Adaptive mutations in the V3 loop of gp120 enhance fusogenicity of human immunodeficiency virus type 1 and enable use of a CCR5 coreceptor that lacks the amino-terminal sulfated region

Journal of Virology

Volumn 75, Issue 24, 2001, Pages 12266-12278

  Platt, E J ^a   Kuhmann, S E ^a   Rose, P P ^a   Kabat, D ^a  

^a OREGON HEALTH AND SCIENCE UNIVERSITY   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CD4 ANTIGEN; CHEMOKINE RECEPTOR CCR5; GLYCOPROTEIN GP 120;

ACQUIRED IMMUNE DEFICIENCY SYNDROME; ADAPTATION; AMINO TERMINAL SEQUENCE; ANIMAL CELL; ARTICLE; BINDING AFFINITY; CELL FUSION; CELL SURFACE; CONCENTRATION RESPONSE; CONTROLLED STUDY; EMBRYO; HUMAN; HUMAN CELL; HUMAN IMMUNODEFICIENCY VIRUS 1; HUMAN IMMUNODEFICIENCY VIRUS INFECTION; MOLECULAR CLONING; NONHUMAN; PRIORITY JOURNAL; RECEPTOR BINDING; SULFATION; VIRION; VIRUS ASSEMBLY; VIRUS ENVELOPE; VIRUS MUTATION; VIRUS REPLICATION;

AMINO ACID SEQUENCE; ANIMALS; CRICETINAE; HELA CELLS; HIV ENVELOPE PROTEIN GP120; HIV-1; HUMANS; MEMBRANE FUSION; MOLECULAR SEQUENCE DATA; RECEPTORS, CCR5; SULFATES;

EID: 0035202075     PISSN: 0022538X     EISSN: None     Source Type: Journal    
DOI: 10.1128/JVI.75.24.12266-12278.2001     Document Type: Article

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