Glycoforms of α1-Acid Glycoprotein in Sera of Human Immunodeficiency Virus-Infected Persons

In acute infections thus far studied, there is a relative increase in plasma protein glycoforms rich in biantennary complex type N-glycans (type I), while in some diseases with chronic inflammatory changes, there is increase in glycoforms with more branched N-glycans (type II). In sera of 109 human...

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Published inThe Journal of infectious diseases Vol. 169; no. 6; pp. 1360 - 1363
Main Authors Mackiewicz, Andrzej, Khan, Muhammad A., Górny, Aleksander, Kapcińska, Małgorzata, Juszczyk, Jacek, Calabres, Leonard H., Espinosa, Louis R.
Format Journal Article
LanguageEnglish
Published Chicago, IL The University of Chicago Press 01.06.1994
University of Chicago Press
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Summary:In acute infections thus far studied, there is a relative increase in plasma protein glycoforms rich in biantennary complex type N-glycans (type I), while in some diseases with chronic inflammatory changes, there is increase in glycoforms with more branched N-glycans (type II). In sera of 109 human immunodeficiency virus (HIV)-infected persons, 38 rheumatoid arthritis patients, and 44 healthy subjects, the composition of α1-acid glycoprotein (AGP) glycoforms was studied using crossed immunoaffinity electrophoresis with concanavalin A as a ligand. In patients in CDC classifications I, II, and III, distribution of AGP glycoforms was analogous to that in normal subjects. Type I alterations were observed in patients in group IV who had no signs of arthritis. Type II changes, analogous to those found in rheumatoid arthritis, were seen in group IV patients who developed arthritis. Most significant type I changes were associated with Pneumocystis carinii pneumonia (specificity, 100%;sensitivity, 96%).
Bibliography:ark:/67375/HXZ-JJP90KX2-F
istex:E0CD1B0EADE8CCD9D66DC0D665A543E57365FBE2
Reprints or correspondence: Dr. Andrzej Mackiewicz, Dept. of Cancer Immunology, Academy of Medicine at GreatPoland Medical Center, Garbary 15, 61866 Poznań, Poland.
ISSN:0022-1899
1537-6613
DOI:10.1093/infdis/169.6.1360