壮族大学生中HIV-1感染相关基因CCR5多态性的初步研究

目的:了解CCR5Δ32基因突变在广西壮族人群基因组中的分布,初步估计壮族人群对人类免疫缺陷病毒(HIV-1)感染的遗传易感性.方法:分别抽取50名壮族大学生外周血6 ml,从血中提取DNA样品,对其基因组DNA中CCR5基因进行PCR扩增.结果:在50名壮族大学生外周血中未检测到CCR5Δ32基因突变.结论:50名壮族大学生对HIV-1可能较易感.     

延边朝鲜族低密度脂蛋白受体基因PvuⅡ多态位点的研究

[目的 ]研究延边朝鲜族人群低密度脂蛋白受体基因内含子 15PvuⅡ多态性位点的存在和等位基因频率 ,以探讨该群体的遗传结构及遗传背景 .[方法 ]按酚 /氯仿抽提法提取基因组DNA ;用聚合酶链反应 限制性片段长度多态性技术从人类外周血基因组DNA中分离到一个长约 810bp的片段 ,采用Dynabeads固相单链分离直接测序法测定 ,证明分离的片段是否是低密度脂蛋白受体基因内含子 15 ;用限制性内切酶PvuⅡ酶进行酶切 ,进行琼脂糖凝胶电泳 ,在凝胶自动成像系统紫外线检测仪上观察酶切结果 .[结果 ]延边朝鲜族人群低密度脂蛋白受体基因存在PvuⅡ多态性 .12 0名朝鲜族中无酶切位点的纯合个体 92例 ,基因型 (P-P-)频率为 76 6 % ;有酶切位点的杂合个体 2 0例 ,基因型 (P+ P-)频率为16 7% ;有酶切位点的纯合个体 8例 ,基因型 (P+ P+ )频率为 6 7% .2 4 0个低密度脂蛋白受体等位基因中PvuⅡ酶切位点基因 (P+ )的出现频率为 15 % .[结论 ]延边朝鲜族人群低密度脂蛋白受体基因也存在PvuⅡ多态性位点 ,说明PvuⅡ多态性特点可以作为延边朝鲜族的遗传标记 .     

我国人群中人类免疫缺陷病毒1感染的协同受体CCR5△32基因突？…

目前 ,中国人群对人类免疫缺陷病毒 (ＨＩＶ)的遗传易感性已引起我国学者的高度关注。我们取中国人外周血单个核细胞来源的基因组ＤＮＡ ,应用ＰＣＲ扩增和ＤＮＡ序列分析等技术 ,分析ＣＣＲ5Δ32基因纯合子和杂合子在中国人群中的分布 ,初步评估我国人群ＨＩＶ 1感染的遗传易感性。此外 ,希望从分子遗传学角度为我国卫生主管部门对艾滋病防治的决策提供科学依据。一、材料与方法1 标本来源 :我们收集了 915例土生土长的中国人外周静脉血标本 ,他们均为中国人民解放军第三○二医院的住院病人 (主要是患各种急慢性肝炎、菌痢、高血压和肿瘤等…     

DYS452基因座在延边地区朝鲜族和汉族群体中的遗传多态性研究

[目的]研究STR基因座DYS452在延边地区朝鲜族和汉族人群中的遗传多态性.[方法]设计DYS452荧光标记引物,利用PCR扩增与ABI310基因分析仪对无关联的各200份朝鲜族和汉族个体的DYS452基因座进行检测,用GeneMapperID v3.2软件分析电泳结果并分析获得群体遗传多态性数据.[结果]朝鲜族和汉族人群在DYS452基因座上共检测出7个等位基因,朝鲜族人群中检测出5个等位基因,分别为29~33号等位基因;汉族人群中检测出7个等位基因,分别为27~33号等位基因.朝鲜族和汉族人群的GD值分别是0.660 7和0.696 4.将DYS452基因座在朝鲜族和汉族中的遗传分布分别与不同地区、民族及种族进行比较,获得不同群体间的P值和遗传距离.[结论]DYS452基因座在延边地区朝鲜族和汉族群体中具有较高的遗传多态性,可为该地区的法医学个人识别、亲权鉴定及人类遗传学调查提供依据.     

