1 or gp120[J]. Virology, 2003,312(1): 60-73.[21] Zhang Y, Shi Y, Qiao L, et al. Sigma-1 receptor agonists provide neuroprotection against gp120 via a change in bcl-2 expression in mouse neuronal cultures[J]. Brain Res, 2012,1431: 13-22. |