High levels of divergent HIV-1 quasispecies in neurological opportunistic infections in China

doi:10.3969/j.issn.1006-7795.2014.01.018

Abstract

Abstract:

Objective To investigate virological characteristics of central nervous system (CNS) HIV-1 in AIDS patients with CNS opportunistic infection (OIs).Methods Totally 24 cases with CNS OIs and 16 non-CNS-OIs (control) cases were selected from AIDS patients who were infected with HIV-1 by paid blood donor in Henan province. HIV-1 loads of plasma and cerebrospinal fluid (CSF) were detected by reverse transcriptase polymerase chain reaction, and C2-V5 area of HIV-1 envelope region was amplified from viral quasispecies isolated from CSF by nest polymerase chain reaction. Results CSF HIV-1 load was significantly higher in cases with CNS OIs, but no high plasma HIV-1 load was found in these patients. CD4 counts were not significantly different between two groups. And, no straight linear correlations were found between CSF viral load and plasma viral load, CSF viral load and CD4 counts in either group. HIV-1 quasispecies isolated from the CSF of CNS OIs patients had a high diversity as the nucleotide sequence analysis of C2-V5 region.Conclusion These results suggest that high levels of divergent HIV-1 quasispecies in the CNS which probably contribute to opportunistic infections.

Key words: acquired immuno deficiency syndrome(AIDS), central nervous system, HIV-1, opportunistic infections, viral load, divergence

CLC Number:

R512.91

Liu Yuanzhi, Chen Binggang, Ding Wei, Qiao Luxin, Zhao Qingxia, Wu Hao, Chen Dexi, Zhang Yulin. High levels of divergent HIV-1 quasispecies in neurological opportunistic infections in China[J]. Journal of Capital Medical University, 2014, 35(1): 81-86.

0
/ / Recommend

Add to citation manager EndNote|Reference Manager|ProCite|BibTeX|RefWorks

URL: https://journal03.magtech.org.cn/Jweb_sdykdxxb/EN/10.3969/j.issn.1006-7795.2014.01.018

https://journal03.magtech.org.cn/Jweb_sdykdxxb/EN/Y2014/V35/I1/81

References

[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.