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Cellular effects of Vpr in astrocytes and neurons (LB61)
Author(s) -
Santiago Ismael,
Torres Lilith,
Noel Richard
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.lb61
Subject(s) - biology , apoptosis , viral replication , viability assay , transfection , neurotoxin , virology , neurotoxicity , toxicity , virus , astrocyte , microbiology and biotechnology , cell culture , chemistry , central nervous system , neuroscience , genetics , biochemistry , organic chemistry
Combined Antiretroviral Therapy (cART) reduces viral loads of HIV by preventing virus replication to slow down the progression to AIDS. Therapy does not prevent all viral gene expression and so morbidities continue to present in HIV infected people. HIV associated neurocognitive disorders (HAND) affect approximately 50% of HIV‐1 positive individuals. Viral protein expression in astrocytes may contribute to HAND. Viral protein R (Vpr) is an important factor in HIV replication and a neurotoxin. We hypothesized Vpr can be toxic to astrocytes or neurons. To test our hypothesis we measured cell markers of apoptosis, viability and toxicity using fluorescent assays in co‐cultures of Vpr‐transfected SVGA astrocytes and SH‐SY5Y neurons. Vpr treated cultures exhibited modestly higher cytotoxicity and unchanged viability or apoptosis in neurons. In conclusion, the results suggest that Vpr has sub‐lethal effects and may cause milder toxicity, such as changes in morphology. Future experiments will be directed at testing for actin changes caused by Vpr expression in astrocytes.