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Porcine Fc?RIIb mediates enhancement of porcine reproductive and respiratory syndrome virus (PRRSV) infection.

ABSTRACT: Antibody-dependent enhancement (ADE) of virus infection caused by the uptake of virus-antibody complexes by Fc?Rs is a significant obstacle to the development of effective vaccines to control certain human and animal viral diseases. The activation Fc?Rs, including Fc?RI and Fc?RIIa have been shown to mediate ADE infection of virus. In the present paper, we showed that pocine Fc?RIIb, an inhibitory Fc?R, mediates ADE of PRRSV infection. Stable Marc-145 cell lines expressing poFc?RIIb (Marc-poFc?RII) were established. The relative yield of progeny virus was significantly increased in the presence of sub-neutralization anti-PRRSV antibody. The Fab fragment and normal porcine sera had no effect. Anti-poFc?RII antibody inhibited the enhancement of infection when cells were infected in the presence of anti-PRRSV antibody, but not when cells were infected in the absence of antibody. These results indicate that enhancement of infection in these cells by anti-PRRSV virus antibody is Fc?RII-mediated. Identification of the inhibitory Fc?R mediating ADE infection should expand our understanding of the mechanisms of pathogenesis for a broad range of infectious diseases and may open many approaches for improvements to the treatment and prevention of such diseases.

SUBMITTER: Qiao S

PROVIDER: S-EPMC3248417 | biostudies-literature | 2011

REPOSITORIES: biostudies-literature

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Porcine FcγRIIb mediates enhancement of porcine reproductive and respiratory syndrome virus (PRRSV) infection.

Qiao Songlin S Jiang Zhizheng Z Tian Xiaohui X Wang Rui R Xing Guangxu G Wan Bo B Bao Dengke D Liu Yonghui Y Hao Huifang H Guo Junqing J Zhang Gaiping G

PloS one 20111229 12

Antibody-dependent enhancement (ADE) of virus infection caused by the uptake of virus-antibody complexes by FcγRs is a significant obstacle to the development of effective vaccines to control certain human and animal viral diseases. The activation FcγRs, including FcγRI and FcγRIIa have been shown to mediate ADE infection of virus. In the present paper, we showed that pocine FcγRIIb, an inhibitory FcγR, mediates ADE of PRRSV infection. Stable Marc-145 cell lines expressing poFcγRIIb (Marc-poFcγR ...[more]

PMID: 22220194

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Project description:BackgroundMechanisms of fetal death following maternal PRRSV2 infection remain uncharacterized, although hypoxia from umbilical cord lesions and/or placental detachment due to apoptosis are hypothesized. We performed two experiments examining hypoxia and apoptosis in PRRSV-infected and non-infected, third-trimester fetuses to elucidate possible associations with fetal death. Fetuses were selected based on four phenotypic infection groups: fetuses from non-challenged control gilts (CTRL); low viral load fetuses (LVL; Exp 1) or uninfected fetuses (UNINF; Exp 2) from inoculated gilts; viable high viral load fetuses (HVL-VIA); and HVL meconium-stained fetuses (HVL-MEC).ResultsIn experiment 1, paraffin embedded fetal tissues collected 21 days post maternal infection (DPI) were examined for DNA fragmentation associated with apoptosis. Positively stained foci were larger and more numerous (P < 0.05) in heart, liver, and thymus of HVL-VIA and HVL-MEC compared to CTRL and LVL fetuses. In experiment 2, group differences in gene expression within the hypoxia (HIF1a, IDO1, VEGFa, LDHA, NOS2, NOX1) and apoptosis (CASP3, CASP7, CASP8, CASP9, RIPK1, RIPK3) pathways were assessed by RT-qPCR in fetal tissues collected at 12 DPI. High viral load fetuses showed differential expression relative to the CTRL and UNINF (P < 0.05 for all). Brain tissue from HVL-VIA and HVL-MEC fetuses presented increased expression of CASP7, CASP8, RIPK3, HIF1a and IDO1. Fetal heart showed increased expression of CASP8, HIF1a, IDO and NOX1 and a decrease in NOS2 expression in infected groups. CASP7, CASP9, RIPK1 and RIPK3 were only increased in the heart of HVL-VIA while VEGFa was only increased for HVL-MEC fetuses. Thymus from HVL-MEC had decreased expression of CASP9 and there was increased IDO1 in all infected fetuses.ConclusionsThere is strong evidence of apoptosis occurring in the heart, liver and thymus of highly viral load fetuses at 21 DPI. Furthermore, there was clear upregulation of apoptotic genes in the heart of high viral load infected fetuses and less prominent upregulation in the brain of PRRSV-infected fetuses, whereas thymus appears to be spared at 12 DPI. There was no strong evidence of hypoxia at 12 DPI in brain and thymus but some indication of hypoxia occurring in fetal heart.

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Porcine Fc?RIIb mediates enhancement of porcine reproductive and respiratory syndrome virus (PRRSV) infection.

Publications

Porcine FcγRIIb mediates enhancement of porcine reproductive and respiratory syndrome virus (PRRSV) infection.

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