Host Transcriptional Response to Persistent Infection with a Live-Attenuated Porcine Reproductive and Respiratory Syndrome Virus Strain

Authors

Jayeshbhai Chaudhari, University of Nebraska-LincolnFollow
Chia-Sin Liew, University of Nebraska-LincolnFollow
Aspen M. Workman, USDA, ARS, U.S. Meat Animal Research CenterFollow
Jean-Jack Riethoven, University of Nebraska - LincolnFollow
David J. Steffen, University of Nebraska-LincolnFollow
Sarah Vitosh-Sillman, University of Nebraska–LincolnFollow
Hiep Vu, University of Nebraska-lincolnFollow

Document Type

Article

Date of this Version

2020

Citation

2020 by the authors

Comments

Viruses 2020, 12, 817; doi:10.3390/v12080817

www.mdpi.com/journal/viruses

Abstract

Both virulent and live-attenuated porcine reproductive and respiratory syndrome virus (PRRSV) strains can establish persistent infection in lymphoid tissues of pigs. To investigate the mechanisms of PRRSV persistence, we performed a transcriptional analysis of inguinal lymphoid tissue collected from pigs experimentally infected with an attenuated PRRSV strain at 46 days post infection. A total of 6404 differentially expressed genes (DEGs) were detected of which 3960 DEGs were upregulated and 2444 DEGs were downregulated. Specifically, genes involved in innate immune responses and chemokines and receptors associated with T-cell homing to lymphoid tissues were down regulated. As a result, homing of virus-specific T-cells to lymphoid tissues seems to be ineffective, evidenced by the lower frequencies of virus-specific T-cell in lymphoid tissue than in peripheral blood. Genes associated with T-cell exhaustion were upregulated. Likewise, genes involved in the anti-apoptotic pathway were upregulated. Collectively, the data suggested that the live-attenuated PRRSV strain establishes a pro-survival microenvironment in lymphoid tissue by suppressing innate immune responses, T-cell homing, and preventing cell apoptosis.