z-logo
Premium
Low induction of varicella‐zoster virus‐specific secretory IgA antibody after vaccination
Author(s) -
Terada Kihei,
Niizuma Takahiro,
Yagi Yoshina,
Miyashima Hiroko,
Kataoka Naoki,
Sadahiro Tomio
Publication year - 2000
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/1096-9071(200009)62:1<46::aid-jmv8>3.0.co;2-y
Subject(s) - vaccination , chickenpox , immunology , varicella zoster virus , virus , virology , secretory iga , antibody , herpesviridae , medicine , immunoglobulin a , biology , viral disease , immunoglobulin g
Breakthrough after varicella vaccination occurs in approximately 2.6%∼18.6% of immunocompetent children, but the reason has not been demonstrated clearly. As a first defense, specific secretory IgA antibody on the mucosa plays an important role in preventing invasion of microorganisms. To examine induction of varicella‐zoster virus (VZV) specific secretory IgA after natural infection and vaccination and its booster mechanisms, 143 salivary samples were tested by ELISA. The VZV‐secretory IgA values were significantly higher in the matched children after natural chickenpox than in those after vaccination, although the total secretory IgA did not differ between them. Two (7%) of the vaccinees lacked the sIgA antibody. In the elderly and in immunocompromised children, the VZV‐secretory IgA values were no lower than those in healthy children, and they did not lack VZV‐secretory IgA. The doctors and nurses taking care of patients with chickenpox had higher values than the other groups as did individuals who had had herpes zoster recently. VZV‐secretory IgA was thought to be stimulated by exogenous and reactivated endogenous VZV to neutralize VZV with weak activity. These results suggest that low or no induction of VZV‐secretory IgA antibody after vaccination may be one of the possible explanations for a breakthrough. J. Med. Virol. 62:46–51, 2000. © 2000 Wiley‐Liss, Inc.

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here