Related Experiment Video
Updated: Apr 13, 2026

05:59
Nasal Wipes for Influenza A Virus Detection and Isolation from Swine
Published on: December 4, 2015
10.0K
Postnatal persistent infection with classical Swine Fever virus and its immunological implications
Sara Muñoz-González1, Nicolas Ruggli2, Rosa Rosell3
1Centre de Recerca en Sanitat Animal (CReSA), IRTA-Universitat Autònoma de Barcelona (UAB), Campus de la UAB, Bellaterra, Barcelona, Spain.
Plos One
|May 5, 2015
Summary
Classical swine fever virus (CSFV) can cause persistent infections in piglets after birth, leading to immunosuppression and thymus atrophy. These persistently infected pigs may evade detection through standard serological surveillance methods.
Area of Science:
- Veterinary Virology
- Immunology
- Animal Pathology
Background:
- Trans-placental transmission of classical swine fever virus (CSFV) during mid-gestation causes persistently infected offspring.
- The mechanisms and outcomes of early postnatal CSFV infection remain less understood.
Purpose of the Study:
- To investigate the potential of CSFV to induce viral persistence following early postnatal infection.
- To characterize the immunological and pathological consequences of postnatal CSFV persistence.
Main Methods:
- Piglets were intranasally infected at birth with CSFV isolates of low and moderate virulence.
- Clinical health, virus titers, immune responses (humoral and cellular), and pathological lesions were monitored for six weeks.
- Peripheral blood mononuclear cells (PBMCs) were stimulated to assess interferon-gamma (IFN-γ) production and interleukin-10 (IL-10) levels.
Main Results:
- Postnatally infected piglets remained clinically healthy but showed persistent high virus titers and failed to mount detectable immune responses.
- Severe thymus atrophy was observed, and PBMCs exhibited unresponsiveness to CSFV and mitogen stimulation.
- While IL-10 was produced by CSFV-stimulated PBMCs, adding an anti-IL-10 antibody did not restore T-cell responses, suggesting other immunosuppressive factors.
Conclusions:
- CSFV can establish persistent infections after early postnatal infection, leading to significant immunosuppression and thymus atrophy.
- This postnatal persistence model offers insights into viral persistence mechanisms and highlights potential surveillance challenges.
- The findings underscore the epidemiological and economic importance of understanding CSFV persistence beyond trans-placental transmission.