延边朝鲜族人群Ⅰ型胶原蛋白A2基因MspI多态性位点研究

[目的 ]了解中国朝鲜族人群的Ⅰ型胶原蛋白A 2基因MspI多态性位点的存在和等位基因频率 ,并与其它地区人群进行比较 .[方法 ]按酚 氯抽提法提取人类基因组DNA ,采用聚合酶链反应 限制性片段长度多态性方法对Ⅰ型胶原蛋白A 2基因MspI多态性位点进行检测 .[结果 ]12 0名个体中 ,无酶切位点的纯合个体为 89例 ,P-P-基因型频率为 74 2 % ;有酶切位点的杂合个体为 2 2例 ,P+ P-基因型频率为 18 3% ;有酶切位点的纯合个体为 9例 ,P+ P+ 基因型频率为 7 5 % ;2 4 0个等位基因中MspI酶切位点基因P+ 的频率为 16 7% .[结论 ]延边朝鲜族人群Ⅰ型胶原蛋白A 2基因存在多态性 ,Ⅰ型胶原蛋白A 2基因MspI多态性分布与其它地区人群的分布有所不同 ,可以作为朝鲜族的一个遗传标记 .     

广西壮族人群CCR5等位基因多态性的研究

目的:了解广西壮族人群中HIV-1辅助受体趋化因子受体5(CCR5)及其突变体CCR5Δ32等位基因的频率.方法:以60名土生土长的广西壮族人群为研究对象,根据CCR5Δ32碱基缺失位置采用3对特异性引物,用PCR扩增全血DNA样本,根据扩增结果判断CCR5野生型和CCR5Δ32突变体.从中随机抽取3份PCR扩增产物进行测序,通过测序结果与野生型的U95626序列比较来验证PCR扩增结果.结果:60份样本均为CCR5野生型,未发现CCRΔ32突变体.结论:广西壮族人群对HIV-1病毒感染可能具有较高的遗传易感性.     

延边地区朝鲜族和汉族男性人群DYS444基因座遗传多态性

[目的]探讨Y染色体特异性STR基因座DYS444的遗传多态性在延边地区朝鲜族和汉族男性人群中的分布情况.[方法]应用聚合酶链式反应、变性聚丙烯酰胺凝胶电泳和银染显带技术对205份朝鲜族及207份汉族男性DYS444基因座进行检测.[结果]在朝鲜族人群DYS444基因座中检测出5个等位基因,频率分别为0.058 5,0.365 9,0.341 5,0.229 3,0.004 9,个人识别能力为0.693 5;汉族人群中检测出6个等位基因,频率分别为0.091 8,0.338 2,0.372 0,0.164 3,0.024 2,0.009 7,个人识别能力为0.711 1.[结论]所得到的等位基因频率数据可为朝鲜族和汉族人群法医学个人识别、亲权鉴定及遗传学研究提供依据.     

朝鲜族男性人群DYS388基因座遗传多态性分布研究

[目的]探讨Y染色体特异性短串联重复序列(STR)基因座DYS 388的遗传多态性在延边地区朝鲜族人群中的分布情况.[方法]应用PCR,PAGE技术分离扩增产物,结合银染显带技术对DYS388基因座进行检测.[结果]在DYS 388基因座中检测出6个等位基因,其频率分别为0.110,0.006,0.638,0.220,0.017,0.011,个人识别率为0.532 8.[结论]所得到的等位基因频率数据可为朝鲜族人群法医学个人识别、亲权鉴定及遗传学研究提供依据.     

中国延边地区朝鲜族Rh血型分布调查分析

[目的]分析中国延边地区朝鲜族的Rh血型分布情况.[方法]采用血清学方法检测延边地区朝鲜族及汉族人群Rh血型D,C,c,E,e 5种抗原,统计分析Rh表现型、基因组合体频率及基因频率,进行Hardy-Weinberg吻合度及χ~2检验,并与汉族和其他少数民族进行比较.[结果]朝鲜族RhD阴性频率为0.26%,E抗原阳性频率为52.68%;Rh表现型共检出11个,顺序为DCcEe>DCCee>DccEE>DCcee>DccEe>DCCEe>DCcEE>dccee>Dccee>dccEe>dCcee;共计算出8个基因组合体,其频率为DCe>DcE>dce>Dce>dcE>DCE>dCe>dCE,基因频率为C>c,D>d,e>E.[结论]延边地区朝鲜族Rh血型分布较不平衡,RhD阴性频率稀少,集中分布在dccee型;RhD阳性表现型以DCcEe,DCCee两型为主;朝鲜族人群Rh血型呈多态分布.     

