A preliminary study into the protective mechanisms of adaptive immunity against porcine reproductive and respiratory syndrome virus (PRRSV) in piglets (n = 9) born to a gilt challenged intranasally with a type-2 PRRSV. Immune parameters (neutralizing antibodies, CD3⁺CD4⁺, CD3⁺CD8⁺, CD3⁺CD4⁺CD8⁺ T-lymphocytes, and PRRSV-specific interferon (IFN)-γ secreting T-lymphocytes) were compared with infection parameters (macro- and microscopic lung lesion, and PRRSV-infected porcine alveolar macrophages (CD172α⁺PRRSV-N⁺ PAM) as well as with plasma and lymphoid tissue viral loads. Percentages of three T-lymphocyte phenotypes in 14-days post-birth (dpb) peripheral blood mononuclear cell (PBMC) had significant negative correlations with percentages of CD172α⁺PRRSV-N⁺ PAM (p < 0.05) as well as with macroscopic lung lesion (p < 0.01). Plasma and tissue viral loads had significant (p < 0.05) negative correlations with CD3⁺CD4⁺CD8⁺ T-lymphocyte percentage in PBMC. Frequencies of CD3⁺CD8⁺ and CD3⁺CD4⁺ T-lymphocytes in 14-dpb PBMC had significant negative correlations with of lymph node (p = 0.04) and lung (p = 0.002) viral loads. IFN-γ-secreting T-lymphocytes frequency had a significant negative correlation with gross lung lesion severity (p = 0.002). However, neutralizing antibody titers had no significant negative correlation (p > 0.1) with infection parameters. The results indicate that T-lymphocytes contribute to controlling PRRSV replication in young piglets born after in-utero infection.
Adaptive Immunity ; Antibodies ; Antibodies, Neutralizing ; Interferons ; Lung ; Lymph Nodes ; Lymphoid Tissue ; Macrophages, Alveolar ; Phenotype ; Plasma ; Porcine Reproductive and Respiratory Syndrome ; Porcine respiratory and reproductive syndrome virus ; T-Lymphocytes ; Viral Load

A preliminary study into the protective mechanisms of adaptive immunity against porcine reproductive and respiratory syndrome virus (PRRSV) in piglets (n = 9) born to a gilt challenged intranasally with a type-2 PRRSV. Immune parameters (neutralizing antibodies, CD3⁺CD4⁺, CD3⁺CD8⁺, CD3⁺CD4⁺CD8⁺ T-lymphocytes, and PRRSV-specific interferon (IFN)-γ secreting T-lymphocytes) were compared with infection parameters (macro- and microscopic lung lesion, and PRRSV-infected porcine alveolar macrophages (CD172α⁺PRRSV-N⁺ PAM) as well as with plasma and lymphoid tissue viral loads. Percentages of three T-lymphocyte phenotypes in 14-days post-birth (dpb) peripheral blood mononuclear cell (PBMC) had significant negative correlations with percentages of CD172α⁺PRRSV-N⁺ PAM (p < 0.05) as well as with macroscopic lung lesion (p < 0.01). Plasma and tissue viral loads had significant (p < 0.05) negative correlations with CD3⁺CD4⁺CD8⁺ T-lymphocyte percentage in PBMC. Frequencies of CD3⁺CD8⁺ and CD3⁺CD4⁺ T-lymphocytes in 14-dpb PBMC had significant negative correlations with of lymph node (p = 0.04) and lung (p = 0.002) viral loads. IFN-γ-secreting T-lymphocytes frequency had a significant negative correlation with gross lung lesion severity (p = 0.002). However, neutralizing antibody titers had no significant negative correlation (p > 0.1) with infection parameters. The results indicate that T-lymphocytes contribute to controlling PRRSV replication in young piglets born after in-utero infection.