When pregnant gilts are infected with porcine reproductive and respiratory syndrome virus (PRRSV) late in gestation, their fetuses respond very differently depending on where the virus has traveled. A new study in BMC Veterinary Research reports that measurable antiviral gene expression in fetal tissues appeared only when viral load in the fetal thymus exceeded 2.5 log per microgram, and that the heart, rather than the thymus, mounted the strongest transcriptional response in heavily infected fetuses.
The research team, led by K. E. Walker and colleagues including J. K. Lunney, set out to identify tissues and genes that could forecast whether a fetus is resistant, resilient, or susceptible to congenital PRRSV infection. Their hypothesis was that targeted gene expression analysis would reveal mechanisms behind resistance, seen in fetuses showing no infection, and resilience, seen in fetuses that maintained low viral loads despite exposure.
In the study, 27 pregnant gilts were inoculated with PRRSV at day 85 plus or minus 0.9 of gestation. Twenty-one days after maternal inoculation, the gilts and their fetuses were euthanized and fetal tissues were collected for analysis. The researchers selected a subset of fetuses based on PRRS viral load measured in the placenta, fetal serum, and fetal thymus.
From those measurements, the team defined six distinct fetal groups. Control fetuses came from mock-infected sows. From infected sows came uninfected fetuses with zero log viral load in all three compartments; PLCO fetuses with virus only in the placenta; PLCSER fetuses with virus in both placenta and serum; THYL fetuses with virus in placenta and serum plus a low thymic viral load below 2.0 log; and THYM fetuses with virus in placenta and serum plus a medium thymic viral load above 2.5 log.
RNA was extracted from the fetal heart, liver, and thymus, and differential gene expression was evaluated across 168 gene targets and 12 groupings hypothesized to be involved in fetal outcome, using NanoString transcriptomics.
The central finding was striking: antiviral responses were observed only when thymic viral load exceeded 2.5 log per microgram. Almost no differentially expressed genes were detected even in the PLCSER group, where fetuses carried high viral loads in serum.
In the THYM group compared with controls, the heart showed the most robust response, with 34 of the 168 targeted genes differentially expressed. The liver followed with 12 of 168, while the thymus itself exhibited only 2 of 168.
Instead, the study points to non-lymphoid tissues as early responders. The authors conclude that early responsiveness to the virus, as evidenced by differential gene expression in non-lymphoid tissues, appears critical for fetal survival.
PRRS is economically devastating to pork producers worldwide, and understanding which fetuses survive infection has long been a goal of the field. By linking fetal outcome categories to tissue-specific gene expression patterns, the study offers a framework for identifying markers of resistance and resilience. The work is published as an open-access article in BMC Veterinary Research, and the version shared carries a note that it is subject to further edits before the final Version of Record.
Subject of Research: Tissue-specific fetal gene expression responses to congenital PRRSV infection in pigs
Article Title: Probing fetal heart, liver, and thymus gene expression in congenital PRRSV infection: effect of fetal thymic viral load
Article References: Walker, K. E., Pasternak, J. A., Royer, M., Van Goor, A., Harding, J. C. S., & Lunney, J. K. (2026). Probing fetal heart, liver, and thymus gene expression in congenital PRRSV infection: effect of fetal thymic viral load. BMC Veterinary Research. https://doi.org/10.1186/s12917-026-06044-z
Image Credits: AI Generated
DOI: 10.1186/s12917-026-06044-z
Keywords: PRRSV, fetal gene expression, thymus, viral load, NanoString transcriptomics, porcine reproductive and respiratory syndrome, heart, liver, antiviral response, pregnant gilts, BMC Veterinary Research, congenital infection
News Source: Juliet Wilcox. (October 29, 2026). Fetal heart and liver, not thymus, drive early antiviral gene response to PRRSV. Scienmag.