朝鲜族人群DXS7132基因座的遗传多态性研究

[目的]了解朝鲜族人群短串联重复序列(STR)基因座DXS 7132的遗传多态性分布,获取相应多态性的群体遗传学数据.[方法]选择261名(男性为160名,女性为101名)延边地区朝鲜族无血缘关系的个体静脉血,提取DNA,经PCR扩增、聚丙烯酰胺凝胶电泳及银染显色等,对朝鲜族人群DXS7132基因座的基因多态性进行分析.[结果]在DXS 7132基因座中检测出8个等位基因,基因型频率分布符合Hardy-Weinberg平衡定律,杂合度大于0.693 1,多态信息含量高于0.710 0,女性个人识别力为0.897 8,男性单倍型多样性为0.767 2.[结论]DXS 7132基因座具有较高的杂合度和多态信息量,是理想的遗传标记系统,建立数据库对朝鲜族人群的亲子鉴定、个人识别及民族基因库的建立具有重要意义.     

靶向基因编辑系统编辑趋化性细胞因子受体5对HIV感染人体影响的研究进展

趋化性细胞因子受体5（chemotactic cytokine receptor 5, CCR5）是艾滋病病毒感染人体的主要辅助受体之一。CCR5作为目前抗HIV-1病毒感染的首选靶点,主要基于的原理是通过降低或敲除靶细胞表面CCR5的表达量,进而阻断CCR5与gp120之间的相互作用阻断病毒的感染。CCR5Δ32造血干细胞移植成功治愈HIV感染后,引起了学术界的轰动。CCR5Δ32是一种先天性CCR5基因的32个碱基缺失的突变。由于CCR5Δ32自然突变的概率低,研究人员一直在探索通过靶向基因编辑系统来构建CCR5Δ32的方法。靶向基因编辑系统是近年来以CCR5为靶点预防和治疗艾滋病的重要方法。本文总结了近年来国内外靶向基因编辑技术在编辑 CCR5对HIV治疗的研究进展。     

中国彝族人群CCR5基因单核苷酸多态性及其与HIV感染的关联研究

目的对中国彝族人群CCR5基因调节区和结构区的单核苷酸多态性（SNP）进行全面检测,并分析SNP与HIV感染的关联.方法通过巢式-PCR分别扩增102份彝族正常人和68份HIV感染者样本的CCR5基因调节区和结构区,利用变性高压液相色谱法（DHPLC）筛选存在突变的基因片段,对突变片段进行双向DNA序列测定,然后应用Sequence Navigator 软件对CCR5基因的单核苷酸多态性进行分析,并通过SPSS and PPAP 软件分析SNPs与HIV感染的相关性.结果在中国彝族人群CCR5基因的编码区中检测到A77G、G316A、T532C、C921T、G668A五种SNP以及第686-688位的AGA缺失突变（686Del3）,除C921T（Y307Y）为无意义突变外,其他A77G、G316A、T532C、G668A均为有意义突变,它们的氨基酸突变分别为K26R、G106R、C178R、R223Q突变.在这些突变位点中,只有G668A突变的等位基因频率较高,可达0.08, 其余均小于0.01,并且在正常人群和HIV感染者两个群体中的等位基因频率没有显著性差异（P＞0.05）;与编码区所不同的是,在调节区检测到T58934G、G59029A、T59353C、G59402A和C59653T五种SNP,他们的等位基因频率较高,在0.1912-0.2941范围之间. 所检测到的每一个突变在正常人群和HIV感染人群中的分布均差异无统计学意义（P＞0.05）.突变位点间的连锁与HIV感染的相关性,提示T59353C-G59402A单体型与HIV感染可能存在关联.结论 DHPLC是一种快速的高效筛选未知基因突变的高通量方法.SNP与HIV感染的关联性有待于进一步深入研究.     

