CONTINUITY AND DISCONTINUITY IN THE ANTI-V3 IGG RESPONSE OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE 1-INFECTED PERSONS IN A CROSS-SECTIONAL AND LONGITUDINAL-STUDY USING SYNTHETIC PEPTIDES

被引:7
作者
LAWOKO, A
JOHANSSON, B
DASH, R
FALCK, L
DIETRICH, U
PIPKORN, R
NILEHN, B
BLOMBERG, J
机构
[1] LUND UNIV,DEPT MED MICROBIOL,VIROL SECT,S-22362 LUND,SWEDEN
[2] CENT HOSP HELSINGBORG,DEPT BACTERIOL,HELSINGBORG,SWEDEN
[3] CENT HOSP HELSINGBORG,DEPT INFECT DIS,HELSINGBORG,SWEDEN
[4] DEUTSCH KREBSFORSCHUNGSZENTRUM,HEIDELBERG,GERMANY
[5] GEORG SPEYER HAUS,CHEMOTHERAPEUT FORSCHUNGSINST,FRANKFURT,GERMANY
关键词
D O I
10.1093/infdis/172.3.682
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The principal neutralization domain (PND) of the V3 region of human immunodeficiency virus type 1 (HIV-1) gp120 is central to HIV pathogenesis. The IgG antibody response to PND was followed in 15 HIV-1-infected persons from southern Sweden over 2-5 years using 32 synthetic V3 peptides. Five peptides had amino acid sequences derived from isolates from each of 5 patients. Sera obtained simultaneously with isolate almost always reacted strongly with these cognate peptides; however, reactivity was undetectable in 1 patient's serum and short lived in the sera of another, indicating inducible holes in the antibody repertoire, which would facilitate dissemination of the corresponding virus strains. Reactivity to other V3 peptides correlated with sequence similarity to the cognate peptide. Strong, stable reactivity to peptides with sequences similar to a south Swedish V3-consensus was accompanied by transient activity to less similar ones. The latter may reflect viral variation, B lymphocyte clonal depletion, or both. Certain IgG responses appeared to preclude others, suggesting clonal dominance.
引用
收藏
页码:682 / 690
页数:9
相关论文
共 45 条
[1]  
AHLERS JD, 1993, J IMMUNOL, V150, P5647
[2]   SEQUENCE VARIATION WITHIN THE HUMAN-IMMUNODEFICIENCY-VIRUS V3 LOOP AT SEROCONVERSION [J].
AITKHALED, M ;
EMERY, VC .
JOURNAL OF MEDICAL VIROLOGY, 1993, 41 (04) :270-274
[3]   RAPID DEVELOPMENT OF ISOLATE-SPECIFIC NEUTRALIZING ANTIBODIES AFTER PRIMARY HIV-1 INFECTION AND CONSEQUENT EMERGENCE OF VIRUS VARIANTS WHICH RESIST NEUTRALIZATION BY AUTOLOGOUS SERA [J].
ALBERT, J ;
ABRAHAMSSON, B ;
NAGY, K ;
AURELIUS, E ;
GAINES, H ;
NYSTROM, G ;
FENYO, EM .
AIDS, 1990, 4 (02) :107-112
[4]   SIMPLE, SENSITIVE, AND SPECIFIC DETECTION OF HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 IN CLINICAL SPECIMENS BY POLYMERASE CHAIN-REACTION WITH NESTED PRIMERS [J].
ALBERT, J ;
FENYO, EM .
JOURNAL OF CLINICAL MICROBIOLOGY, 1990, 28 (07) :1560-1564
[5]   IMPROVED TISSUE-CULTURE TECHNIQUE FOR PRODUCTION OF POORLY REPLICATING HUMAN IMMUNODEFICIENCY VIRUS-STRAINS [J].
ASJO, B ;
ALBERT, J ;
CHIODI, F ;
FENYO, EM .
JOURNAL OF VIROLOGICAL METHODS, 1988, 19 (3-4) :191-196
[6]  
AYEHUNIE S, 1991, VIRUS GENES, V5, P359
[7]   NATURAL VARIANTS OF CYTOTOXIC EPITOPES ARE T-CELL RECEPTOR ANTAGONISTS FOR ANTIVIRAL CYTOTOXIC T-CELLS [J].
BERTOLETTI, A ;
SETTE, A ;
CHISARI, FV ;
PENNA, A ;
LEVRERO, M ;
DECARLI, M ;
FIACCADORI, F ;
FERRARI, C .
NATURE, 1994, 369 (6479) :407-410
[8]   A SURVEY OF SYNTHETIC HIV-1 PEPTIDES WITH NATURAL AND CHIMERIC SEQUENCES FOR DIFFERENTIAL REACTIVITY WITH ZIMBABWEAN, TANZANIAN AND SWEDISH HIV-1-POSITIVE SERA [J].
BLOMBERG, J ;
LAWOKO, A ;
PIPKORN, R ;
MOYO, S ;
MALMVALL, BE ;
SHAO, J ;
DASH, R ;
TSWANA, S .
AIDS, 1993, 7 (06) :759-767
[9]  
BLOMBERG J, 1989, J CLIN MICROBIOL, V17, P1081
[10]   SEQUENCE-ANALYSIS OF THE GP120 REGION OF THE ENV GENE OF UGANDAN HUMAN IMMUNODEFICIENCY PROVIRUSES FROM A SINGLE INDIVIDUAL [J].
BRUCE, C ;
CLEGG, C ;
FEATHERSTONE, A ;
SMITH, J ;
ORAM, J .
AIDS RESEARCH AND HUMAN RETROVIRUSES, 1993, 9 (04) :357-363