Molecular Microbiology Research, 2025, Vol.15, No.1, 10-17 http://microbescipublisher.com/index.php/mmr 12 3.2 Adaptive immune response and related gene expression 3.2.1 B-cell-mediated humoral immune response and antibody production After adaptive immunity is initiated, B cells are activated and then specific antibodies are started. These antibodies recognize and neutralize FMDV, preventing the virus from entering the cells. In this process, a gene called C1QB also plays a role, which enhances the complement system and thus improves the efficiency of the antibody (Lüet al., 2018). 3.2.2 T-cell-mediated cellular immune response (differentiation and activation of CD4+ and CD8+ T cells) In addition to B cells, T cells are also very important, especially CD4+ and CD8+. They are activated after the antigen is recognized and then are involved in the removal of infected cells. Some studies have pointed out that genes like TIMD4 are related to T cell activation, which shows that T cells play a very critical role in fighting FMDV (Chen et al., 2021). 3.2.3 Establishment of immunological memory and its role in secondary infection The immune system also "remembers" the virus. This is immune memory. After the initial infection, some B and T cells are converted into memory cells. When FMDV appears again, they can react quickly and effectively control the virus. This is important in preventing recurrence (Hussain et al., 2019). 3.2.4 Role of MHC molecules in antigen presentation and gene polymorphism To make T cells work, the first thing to do is to have an antigen "display". This process relies on MHC molecules. They deliver viral antigens to T cells, guiding the direction of the immune response. There are differences in MHC genes, and this diversity will affect their efficiency and will also affect the ability of the entire immune system to respond to FMDV (Nahas et al., 2021). 3.3 Cytokine network function in the antiviral process Cytokines are also very active during FMDV infection. These small molecules, like "messengers", are responsible for transmitting immune signals between cells. For example, TNF, IL-6 and IL-10 are involved in the inflammatory response and the mobilization of immune cells. Studies have found that the pathways related to these cytokines are significantly activated in FMDV infection (Wani et al., 2018). They can help control virus replication and also help the body quickly start defense. 4 Immune Gene Expression Analysis Results 4.1 Differential expression of immune genes in early, middle, and late stages of infection When FMDV infects goats, the expression of immune genes changes at different stages. In the early stages of infection, the expression of cytokines such as IL6, CXCL2, CCL20, CCL4, and transcription factors such as NFKBIA will be increased. These genes and molecules are primarily responsible for initiating inflammation and immune responses (Zhang et al., 2018). In the mid-term, some chemokines have been downregulated, such as CCL23 and CXCL17. This change may affect the arrival of immune cells, making it easier for the virus to stay and continue to infect (Zhu et al., 2020). In the late stages, the situation was more complicated. The study found that some genes associated with Th17 immune response are upregulated, while the classic NF-κB pathway is downregulated. This combination may make the virus easier to stay in the body and less easily cleared (Zhu et al., 2022). 4.2 Functional analysis of upregulated and downregulated genes The study also analyzed what all genes with obvious expression changes did during the infection process. It was found that many upregulated genes are related to immune and inflammatory pathways, such as those involved in the cytokine-receptor interaction pathway or the TNF signaling pathway. These pathways are important to fight viruses. Some downregulated genes are often related to cell apoptosis or cell killing. If these genes are attenuated, the body may not be able to remove the virus smoothly, resulting in the persistence of the virus (Eschbaumer et al., 2016). In addition, some chemokines that attract neutrophils or T cells are also inhibited after infection. This may leave the immune system “cannot find the direction” and thus allow the virus to escape (Wani et al., 2019).
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