Single-cell transcriptomic profiling of bronchial lymph nodes reveals mechanisms of PRRSV escape from host adaptive immunity

Category	Detail
Condition	Porcine reproductive and respiratory syndrome (PRRS)
Key Mechanisms	Impaired adaptive immune responses, including delayed neutralizing antibody development and defective T-cell responses.
Target Population	Piglets infected with highly pathogenic PRRSV (HP-PRRSV).
Care Setting	Veterinary clinical research.

HP-PRRSV infection reduces multiple T-cell subsets while increasing B cells in bronchial lymph nodes.
Infection disrupts T-cell egress, leading to accumulation of cytotoxic T lymphocytes.
Impaired crosstalk between T follicular helper cells and germinal center B cells may suppress neutralizing antibody production.
Identification of a novel RAG1+ CD4+CD8+ double-positive T-cell subset associated with PRRSV.
Study provides insights into mechanisms of PRRSV-induced adaptive immunosuppression.

Single-cell RNA sequencing can be utilized to analyze immune responses in PRRSV infection.

Further research is needed to develop effective vaccines and antiviral strategies against PRRSV.

Monitor T-cell and B-cell responses in infected populations to assess immune status.

Delayed neutralizing antibody production may lead to prolonged viral replication and persistence.

Piglets infected with HP-PRRSV.

Currently, no broad-spectrum, highly effective, and safe vaccine is available for PRRSV.

Utilize single-cell transcriptomic analysis to understand immune landscape changes in PRRSV infection.
Focus on enhancing T-cell and B-cell interactions to improve vaccine efficacy.

Clinical Scorecard: Single-cell RNA sequencing of bronchial lymph nodes uncovers strategies used by PRRSV to evade host adaptive immune responses