Retrovirus infection in pigs: a possible factor in poor health

UK - Researchers at Cambridge and Glasgow Universities recently reported the novel discovery of age-related titres of circulating retroviral elements in serum samples taken from commercial pigs and a preliminary association with background disease status and mortality (5, 7).
calendar icon 13 October 2006
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All mammals have within their genetic makeup leftover traces of past virus infections, especially those within the retrovirus family. These agents are unusual in that part of their replication strategy is to put their genome into the host's genetic material. If this occurs in germ line cells then the virus becomes fixed as part of the host's genetic makeup and does not need to replicate itself; these are called endogenous retroviruses. Other retroviruses survive by infecting new host animals and undergoing replication to produce infectious progeny which are shed to infect in contact susceptible animals (e.g. equine infectious anaemia virus) and these are called exogenous retroviruses. There is, as yet, no clear link with disease caused by endogenous retroviruses but exogenous retroviruses do cause many important veterinary and human diseases.

This preliminary data indicates that commercial pigs carry high and variable titres of retroviral RNA in blood, with statistically significant differences in titre according to age (weaners versus growers versus adults), and herd health status. The initial study assessed herd health status according to over-all herd mortality rate and presence or absence of 2 endemic diseases: post-weaning mortality and wasting syndrome (PMWS) and porcine reproductive and respiratory syndrome (PRRS).

Only 4 farms, a total of 89 pigs, were included in the initial study but evidence was found for increased retroviral titres in weaner and grower pigs on the low health status units versus the higher health units. Initial sequencing studies indicate the presence of a retrovirus previously proposed to be exogenous in miniature swine (3, 6).

There are plans to initiate a joint Cambridge (Dr Dan Tucker), Glasgow (Dr Linda Scobie) and Bristol Veterinary School-based (Professor Mick Bailey) study in March, subject to funding. The primary goals will be to expand these initial data, to understand the cause or effect relationship between retroviraemia and low health status, and to develop prototype diagnostic tools and control methods if appropriate.

Relevant Paper

Evidence of retroviraemia in commercial pigs and its preliminary association with low health status.

Authors: L Scobie^ and AW Tucker*

^ Institute of Comparative Medicine, Faculty of Veterinary Medicine, University of Glasgow, Glasgow, Scotland. G61 1QH. Email: [email protected]. Telephone: +44 (0)141 330 2402.

* Department of Veterinary Medicine, University of Cambridge, Madingley Rd., Cambridge, UK. CB3 0ES. Email: [email protected]. Telephone: +44 (0)1223 330885.

References

  1. BRATANICH A., W. HENEINE, C. KONOBY, ET AL. 1999. Lack of evidence of conserved lentiviral sequences in pigs with post weaning multisystemic wasting syndrome. Can J Vet Res 63:207-211.
  2. GREEN, L. May 2005 2005, posting date. PMWS Study - First Results. Warwick University. [Online.]
  3. SCOBIE, L., S. TAYLOR, J. C. WOOD, ET AL. 2004. Absence of replication-competent human-tropic porcine endogenous retroviruses in the germ line DNA of inbred miniature Swine. J Virol 78:2502-9.
  4. TAKEUCHI, Y., C. PATIENCE, S. MAGRE, ET AL. 1998. Host range and interference studies of three classes of pig endogenous retrovirus. J Virol 72:9986-91.
  5. TUCKER, A.W., M. A. MELLENCAMP, M. DONADEU, L. SCOBIE. 2006. Retroviraemia in commercial pigs and its preliminary association with low health status. Journal of Clinical Microbiology 44(10): 3846-3847.
  6. WOOD, J. C., G. QUINN, K. M. SULING, ET AL. 2004. Identification of exogenous forms of human-tropic porcine endogenous retrovirus in miniature Swine. J Virol 78:2494-501.
  7. TUCKER, A.W., L. SCOBIE. 2006. Retroviraemia and low health status in pigs. Vet. Rec. 159(11):367-8.
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