Amyloidogenic, neuroinflammatory and memory dysfunction effects of HIV-1 gp120

Young Jung Lee, In Jun Yeo, Dong Young Choi, Jaesuk Yun, Dong Ju Son, Sang Bae Han, Jin Tae Hong

Research output: Contribution to journalArticlepeer-review

7 Scopus citations


Human immunodeficiency virus 1 (HIV-1) infection can cause several HIV-associated neurocognitive disorders a variety of neurological impairments characterized by the loss of cortical and subcortical neurons and decreased cognitive and motor function. HIV-1 gp120, the major envelope glycoprotein on viral particles, acts as a binding protein for viral entry and is known to be an agent of neuronal cell death. To determine the mechanism of HIV-1 gp120-induced memory dysfunction, we performed mouse intracerebroventricular (i.c.v.) infusion with HIV-1 gp120 protein (300 ng per mouse) and investigated memory impairment and amyloidogenesis. Infusion of the HIV-1 gp120 protein induced memory dysfunction, which was evaluated using passive avoidance and water maze tests. Infusion of HIV-1 gp120 induced neuroinflammation, such as the release of iNOS and COX-2 and the activation of astrocytes and microglia and increased the mRNA and protein levels of IL-6, ICAM-1, M-CSF, TIM, and IL-2. In particular, we found that the infusion of HIV-1 gp120 induced the accumulation of amyloid plaques and signs of elevated amyloidogenesis, such as increased expression of amyloid precursor protein and BACE1 and increased β-secretase activity. Therefore, these studies suggest that HIV-1 gp120 may induce memory impairment through Aβ accumulation and neuroinflammation.

Original languageEnglish
Pages (from-to)689-701
Number of pages13
JournalArchives of Pharmacal Research
Issue number7
StatePublished - Jul 2021


  • Amyloid beta
  • gp120
  • HIV-1
  • Neuroinflammation


Dive into the research topics of 'Amyloidogenic, neuroinflammatory and memory dysfunction effects of HIV-1 gp120'. Together they form a unique fingerprint.

Cite this