Abstract
Despite the inability of HIV-1 to infect neurons, over half of the HIV-1-infected population in the USA suffers from neurocognitive dysfunction. HIV-infected immune cells in the periphery enter the central nervous system by causing a breach in the blood-brain barrier. The damage to the neurons is mediated by viral and host toxic products released by activated and infected immune and glial cells. To evaluate the toxicity of any viral isolate, viral protein, or host inflammatory protein, we describe a protocol to assess the neuronal apoptosis and synaptic compromise in primary cultures of human neurons and astrocytes.
Original language | English (US) |
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Title of host publication | Methods in Molecular Biology |
Publisher | Humana Press Inc. |
Pages | 367-376 |
Number of pages | 10 |
DOIs | |
State | Published - Jan 1 2016 |
Externally published | Yes |
Publication series
Name | Methods in Molecular Biology |
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Volume | 1354 |
ISSN (Print) | 1064-3745 |
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Keywords
- Chemokines
- Cytokines
- Gp120
- HAD
- HAND
- HIV-1
- HIV-associated dementia
- HIV-associated neurocognitive dysfunction
- Neuro-inflammation
- Neuronal apoptosis
- Neuronal damage
- Tat
ASJC Scopus subject areas
- Molecular Biology
- Genetics
Cite this
Evaluating the role of viral proteins in HIV-mediated neurotoxicity using primary human neuronal cultures. / Rao, Vasudev R.; Eugenin, Eliseo; Prasad, Vinayaka R.
Methods in Molecular Biology. Humana Press Inc., 2016. p. 367-376 (Methods in Molecular Biology; Vol. 1354).Research output: Chapter in Book/Report/Conference proceeding › Chapter
}
TY - CHAP
T1 - Evaluating the role of viral proteins in HIV-mediated neurotoxicity using primary human neuronal cultures
AU - Rao, Vasudev R.
AU - Eugenin, Eliseo
AU - Prasad, Vinayaka R.
PY - 2016/1/1
Y1 - 2016/1/1
N2 - Despite the inability of HIV-1 to infect neurons, over half of the HIV-1-infected population in the USA suffers from neurocognitive dysfunction. HIV-infected immune cells in the periphery enter the central nervous system by causing a breach in the blood-brain barrier. The damage to the neurons is mediated by viral and host toxic products released by activated and infected immune and glial cells. To evaluate the toxicity of any viral isolate, viral protein, or host inflammatory protein, we describe a protocol to assess the neuronal apoptosis and synaptic compromise in primary cultures of human neurons and astrocytes.
AB - Despite the inability of HIV-1 to infect neurons, over half of the HIV-1-infected population in the USA suffers from neurocognitive dysfunction. HIV-infected immune cells in the periphery enter the central nervous system by causing a breach in the blood-brain barrier. The damage to the neurons is mediated by viral and host toxic products released by activated and infected immune and glial cells. To evaluate the toxicity of any viral isolate, viral protein, or host inflammatory protein, we describe a protocol to assess the neuronal apoptosis and synaptic compromise in primary cultures of human neurons and astrocytes.
KW - Chemokines
KW - Cytokines
KW - Gp120
KW - HAD
KW - HAND
KW - HIV-1
KW - HIV-associated dementia
KW - HIV-associated neurocognitive dysfunction
KW - Neuro-inflammation
KW - Neuronal apoptosis
KW - Neuronal damage
KW - Tat
UR - http://www.scopus.com/inward/record.url?scp=84952837971&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84952837971&partnerID=8YFLogxK
U2 - 10.1007/978-1-4939-3046-3_25
DO - 10.1007/978-1-4939-3046-3_25
M3 - Chapter
C2 - 26714725
AN - SCOPUS:84952837971
T3 - Methods in Molecular Biology
SP - 367
EP - 376
BT - Methods in Molecular Biology
PB - Humana Press Inc.
ER -