作者: Stephen Norley , Reinhard Kurth
DOI: 10.1128/9781555817213.CH9
关键词: Genetics 、 Virus 、 Glycoprotein 、 Immune system 、 Genome 、 CTL* 、 Epitope 、 Virology 、 Cytotoxic T cell 、 Antibody 、 Biology
摘要: This chapter describes the scale and driving force behind profound genomic plasticity of human immunodeficiency virus (HIV). It discusses intense interplay between immune system host. also speculates on impact this variability prospects for development effective vaccines novel therapies. The evolution HIV is, as with all organisms, driven predominantly by Darwinian natural selection that comprises two fully independent but essential components. first is production random mutations form a pool organisms differing slightly in pheno-type. Second, selective pressure drives rapid spectacular HIV. Neutralizing antibodies produced are relatively type specific targeted to one or regions envelope glycoprotein free mutate without taking significant fitness hit. options open escaping cytotoxic T lymphocyte (CTL) recognition numerous. First, it may alter amino acids epitope necessary corresponding CTL T-cell receptor. In addition extreme exerted system, there an additional "artificial" evolution, particularly industrialized countries.