With the introduction of combinatory antiretroviral therapy, patients infected with human immunodeficiency virus type 1 (HIV-1) can live much longer than before. However, the identification of HIV-associated neurocognitive disorder (HAND), especially HIV-associated dementia in 15-20% of patients infected with HIV-1, indicates additional complexity. These disorders turn out to be subtype dependent. Recently, many studies are ongoing trying to understand how the virus induces neuronal injury which could lead to neurological dysfunction. Most of these studies are focusing on the HIV-1 release of proteins such as Tat. However, the exact role of these proteins and their involvement in neuronal degeneration remains unidentified; this is especially true since viral proteins from different HIV-1 subtypes differ in their ability to cause neuronal damage. This review describes the role of different HIV-1 subtypes, identifies probable pathways involved in neuronal damage, the contribution of different HIV-1 subtypes to the progression of HAND, and potential treatments for HAND.

中文翻译：

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HIV-1 B和C型亚型对神经系统疾病的不同贡献：机制和可能的治疗方法。

随着组合抗逆转录病毒疗法的引入，感染了人类免疫缺陷病毒1型（HIV-1）的患者的寿命可以比以前更长。但是，在15-20％感染HIV-1的患者中鉴定出与HIV相关的神经认知障碍（HAND），尤其是与HIV相关的痴呆症，这表明了额外的复杂性。这些疾病证明是亚型依赖性的。最近，许多研究正在进行，试图了解该病毒如何诱导神经元损伤，这可能导致神经功能障碍。这些研究大多数都集中在诸如Tat等蛋白质的HIV-1释放上。然而，这些蛋白的确切作用及其在神经元变性中的作用尚不清楚。尤其如此，因为来自不同HIV-1亚型的病毒蛋白引起神经元损伤的能力不同。