ABSTRACT
Objective To study the correlation between genotype drug resistance and CD4+ T-lymphocyte of AIDS patients who received antiretroviral treatment in Henan province. Methods Several indicators were studied through questionnaires and whole blood was collected to analyze CD4+ T-lymphocyte as well as the virus load. In-House technique was used to detect the genotype drug resistance. Results 32.21% and 29.17% of the patients were identified as genotype drug resistant to AIDS when used first and second generation medicine schemes but the improvement (P=0.7538) of disease process was not influenced much. However, if the genotype drug resistance of patients with HAART last longer than two years (33.20%) or patients with HAART less than one year (18.97%), a greater impact on the improvement was noticed. Age (OR=0.68) and the interval on distribution of medicines (OR=1.93) had a great impact on the improvement with the genotype drug resistance through logistic regression analysis. Medicine scheme (OR=0.51), genotype drug resistance (OR=3.20) and the rate of regular dose in a month (OR=0.51) all had a great impact on the improvement to CD4+ T-lymphocyte by logistic regression analysis. Conclusion Part of HIV/AIDS patients showed resistant to genotype drugs in Henan province, suggesting that we must reinforce the surveillance on HAART and program on drug administration to the patients, in order to increase the number of CD4+ T-lymphocyte so as to avoid the development of drug resistance.
ABSTRACT
Objective:To investigate the role of CCR5 key residues as a co-recptor for the cellular entry of human immunodeficiency virus type Ⅰ(HIV-Ⅰ).Methods: Mutation of amino acids was introduced in different extracellular loops of CCR5 by site-directed mutagenesis technique,turning the non-polar amino acids into polar ones,the non-hydrophilic into hydrophilic,and the aromatic into non-aromatic.The mutants of CCR5 were expressed in BamHⅠ/XhoⅠ and were allowed to bind with gp120,and the binding activity of the mutants was compared with that of wild-type CCR5.Results: The coreceptor activity of CCR5 was reduced greatly when Cys in the first extracellular loop was replaced by Tyr and Pro in the third extracellular loop was replaced by Ser.There was no obvious change in the coreceptor activity of CCR5 when other replacements were introduced.Conclusion: HIV-Ⅰ virus needs receptor and co-receptor to achieve its cellular entry.CCR5 is a co-receptor and some of its extracellular loop amino acids are essential for gp120 recognition of HIV-Ⅰ.