Abstract
Porcine reproductive and respiratory syndrome virus (PRRSV) is a problematic virus that is difficult to control. The principal target cells for PRRSV infection are porcine alveolar macrophages (PAMs). Increasing evidence has demonstrated that CD163 is the determinant receptor for PRRSV infection. However, the relationship between CD163 abundance and PRRSV infection is unclear. In this study, we first generated primary immortalized PAMs (iPAMs) using SV40 large T antigen and demonstrated that CD163 expression is suppressed by the alternative splicing of mRNA in iPAMs. Two forms of CD163 transcripts were discovered, and most iPAMs expressed a short-form CD163 transcript that lacked from scavenger receptor cysteine-rich tandem repeat 1 (SRCR1) to SRCR5 of the functional domain. More importantly, using flow cytometric cell sorting technology, we isolated CD163-positive single-cell-derived clones with varying CD163 abundances to investigate the relationship between CD163 abundance and PRRSV infection. For the first time, we showed that cells with low CD163 abundance (approximately 20%) do not initiate PRRSV infection, while cells with moderate CD163 abundance display limited infection. PRRSV initiated efficient infection only in cells with high CD163 abundances. Our results demonstrate that CD163 abundance is a pivotal switch for PRRSV replication.
Highlights
Porcine reproductive and respiratory syndrome virus (PRRSV) is a dangerous pathogen in the swine industry worldwide, especially with the emergence of highly pathogenic PRRSV [1, 2]
Primary porcine alveolar macrophages (PAM) immortalized by introducing SV40 large T antigen fail to support PRRSV replication
The primary PAMs were plated at a low density in a 6-well plate, and SV40 large T antigen was introduced via an murine leukemia virus (MLV)-mediated lentiviral vector
Summary
Porcine reproductive and respiratory syndrome virus (PRRSV) is a dangerous pathogen in the swine industry worldwide, especially with the emergence of highly pathogenic PRRSV [1, 2]. According to recent taxonomic classifications, the Arteriviridae family includes three other viruses, namely, equine arteritis virus (EAV), lactate dehydrogenase-elevating virus (LDV) and simian hemorrhagic fever virus (SHFV). PRRSV infection is limited to porcine alveolar macrophages (PAMs), differentiated blood monocytes (BMos), dendritic cells (DCs) and a subset of bone marrow (BM) cells [4]. Several putative receptors have been demonstrated to participate in PRRSV infection. These putative PRRSV receptors include CD163 [5], CD151 [6], CD169 [7], Heparin sulfate (HS) [3], vimentin [8], DC-SIGN (dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin/CD209)
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