TY - JOUR
T1 - Proteomic fingerprinting of HIV-1-infected human monocyte-derived macrophages
T2 - A preliminary report
AU - Carlson, Kimberly A.
AU - Ciborowski, Pawel
AU - Schellpeper, Courtney N.
AU - Biskup, Toni M.
AU - Shen, Rong Fong
AU - Luo, Xiaoguang
AU - Destache, Christopher J.
AU - Gendelman, Howard E.
N1 - Funding Information:
The authors would like to thank Dr. Greg Schneider of Ciphergen Biosystems for helpful conversations and technical assistance. Dr. Jenae Limoges and Ms. Robin Taylor are thanked for their technical and editorial assistance. This work was supported by grants supported by NIH grants 2R37 NS36136, PO1 NS31492, 2R01 NS34239 and 1 U54 NS43011.
PY - 2004/2
Y1 - 2004/2
N2 - Mononuclear phagocytes (MP; blood monocytes, alveolar, lymph node, and brain macrophages and microglia) are vehicles for dissemination and principle target cells for human immunodeficiency virus type 1 (HIV-1) infection. Notably, viral persistence in macrophages occurs despite ongoing phagocytic, intracellular killing, innate and adaptive immune responses. To assess potential pathways for how HIV-1 may bypass antiviral MP responses, we used proteomic tests to evaluate protein fingerprints of HIV-1-infected human monocyte-derived macrophages 7 days after viral infection. By using weak cation exchange chips, 58 proteins were found up- or down-regulated after HIV-1 ADA infection. Several of these proteins were identified by microsequencing. It is probable that cellular proteins identified by proteomic fingerprinting could assist in unraveling how persistent viral infection occurs in MP lineage cells. Moreover, this evolving technology can be utilized to unravel changes in immune activities initiated by interactions between virus, environmental cues and drugs of abuse.
AB - Mononuclear phagocytes (MP; blood monocytes, alveolar, lymph node, and brain macrophages and microglia) are vehicles for dissemination and principle target cells for human immunodeficiency virus type 1 (HIV-1) infection. Notably, viral persistence in macrophages occurs despite ongoing phagocytic, intracellular killing, innate and adaptive immune responses. To assess potential pathways for how HIV-1 may bypass antiviral MP responses, we used proteomic tests to evaluate protein fingerprints of HIV-1-infected human monocyte-derived macrophages 7 days after viral infection. By using weak cation exchange chips, 58 proteins were found up- or down-regulated after HIV-1 ADA infection. Several of these proteins were identified by microsequencing. It is probable that cellular proteins identified by proteomic fingerprinting could assist in unraveling how persistent viral infection occurs in MP lineage cells. Moreover, this evolving technology can be utilized to unravel changes in immune activities initiated by interactions between virus, environmental cues and drugs of abuse.
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U2 - 10.1016/j.jneuroim.2003.10.039
DO - 10.1016/j.jneuroim.2003.10.039
M3 - Article
C2 - 14741425
AN - SCOPUS:1642493593
VL - 147
SP - 35
EP - 42
JO - Journal of Neuroimmunology
JF - Journal of Neuroimmunology
SN - 0165-5728
IS - 1-2
ER -