Gene expression of cytokines and chemokines on porcine alveolar macrophage cells (PAM) infected with recombinant genotype I and II strains of African swine fever virus isolated from field in Vietnam
Keywords:
African swine fever, chemokine, cytokine, gene expression, PAMsAbstract
African swine fever (ASF) is a highly contagious and fatal disease in pigs, with mortality rates reaching 100%, causing devastating economic impacts globally. Currently, the efficacy of available vaccines remains limited, particularly against the recombinant ASF virus (ASFV) genotype I/II. While cytokines and chemokines play a pivotal role in initiating and coordinating the host’s immune response, their expression mechanisms during infection are not yet fully understood. This study evaluated the gene expression of various cytokines and chemokines in porcine alveolar macrophages (PAMs) infected with the recombinant ASFV genotype I/II using quantitative real-time PCR (qRT-PCR). Our results demonstrated that the antiviral cytokines (IFN-γ, IFN-α, IFN-β, and TNF-α) showed strong upregulation, peaking at 48 hours post-infection (hpi) and remaining elevated until 72 hpi. Proinflammatory cytokines (IL-1α, IL-1β, IL-12p40, and IL-17A) increased significantly between 24 and 48 hpi, functioning to initiate and amplify the inflammatory response. Concurrently, Th2 cytokines (IL-4, IL-10, IL-11, and IL-13), reached peak levels at 48-72 hpi to balance inflammation and promote humoral immunity. Furthermore, various chemokines (CCL2, CCL3, CCL14, and CXCL9) exhibited substantial increases, with CXCL9 peaking early at 24 hpi, suggesting a key role in recruiting immune cells to the site of infection. These findings indicate a tightly regulated coordination between cytokines and chemokines during the 24-48 hpi, providing critical insights into viral control and the host’s adaptive immune regulation against recombinant ASFV strains in Vietnam.
DOI:
https://doi.org/10.31276/VJST.2025.3757Classification number
1.6, 4.3
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Published
Received 28 November 2025; revised 26 December 2025; accepted 9 January 2026

