Lymphoid tissue tropism of porcine reproductive and respiratory syndrome virus replication during persistent infection of pigs originally exposed to virus in utero

Raymond R.R. Rowland, Steven Lawson, Kurt Rossow, David A. Benfield

Research output: Contribution to journalArticlepeer-review

73 Scopus citations

Abstract

The ability of porcine reproductive and respiratory syndrome virus (PRRSV) to establish a persistent infection is the principal contributing factor to the world-wide spread of the disease. Several studies have documented the course of viral infection in postnatally infected pigs; however, very little is known regarding sites of virus replication during persistent infection of pigs exposed to PRRSV in utero. In this study, virus replication and PRRSV-specific antibody were followed for several hundred days in a group of pigs derived from three sows infected at 90 days of gestation with PRRSV isolate VR-2332. Eighty-four percent of pigs were born viremic with a mortality of 54% within 21 days after birth. At approximately 60 days sera from pigs were negative for virus by virus isolation. Analysis of virus replication in the tissues of pigs randomly sacrificed between 63 and 132 days showed no evidence of virus in lung and other non-lymphoid organs. However, virus was easily recovered from tonsil and lymph nodes and in situ hybridization identified these tissues as sites of virus replication. Even though replication was at a low level, virus was easily transmitted to sentinel pigs. By 260 days pigs became seronegative and did not transmit virus to sentinel pigs. Sacrifice of remaining pigs after 300 days showed no evidence of virus in blood and tissues. This study shows that congenital PRRSV-infected pigs can support virus replication for an extended period during which virus replication is primarily restricted to tonsil and lymph nodes.

Original languageEnglish (US)
Pages (from-to)219-235
Number of pages17
JournalVeterinary Microbiology
Volume96
Issue number3
DOIs
StatePublished - Oct 30 2003

Bibliographical note

Funding Information:
This work was supported by the USDA National Research Initiative for Competitive Grants Program Grants # 95-37204-2233 and # 97-35204-5071, National Pork Producer Council Grant # 1795, National Science Foundation Grant # OSR-9108773, South Dakota Agricultural Experiment Station and the South Dakota Future Fund. We thank Curt Nelson and Scott Kistler for their excellent assistance in the care and welfare of the animals.

Keywords

  • Congenital infection
  • Persistence
  • Pig-viruses
  • Porcine reproductive and respiratory syndrome virus (PRRSV)

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