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CD1D knockout swine are permissive to African swine fever virus genotype II infection
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DOI：10.1080/22221751.2026.2671519.png)
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Abstract
En 中文
African swine fever virus (ASFV) is an important pathogen of domestic and wild suids and the causative agent of African swine fever (ASF). ASFV displays a tropism for myeloid cells, predominately of the monocyte/macrophage lineage, which is critical for ASFV pathogenesis. However, the mechanisms that govern the cellular tropism of ASFV are complex and incompletely understood. ASFV can enter susceptible cells through several mechanisms. One way is by clathrin-mediated endocytosis (CME) via interaction with the host glycoprotein CD1d, encoded by the CD1D gene, and disruption of CD1D expression significantly reduces ASFV replication in cell culture. In order to evaluate the role of CD1d in the replication and pathogenesis of ASF in vivo, CD1D knockout (KO) pigs, generated using a CRISPR-Cas9 system, were challenged with the highly virulent genotype II ASFV isolate MNG19. Notably, CD1D KO pigs were highly permissive to ASFV infection and developed severe acute ASF similar to age-matched wildtype (WT) controls. No significant differences in disease severity or mortality between ASFV-infected WT and KO pigs were observed. ASFV DNA levels in blood or in the majority of visceral and lymphoid tissues were also not significantly different between ASFV-infected wild-type and KO pigs. In addition, pathological changes were similar between both groups and typical of acute ASF, such as fibrinous polyserositis, haemorrhagic lymphadenopathy, and systemic coagulopathy. This work demonstrates that porcine CD1d is not critical for genotype II ASFV replication and virulence in vivo, and that CD1D KO piglets possess no resistance to virulent genotype II ASFV infection.
Keywords:
African swine fever virus
pathogenesis
CD1d
CRISPR-Cas9
disease resistance
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