Novel structurally related compounds reactivate latent HIV-1 in a bcl-2-transduced primary CD4+ T cell model without inducing global T cell activation

Journal of Antimicrobial Chemotherapy

Volumn 67, Issue 2, 2012, Pages 398-403

  Xing, Sifei ^a   Bhat, Shridhar ^a   Shroff, Neeta S ^b   Zhang, Hao ^c   Lopez, Joseph A ^c   Margolick, Joseph B ^c   Liu, Jun O ^a   Siliciano, Robert F ^a,b  

^a JOHNS HOPKINS UNIVERSITY SCHOOL OF MEDICINE   (United States)

^b HOWARD HUGHES MEDICAL INSTITUTE   (United States)

^c JOHNS HOPKINS UNIVERSITY   (United States)

Author keywords

Latency; Primary cell model; Quinolin 8 ol; Reactivation; Virus

Indexed keywords

CD28 ANTIGEN; CD3 ANTIGEN; DISULFIRAM; JUGLONE; PROTEIN BCL 2; QUINOLINE DERIVATIVE;

ANTIVIRAL ACTIVITY; ARTICLE; CD4+ T LYMPHOCYTE; CELL VIABILITY; CONCENTRATION RESPONSE; CONTROLLED STUDY; CYTOKINE RELEASE; CYTOTOXICITY; DRUG STRUCTURE; GENETIC TRANSDUCTION; HUMAN; HUMAN CELL; HUMAN IMMUNODEFICIENCY VIRUS 1; LYMPHOCYTE ACTIVATION; MOLECULAR WEIGHT; T LYMPHOCYTE ACTIVATION; VIRUS LATENCY; VIRUS REACTIVATION;

ADULT; CD4-POSITIVE T-LYMPHOCYTES; CELLS, CULTURED; CYTOKINES; HIV-1; HUMANS; PROTO-ONCOGENE PROTEINS C-BCL-2; QUINOLONES; TRANSCRIPTIONAL ACTIVATION; TRANSFORMATION, GENETIC; VIRUS ACTIVATION; VIRUS LATENCY;

EID: 84862907673     PISSN: 03057453     EISSN: 14602091     Source Type: Journal    
DOI: 10.1093/jac/dkr496     Document Type: Article

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