中国人群中HIV-1辅助受体CCR5基因新突变位点及CCR5-894C缺失基因多态性分析

目的：研究中国人群HIV-1辅助受体CCR5基因编码区新的单核苷酸多态性（SNP）位点;分析CCR5-894C缺失等位基因在中国普通人群和HIV-1高危人群中的分布特点和相关意义。方法：针对CCR5编码区用2对引物进行PCR扩增,设计测序引物对45例汉族人样本进行PCR产物直接测序,用DNAstar分析测序结果,寻找SNP位点。采用错配PCR-RFLP法对中国汉族、蒙族、藏族普通人群,性传播疾病和静脉吸毒高危人群及HIV-1携带者,共627份样品进行了CCR5-894C缺失等位基因分型。结果：在45例汉族人CCR5基因编码区共发现6个SNP位点,4个（184A→G、503G→T、668G→A、99G→T）引起氨基酸改变,两个无义突变;此外还发现1个单碱基缺失（894C缺失）,引起移码突变和提前终止。其中184A→G、503G→T、999G→T三个中国汉族人所特有的SNP位点为首次发现,它们的等位基因频率分别为1.11％,21.1%和10.0％;其中503G→T分布明显不符合Hardy-Weinberg平衡。汉、藏、蒙等民族的普通人群CCR5-894C缺失等位基因频率为1.11％,0.53%和0.在汉族HIV-1性传播、静脉吸毒传播的高危人群中,HIV-1阳性个体和阴性个体间CCR5-89C缺失等位基因频率差异无显著意义,与汉族普通人群比较差异也无显著意义。结论：中国人CCR5基因的SNP位点有自己的特点,共发现4个引起氨基酸改变的SNP位点（其中3个为首次发现）,1个引起移码突变的单碱基缺失。汉族人群中存在CCR5-894C缺失突变,但突变频率很低。这些SNP和缺失突变对于HIV-1感染和艾滋病病程的影响值得进一步研究。     

朝鲜族人群鼻部肿瘤

[目的 ]了解朝鲜族的各种鼻部肿瘤的发病率并确定针对高发鼻部肿瘤的研究课题 .[方法 ]调查 1990年 1月到 1999年 10月之间在延边大学医学院附属医院病理科经活检确诊为鼻部肿瘤的全部患者的原始记录 .[结果 ]发现了 82例朝鲜族鼻部肿瘤患者 .其中 ,发病率最高的为乳头状瘤 ( 3 6/ 82 ) ,其次为鳞状上皮癌 ( 13 / 82 ) .[结论 ]朝鲜族鼻部乳头状瘤的发病率明显高于国内其它地区 .必须提高对鼻部乳头状瘤的诊断和治疗水平 ,并加快有关鼻部乳头状瘤和人类乳头状瘤病毒之间的关系的研究 .     

人CCR5Delta32基因重组慢病毒载体的构建及表达

目的:构建含人CCR5Delta32基因的重组慢病毒载体并鉴定其表达性能。方法:从CCR5Delta32突变个体外周血单个核细胞(PBMCs)内提取人基因组DNA,利用PCR技术扩增CCR5Delta32全长基因,经EcoRI单酶切后与pUCm-T载体连接,随后转化感受态E.coliDH5α,提取质粒进行酶切鉴定及DNA测序。再将鉴定正确的CCR5Delta32基因亚克隆至慢病毒载体pLenti6/V5-D-TOPO并进行酶切鉴定及DNA序列分析。最后用pLP1、pLP2、pLP/VSVG及pLenti-CCR5Delta32四种质粒共转染293T细胞,产生重组慢病毒并通过Western blot鉴定目的基因在靶细胞内的表达。结果:经PCR扩增获得约650bp的DNA片段,测序结果与发表于GenBank上的序列完全一致。经酶切鉴定,克隆的目的基因已经正确插入到慢病毒载体pLenti6/V5-D-TOPO中。四种质粒共转染293T细胞,产生出5×105TU/ml高滴度的重组慢病毒。用其感染靶细胞,Western blot结果显示有目的蛋白表达。结论:成功构建了含人CCR5Delta32基因的重组慢病毒载体并将其在293T细胞内表达,为进一步AIDS基因治疗研究奠定基础。     

Genotypes and polymorphisms of mutant CCR5-delta 32, CCR2-64I and SDF1-3' a HIV-1 resistance alleles in indigenous Han Chinese.

OBJECTIVE: To evaluate the frequencies and polymorphisms of CCR5-delta 32, CCR2-64I and SDF1-3' A alleles conferring resistance to HIV-1 infection in Chinese population from Han ethnic origin. METHODS: This cohort was comprised of 1251 subjects (915 men and 336 women) aged 15-80 years and none was HIV-1 positive. Genotyping of allelic CCR5-delta 32, CCR2-64I and SDF1-3' A variants was performed using PCR or PCR/RFLP assay, and further confirmed by direct DNA sequencing. RESULTS: Our finding shows that the delta 32 deletion mutation in the CCR5 gene does occur in this population and can be inherited in a Mendelian fashion in indigenous Han Chinese at a very low frequency of 0.00119 (n = 1254). The frequencies of mutant CCR2-64I and SDF1-3' A alleles were 0.20023 (n = 1251) and 0.2873 (n = 893), in this population, which are higher than those found in American Caucasians. Furthermore the polymorphisms of CCR2-64I and SDF1-3' A alleles in the Han Chinese population were different from those in American Caucasians. Statistical analysis showed that the genotype distribution of CCR5-delta 32, CCR2-64I and SDF1-3' A alleles was in equilibrium according to the Hardy-Weinberg equation. CONCLUSION: The CCR5-delta 32 mutation may not be a major resistant factor against HIV-1 infection in indigenous Han Chinese. The significance of higher frequencies of CCR2-641 and SDF1-3' A alleles (0.20023 and 0.2791) in the Han population remains to be clarified in HIV-1-positive carriers and AIDS patients.     

