Sensitivity of Human Immunodeficiency Virus Type 1 to the Fusion Inhibitor T-20 Is Modulated by Coreceptor Specificity Defined by the V3 Loop of gp120
By C. Derdeyn, J. Decker, Jeffrey N. Sfakianos, Xiaoyun Wu, W. O'brien, L. Ratner, J. Kappes, G. Shaw, E. Hunter. Journal of Virology, 2000
786 citations recorded by the source corpus.
Subfields: Epidemiology, Infectious Diseases, Virology
View Paper: https://www.semanticscholar.org/paper/8e0cf6f2d8354e147d3919318f73cfaa5523f2ce
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
- E. Arts
- D. Hazuda
- Xiping Wei
- J. Decker
- G. Shaw
- J. Kappes
- Hongmei Liu
- Xiaoyun Wu
Citations in the corpus
- HIV-1 antiretroviral drug therapy. (2012, background): “Nonetheless, studies of baseline susceptibility to enfuvirtide suggested that large variations in intrinsic susceptibility existed in diverse HIV-1 isolates, and that these variations mapped to regions outside the enfuvirtidebinding site (Derdeyn et al. 2000).”
- RNA motif discovery by SHAPE and mutational profiling (SHAPE-MaP) (2014, neutral): “Viruses were measured for infectivity on TZM-bl indicator cells 53 (using Glo Lysis buffer and the Luciferase Assay System; Promega).”
- Emergence of Resistant Human Immunodeficiency Virus Type 1 in Patients Receiving Fusion Inhibitor (T-20) Monotherapy (2002, background): “(6), these differences appear not to affect susceptibility to T-20.”