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Pathogen Page

Porcine respiratory and reproductive syndrome virus

I. General Information

1. NCBI Taxonomy ID:

2. Disease:

Porcine Reproductive and Respiratory Syndrome (PRRS), Blue-Ear Pig Disease

3. Introduction

The PRRSV is an enveloped, single-stranded positive-sense RNA virus, approximately 50–65 nm in diameter that is classified in the order Nidovirales, family Arteriviridae, genus Arterivirus along with equine arteritis virus, lactate dehydrogenase-elevating virus of mice, and simian hemorrhagic fever virus. Properties of these viruses include the ability to induce prolonged viremia, persistent infections, and replication in macrophages. Being an enveloped virus, PRRSV survivability outside of the host is affected by temperature, pH and exposure to detergents. It is known that PRRSV can survive for extended intervals (>4 months) at temperatures ranging from −70 to −20 °C; however, viability decreases with increasing temperature. Regarding genetic diversity, there are two major prototypes of PRRSV, the European isolate (Lelystad virus, LV) and the North American isolate (VR-2332). Porcine reproductive and respiratory syndrome (PRRS) is an economically important disease of swine, estimated to cost the swine industry in USA approximately US$ 560 million per year. Clinical outbreaks of PRRS were first reported in the late 1980's in the USA; however, the etiology of the disease remained unknown. Clinical signs included severe reproductive failure, post-weaning pneumonia, growth reduction, decreased performance, and increased mortality. Similar clinical outbreaks were reported in Germany in 1990 and were widespread throughout Europe by 1991. In 1991, the etiologic agent, porcine reproductive and respiratory syndrome virus (PRRSV) was identified by investigators in The Netherlands and USA. Today, PRRSV is endemic in the global swine population; however, several countries, including Sweden, Switzerland, New Zealand, and Australia claim to be free of the disease (Cho and Dee, 2006).

4. Host Ranges and Animal Models

Pigs

5. Host Protective Immunity

Infected pigs develop a strong and rapid humoral response but these initial antibodies do not confer protection and can even be harmful by mediating an antibody-dependent enhancement of disease. In contrast, development of neutralising antibodies (NAs) is delayed and generation of cell-mediated immune responses, such as PRRSV-specific interferon (IFN)-gamma secreting cells, is initially erratic. In spite of this, induction of strong and rapid NAs and IFN-gamma responses seem to be required for effective vaccination. PRRSV strongly modulates the host's immune responses. The virus inhibits key cytokines, such as IFN-alpha, and may induce regulatory cytokines, such as interleukin (IL)-10 (Mateu and Diaz, 2008).

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