ELEVATED LEVELS OF TOTAL AND PUUMALA VIRUS-SPECIFIC IMMUNOGLOBULIN-E IN THE SCANDINAVIAN TYPE OF HEMORRHAGIC-FEVER WITH RENAL SYNDROME

Citation
Oa. Alexeyev et al., ELEVATED LEVELS OF TOTAL AND PUUMALA VIRUS-SPECIFIC IMMUNOGLOBULIN-E IN THE SCANDINAVIAN TYPE OF HEMORRHAGIC-FEVER WITH RENAL SYNDROME, Clinical and diagnostic laboratory immunology, 1(3), 1994, pp. 269-272
Citations number
31
Categorie Soggetti
Immunology,"Infectious Diseases","Medical Laboratory Technology",Microbiology
ISSN journal
1071412X
Volume
1
Issue
3
Year of publication
1994
Pages
269 - 272
Database
ISI
SICI code
1071-412X(1994)1:3<269:ELOTAP>2.0.ZU;2-T
Abstract
In a previous study, it was reported that the total immunoglobulin E ( IgE) level was increased in patients with hemorrhagic fever,vith renal syndrome (HFRS). The aim of the present study was to investigate whet her specific IgE is synthesized during the course of the disease. For this purpose, an E-capture enzyme-linked immunosorbent assay was devel oped. A total of 72 patients with HFRS caused by Puumala virus were st udied. Three different control groups were included: 20 blood donors, 20 patients with other viral diseases (influenza A and B virus, acute Epstein-Barr virus, and acute cytomegalovirus infections), and 5 subje cts with high levels of total IgE (median, 1,070 kU/liter; range, 773 to 5,740 kU/liter). The levels of total IgE were significantly higher during the acute phase of HFRS than those of blood donors (P < 0.01) a nd of patients with other viral diseases (P < 0.001). All patients dev eloped a specific IgE response (median, 55 arbitrary units; range, 24 to 123 arbitrary units) in the acute phase of the disease, whereas in the different control groups no specific IgE was detectable. Both tota l and specific IgE levels decreased during convalescence compared with those during the acute phase of HFRS (P < 0.001 and P < 0.001, respec tively). In conclusion, we have shown that both total and specific IgE levels are increased in patients with HFRS compared with levels in pa tients with other viral diseases. The possible pathogenetic role of th e specific IgE response in HFRS is discussed.