Abstract
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-poFcγRII) 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-poFcγRII 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 FcγRII-mediated. Identification of the inhibitory FcγR 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.
Highlights
Porcine reproductive and respiratory syndrome virus (PRRSV) is an enveloped positive-strand RNA virus in the family Arteriviridae [1]
Marc-145 cell line was selected for transfection with poFccRII, because it is a permissive cell for PRRSV infection
Virus infection and virion production were quantified in the absence of PRRSV antibody using both Marc-poFccRII and parent Marc-145 cells (Fig. 2)
Summary
Porcine reproductive and respiratory syndrome virus (PRRSV) is an enveloped positive-strand RNA virus in the family Arteriviridae [1]. PRRS can cause severe reproductive failure in sows and is associated with the porcine respiratory disease complex in combination with secondary infection [2,3,4]. The virus is present in a majority of swine producing countries around the world and gives rise to significant economic losses in pig farming [5]. Swine are the only known host of PRRSV, and myeloid cells, macrophages and dendritic cells, are the primary permissive cells [6]. Various features of PRRSV infection and the ensuing immune response suggest that PRRSV immunity is aberrant. PRRSV infection can induce significant and specific antibody and B-cell responses to a variety of PRRSV protein [8,9]
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