HIV PATHOGENESIS-EMERGING CONCEPTS

CD4 receptor molecules on ‘T’ lymphocytes and macrophages have already been identified as the route of entry for HIV. However CCR5 and CXCR4 are identified only recently as the second receptors for HIV on macrophages and ‘T’ lymphocytes respectively. Presence of homozygous CCR5 Δ 32, a defective CCR5 gene leads to resistance to HIV infection in the risk groups. While heterozygous CCRS Δ 32 leads to delay in the progress of HIV infection to AIDS.KEY WORDS: CCR5, CXCR4, SDF-1, HIVSince the beginning of the HIV pandemic, many a questions still remain unanswered. The most intriguing of them is susceptibility to HIV. Even in the same risk group, exposed to same risk factors only some of the individuals get the infection while others do not. Some of the siblings (about 20%) born from the same HIV infected mother develop AIDS whereas others escape. Another pertinent question is why some HIV infected people progress rather faster than the others towards AIDS? What protects the uninfected? What slows the progress of the HIV to AIDS? After years of research scientists have tried to find some of the answers to these questions.Though possible HLA differences were postulated to be the cause of these differences [1], recent evidences suggest that the good fortune of some individuals, who are partly or fully resistant to HIV infection are due to possession of a particular variant of a gene involved in immunologic function. At present this gene and its variations are intensely studied for strategies to prevent and control HIV infection particularly to HIV-1.Immediately after the discovery of the virus in 1984, at the National Cancer Institute, search for these factors were initiated. In a cohort study, groups of several hundred individuals at high risk of HIV infections-viz. homosexual men, IV drug abusers and hemophiliacs who had received contaminated blood products were monitored for years by physicians. The patients (with their consent) supplied blood, tissue samples and case reports to researchers for study of cell biology and DNA genetic testing. The cohorts were divided into (a) those infected with HIV vs those who remained free of it after extensive exposure (b) infected patients who progressed to AIDS rapidly vs those who progressed to AIDS slowly, if at all (c) infected HIV, who developed a specific type of infection example, Pneumocystis carinii pneumonia vs those who did not. Their genotypes were studied [2].An individual inherits two copies of all genes outside the sex chromosome (one copy from the mother and one copy from the father). The pair of alleles of a particular chromosomal locus or gene address constitute the genotype. One who inherits two identical alleles of a given gene is said to be a homozygote; one who inherits two distinct alleles is said to be a heterozygote. After more than a decade of relentless research for their differences in multiple centres of excellence, finally a ray of hope appeared in 1995 [3]. By 1990 it was well documented that HIV causes immunodeficiency mainly by depletion of white blood cells known as T lymphocytes that displayed a protein CD4 on their surface [4]. Many aspects of immune response against the virus are directed by T cells. Another immune cell, the macrophage also carry the CD4 receptor and are also infected by the HIV virus. As the macrophages are not destroyed by the virus, the infection persists for years. Thus the HIV virus has a cytolytic effect on the T cells but it has no such effect on the macrophages [5].The glycoprotein gp120 of HIV virus attaches to CD4 receptor molecules of the cell to gain entry into them. Though CD4 receptor is essential, it is not sufficient by itself to allow the entry of HIV. The second receptor has been recently known as a chemokine receptor. Chemokines or chemoattractant cytokines, are short 10 kd aminoacid chains which are responsible for luring immune cells to injured or diseased sites. The chemokines viz RANTES (Regulated upon activation normal T-cell expressed and secreted), MIP-1α (Macrophage inflammatory protein), MIP-1ß, possibly interfere with HIV entry into immune cells by binding to and blocking some cell surface proteins that HIV requires for access to the interior [6]. These cell surface proteins are known as receptors and they physiologically mediate the chemotaxis of T-cells and phagocytic cells to areas of inflammation. Choe et al in 1996, discovered the second receptor on CD4 T cells called