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Elevated levels of total and Puumala virus-specific immunoglobulin E in the Scandinavian type of hemorrhagic fever with renal syndrome.

Alexeyev, O A (författare)
Umeå universitet,Virologi
Ahlm, Clas, 1956- (författare)
Umeå universitet,Infektionssjukdomar,Clas Ahlm
Billheden, Jan (författare)
Umeå universitet,Infektionssjukdomar
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Settergren, Bo (författare)
Umeå universitet,Infektionssjukdomar
Wadell, Göran (författare)
Umeå universitet,Virologi
Juto, Per (författare)
Umeå universitet,Virologi
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 (creator_code:org_t)
1994
1994
Engelska.
Ingår i: Clinical and diagnostic laboratory immunology. - 1071-412X. ; 1:3, s. 269-72
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
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  • In a previous study, it was reported that the total immunoglobulin E (IgE) level was increased in patients with hemorrhagic fever with renal syndrome (HFRS). The aim of the present study was to investigate whether specific IgE is synthesized during the course of the disease. For this purpose, an epsilon-capture enzyme-linked immunosorbent assay was developed. A total of 72 patients with HFRS caused by Puumala virus were studied. 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 subjects 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) and of patients with other viral diseases (P < 0.001). All patients developed 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 total and specific IgE levels decreased during convalescence compared with those during the acute phase of HFRS (P < 0.001 and P < 0.001, respectively). In conclusion, we have shown that both total and specific IgE levels are increased in patients with HFRS compared with levels in patients with other viral diseases. The possible pathogenetic role of the specific IgE response in HFRS is discussed.

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