Effects of active HCV replication on neurologic status in HIV RNA virally suppressed patients
Effects of active HCV replication on neurologic status in HIV RNA virally suppressed patients
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DOI：
10.1212/wnl.0b013e3181af7a10
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发表时间：
2009-07-28
期刊：
影响因子：
9.9
通讯作者：
Evans, S. R.
中科院分区：
文献类型：
--
作者：
Clifford, D. B.;Smurzynski, M.;Evans, S. R.
背景：丙型肝炎病毒（HCV）是HIV的常见共同病原体。这两种病毒似乎都在大脑中复制，并且都与神经认知和周围神经病变综合征有关。相互作用的病毒可能是复杂的，更好地了解每个病毒的贡献将是必要的，以证据为基础的治疗decisions.Methods：本研究的目的是确定如果活跃的HCV感染，确定定量HCV RNA测定，与增加的神经认知功能障碍或过度发展的远端感觉周围神经病变的HIV合并感染患者稳定的HIV病毒抑制。艾滋病临床试验组纵向连锁随机试验（ALLRT）研究是已知HIV治疗状态、神经认知和神经病变评估以及HCV状态的受试者的来源。根据HCV抗体状态选择受试者（249例阳性; 310例阴性）。结果：在172例受试者中检测到HCV RNA病毒载量，这些受试者在ALLRT中具有控制的HIV感染和可用的神经系统评价。将这些参与者与同一队列的345名HCV病毒载量检测不到且入选标准相同的参与者进行比较。两组之间通过线索制作A或B和数字符号测试测量的神经认知性能没有差异。此外，活跃的HCV复制和远端感觉neuropathy.Conclusion之间没有显着的关联：临床上显着的神经认知功能障碍和周围神经病变的活动性丙型肝炎病毒感染的最佳治疗的HIV感染的设置没有加剧。神经病学（R）2009; 73：309-314
Background: Hepatitis C virus (HCV) is a frequent copathogen with HIV. Both viruses appear to replicate in the brain and both are implicated in neurocognitive and peripheral neuropathy syndromes. Interaction of the viruses is likely to be complicated and better understanding of the contributions of each virus will be necessary to make evidence-based therapeutic decisions.Methods: This study was designed to determine if active HCV infection, identified by quantitative HCV RNA determination, is associated with increased neurocognitive deficits or excess development of distal sensory peripheral neuropathy in HIV coinfected patients with stable HIV viral suppression. The AIDS Clinical Trials Group Longitudinal Linked Randomized Trials (ALLRT) study was the source of subjects with known HIV treatment status, neurocognitive and neuropathy evaluations, and HCV status. Subjects were selected based on HCV antibody status (249 positive; 310 negative).Results: HCV RNA viral loads were detectable in 172 participants with controlled HIV infection and available neurologic evaluations in the ALLRT. These participants were compared with 345 participants with undetectable HCV viral load and the same inclusion criteria from the same cohort. Neurocognitive performance measured by Trail-Making A or B and digit symbol testing was not dissimilar between the 2 groups. In addition, there was no significant association between active HCV replication and distal sensory neuropathy.Conclusion: Clinically significant neurocognitive dysfunction and peripheral neuropathy were not exacerbated by active hepatitis C virus infection in the setting of optimally treated HIV infection. Neurology (R) 2009; 73: 309-314