the chemokine receptor CXCR4. Simultaneously the second receptor on the macrophages was discovered it is called CCR5 [7]. CXCR4 is an a chemokine where the first two cysteine residues have an intervening aminoacid, whereas CCR5 is a ß chemokine where the first two cysteine residues do not have an intervening aminoacid [8].To keep the records of pathogenicity straight, the HIV virus initially infects macrophages by its gp 120 molecule by attaching to two receptors, i.e., CD4 and CCR5 (Fig-1). These are called the macrophagetropic strains or M-tropic strain or R5 strains. They are also known as transmitted strains [9]. Once inside the macrophages, it synthesizes large quantities of the virus. After years of infection the constantly mutating virus alters the gene for gp120 which changes its allegiance to CXCR4 instead of CCR5. Thus it becomes T lymphotropic as it gains entry via CD4 and CXCR4 receptor on its surface (Fig-2). These HIV strains are known as T-tropic strain or X4 strains. But here the disease takes a dramatic turn. The virus behaves here as cytolytic and kills the T lymphocytes after multiplying within it. The T lymphocyte count steadily dips from 1000/cmm to <200/cmm when opportunistic infections set in and it becomes an AIDS defining condition [10]. However in another cohort study Winkler et al in National Cancer Institute, USA, found stromal derived factor (SDF-1) which is a principal ligand for CXCR4 has protective effect when its structural defective homozygous variant SDF1-3’A/3’A is present in some individuals. The protective effect against AIDS is twice as strong as that conferred by variants of CCR5 [11].Open in a separate windowFig. 1Entry of HIV into macrophages and entry inhibition (M-Tropic Strain)Open in a separate windowFig. 2Entry of HIV into T lymphocytes and entry inhibition (T-Tropic Strains)Liu and colleagues in July 1996 characterized the genetic sequence of CCR5 in both the groups of individuals in the cohort studies. It was found that the groups which were protected from HIV infection were having 32 nucleotides missing from the gene of CCR5 known as CCR5 A 32 gene. The 32 base pair deletion in the CCR5 gene correspond to the second intracellular loop of CCR5 and encodes a severely truncated molecule. They experimentally found that this CCR5 A 32 was producing a truncated CCR5 receptor protein which either fails to reach the cell surface or is so deformed that it cannot attach to HIV [12]. They found that the deletion mutant for the protection against HIV was highly significant statistically. Those individuals who are homogeneous for CCR5 A allele are resistant to HIV infection but those who are heterozygous may be infected with HIV, but progress slowly to AIDS, if at all and they have a lower level of viremia. In these cases the virus has 4-10 fold reduced ability to replicate [13]. Mishrahi in one study found that children with CCR5 A 32 heterozygocity are not protected against mother to infant transmission but, if, infected, there is a longer time before adverse clinical outcome develops than in children with wild type CCR5 geno-type [14]. With increasing HIV exposure the prevalence of A 32/ A 32 CCR5 genotype increases. The wild type CCR5 and CCR5 A 32alleles can be detected easily by polymerase chain reaction (PCR) technique using EcoR1 restriction enzyme digestion and running the digested DNA in agarose gel electrophoresis [15].This recent knowledge has important bearing on the pathogenicity of HIV and potential for a possible therapeutic agent against CCR5-HIV-1 interaction.On full analysis of the available data, it was found that Russians have the mutant allele in 13% of the population, Caucasian Americans have 11.1% for Caucasian European it is 10.0%, African American 1.7% and for Native American, African and Asian population it is 0% [16]. A study on the Indian population is yet to be done about this protective factor which limits HIV infections.The final word about the protective factors against HIV has not yet been told as HIV infection has been reported in a person with hemophilia and several homosexual men with CCR5 Δ 32 homozygotes [8]. This only shows that research has to go on, for, the war on HIV seems to be endless.     

延边地区朝鲜族和汉族的艾滋病知识现况分析

[目的 ]比较延边地区朝鲜族和汉族出国劳务人员的艾滋病知识水平 .[方法 ]采用整群抽样法 ,对延边地区朝鲜族和汉族出国劳务人员 85 8人进行艾滋病知识的现况调查 ,其中朝鲜族 5 2 5名 ,汉族 333名 .[结果 ]在艾滋病基本知识测试中出现明显的民族差异 ,汉族的艾滋病预防知识平均得分明显高于朝鲜族 .2个民族人群获得艾滋病知识的前 3位途径分别是电视、报刊杂志及广播 .[结论 ]应加强延边地区艾滋病健康教育 ,而在制定健康教育计划时 ,应考虑民族因素 .