PRRSV infection facilitates the shedding of soluble CD163 to induce inflammatory responses.

Porcine reproductive and respiratory syndrome (PRRS), which poses substantial threats to the global pig industry, is primarily characterized by interstitial pneumonia. Cluster of differentiation 163 (CD163) is the essential receptor for PRRSV infection. Metalloproteinase-mediated cleavage of CD163 leads to the shedding of soluble CD163 (sCD163), thereby inhibiting PRRSV proliferation.

Enteric coronavirus PDCoV evokes a non-Warburg effect by hijacking pyruvic acid as a metabolic hub.

The Warburg effect, also referred as aerobic glycolysis, is a common metabolic program during viral infection. Through targeted metabolomics combined with biochemical experiments and various cell models, we investigated the central carbon metabolism (CCM) profiles of cells infected with porcine deltacoronavirus (PDCoV), an emerging enteropathogenic coronavirus with zoonotic potential. We found that PDCoV infection required glycolysis but decreased glycolytic flux, exhibiting a non-Warburg effect characterized by pyruvic acid accumulation.

PRRSV-induced inflammation in pulmonary intravascular macrophages (PIMs) and pulmonary alveolar macrophages (PAMs) contributes to endothelial barrier function injury.

Porcine reproductive and respiratory syndrome (PRRS) is a severe infectious disease currently devasting the global pig industry. PRRS is characterized by intense inflammation and severe damage to the alveolar-capillary barrier. Therefore, it is crucial to uncover the underlying mechanism by which the PRRS virus (PRRSV) induces inflammatory responses and barrier function damage.

Porcine reproductive and respiratory syndrome virus infection manipulates central carbon metabolism.

The metabolic pathways of central carbon metabolism (CCM), glycolysis and the tricarboxylic acid (TCA) cycle, are important host factors determining the outcome of viral infection. Thus, it is not surprising that viruses easily manipulate CCM for optimized replication. Porcine reproductive and respiratory syndrome virus (PRRSV) is an Arterivirus that has devastated the swine industry worldwide for over 30 years.

Itaconate derivative 4-OI inhibits PRRSV proliferation and associated inflammatory response.

Itaconate, a metabolite of the tricarboxylic acid (TCA) cycle produced by immunoresponsive gene 1 (IRG1) via catalyzation of cis-aconitate, plays important roles in metabolism and immunity. Porcine reproductive and respiratory syndrome virus (PRRSV) is an Arterivirus that has devastated the swine industry worldwide for over 30 years. Here, we found that 4-octyl itaconate (4-OI), a cell-permeable itaconate derivative, dose-dependently inhibited PRRSV proliferation by interfering with viral attachment, replication, and release.