Is parvovirus B19 the cause for autoimmunity against the angiotensin II type receptor?
Initial studies have demonstrated the significance of the agonistic angiotensin II receptor AT1 autoantibody (AT1-AA) in preeclampsia, although it is unclear what factors induce its generation. Since the epitope recognized by AT1-AA shares high homology with parvovirus B19 (PVB19) capsid proteins, we have investigated the relationship between the presence of AT1-AA in maternal circulation and PVB19 sero-prevalence in normal and abnormal pregnancy. We determined the parvovirus IgG sero-prevalence in normal pregnancies in the second trimester and those with abnormal uterine perfusion that are at risk for preeclampsia. Secondly, pregnancies at delivery with preeclampsia or intrauterine growth restriction were included. All women with normal perfusion were AT1-AA-negative and 80% were parvovirus-IgG-positive. Sixty-three percent of pregnancies with abnormal uterine perfusion were AT1-AA-positive and 71% IgG-positive. Fifty-two percent of the IgG-positive pregnancies in this subgroup were also AT1-AA-positive, and 9 of the 10 parvovirus IgG-negative women were AT1-AA-positive. In the third trimester, 87% of pregnancies with manifest disease were AT1-AA-positive and 58% IgG-positive. While 79% of the PVB19 IgG-positive pregnancies were also AT1-AA-positive, all parvovirus IgG-negative women were AT1-AA-positive. In all groups, AT1-AA activity did not differ between parvovirus IgG-negative and positive women. We find parvovirus IgG-positive pregnant women in all subgroups without relation to AT1-AA presence. This favors AT1-AA generation to be independent of epitope mimicry between parvovirus B19 capsid proteins and the AT1 receptor.
Stepan
Holger
H
Department of Obstetrics and Gynecology, University of Leipzig, Germany.
Wallukat
Gerd
G
Max-Delbrück-Center for Molecular Medicine, Berlin, Germany.
Schultheiss
Heinz-Peter
HP
Department of Cardiology and Pneumology, Charité, Campus Benjamin Franklin (CBF), Hindenburgdamm 30, 12200 Berlin, Germany.
Faber
Renaldo
R
Department of Obstetrics and Gynecology, University of Leipzig, Germany.
Walther
Thomas
T
Department of Cardiology and Pneumology, Charité, Campus Benjamin Franklin (CBF), Hindenburgdamm 30, 12200 Berlin, Germany; Department of Pharmacology, Erasmus Medical Center, Rotterdam, The Netherlands. Electronic address: thomas.walther@charite.de.
D000818:Animals; D000914:Antibodies, Viral / Q000097:blood / Q000276:immunology*; D001323:Autoantibodies / Q000097:blood / Q000276:immunology*; D015551:Autoimmunity; D036022:Capsid Proteins / Q000276:immunology*; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood / Q000276:immunology*; D018716:Molecular Mimicry / Q000276:immunology; D010322:Parvoviridae Infections / Q000097:blood / Q000150:complications / Q000276:immunology; D016732:Parvovirus B19, Human / Q000276:immunology*; D011225:Pre-Eclampsia / Q000097:blood / Q000209:etiology / Q000276:immunology*; D011247:Pregnancy; D011262:Pregnancy Trimester, Second / Q000097:blood / Q000276:immunology; D011263:Pregnancy Trimester, Third / Q000097:blood / Q000276:immunology; D051381:Rats; D044140:Receptor, Angiotensin, Type 1 / Q000276:immunology*
D000914:Antibodies, Viral; D001323:Autoantibodies; D036022:Capsid Proteins; D007074:Immunoglobulin G; D044140:Receptor, Angiotensin, Type 1