Abstract
Human astrocyte cells were exposed to HIV-Tat and/or epidermal growth factor (EGF), to monitor the expression of the neuropathogenic MSRV and Syncytin-1 elements of the HERV-W family of endogenous retroviruses and of TNFα. The results indicate that EGF counteracts Tat regulation of HERV-W/MSRVenv/Syncytin-1, throughout EGFR activation; this effect occurs by interfering with the induction of TNFα production by Tat. The novel effect of EGF counteraction of Tat-mediated regulation of the neuropathogenic HERV-Ws could be neuro-protective, but its actual role in the brain remains to be elucidated.
Keywords:
Epidermal growth factor (EGF); Epidermal growth factor receptor (EGFR); HERV-W/MSRV/Syncytin-1 human endogenous retroviruses; NeuroAIDS/neuropathogenicity; Tat; Tumor necrosis factor-α (TNFα).
MeSH terms
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Antibodies, Monoclonal / pharmacology
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Astrocytes / drug effects
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Astrocytes / virology*
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Cell Line
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Endogenous Retroviruses / genetics*
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Endogenous Retroviruses / growth & development
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Endogenous Retroviruses / metabolism
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Epidermal Growth Factor / pharmacology*
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ErbB Receptors / genetics
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ErbB Receptors / metabolism
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Fetus
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Gene Products, env / genetics
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Gene Products, env / metabolism
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HIV Antibodies / pharmacology
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Humans
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Lipopolysaccharides / pharmacology
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Pregnancy Proteins / genetics
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Pregnancy Proteins / metabolism
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Tumor Necrosis Factor-alpha / pharmacology
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tat Gene Products, Human Immunodeficiency Virus / antagonists & inhibitors
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tat Gene Products, Human Immunodeficiency Virus / pharmacology*
Substances
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Antibodies, Monoclonal
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Gene Products, env
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HIV Antibodies
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Lipopolysaccharides
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Pregnancy Proteins
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Tumor Necrosis Factor-alpha
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syncytin
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tat Gene Products, Human Immunodeficiency Virus
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Epidermal Growth Factor
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EGFR protein, human
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ErbB Receptors