Porcine reproductive and respiratory syndrome virus (PRRSV), is a virus that causes a disease of pigs, called porcine reproductive and respiratory syndrome (PRRS), also known as blue-ear pig disease (in Chinese, zhū láněr bìng 豬藍耳病). This economically important, panzootic disease causes reproductive failure in breeding stock and respiratory tract illness in young pigs.
History PRRS earlier known as "mystery swine disease" and "blue ear disease" during 1987–1988 in the United States and Canada caused first undiagnosed outbreaks, characterized by reproductive losses combined with respiratory signs. In 1990-1991, a similar disease was reported in several European countries such as Germany, The Netherlands, Belgium, Denmark, France, the United Kingdom, and Spain. The emergence of PRRS in Japan, Taiwan and mainland China was reported in 1987, 1991 and 1996, respectively. According to the WOAH, the disease is now present throughout the world, especially in countries with major pig production. Australia, New Zealand, Norway, Sweden and Switzerland are PRRS free. A better picture of PRRSV's genetic diversity suggested that the virus was present in the field before the "original" outbreaks. The lack of recorded data concerning the prevalence prior to the epidemic was due to unawareness of PRRS. A hypothesis has been proposed that PRRSV derived of closely related murine lactate dehydrogenase-elevating virus. Phylogeographic analysis of PRRSV epidemiology suggested that the virus diversified into unique subpopulations in Russia and Belarus, approximately 110–140 years ago. However, still there is an uncertainty as to how, when and where the PRRSV emerged. Several important factors allowed PRRSV to expand further. The transformation of the pig industry worldwide in the 20th century plays a key role. The emergence of high-density confinement management practices and adoption of artificial insemination facilitated wide expansion and diversification of PRRSV. There is abundant evidence that PRRSV is present in wild boars. Wild animals may act as a natural reservoir for PRRSV and could be considered as an additional source of viral infections in domestic pigs.
Current situation PRRSV is highly dynamic in nature. Increasing genetic diversity allows emergence of severe outbreaks characterized by an elevated abortion rate as well as mortality in growing pigs and sows. This happened in 1996, 2000 and 2007 in the US and in 2006 in China. Highly pathogenic and virulent "atypical" PRRSV isolates are regularly reported in different European countries: Belarus, Belgium, Hungary, Austria and others. Immunization programs of swine herds worldwide with attenuated vaccines made of both PRRSV genotypes provided initially optimistic results in the 1990s. At present PRRS, is one of the most significant infectious disease affecting the swine industry. It was also named as "pig AIDS" for emerging through accidental transspecies transmission and significant economic losses in worldwide pig production.
Virology
Classification PRRSV is a member of the family Arteriviridae, and order Nidovirales. Other members of the family Arteriviridae include: equine arteritis virus (EAV), simian hemorrhagic fever virus (SHFV), wobbly possum disease virus, and lactate dehydrogenase elevating virus (LDV).
Structure and genome PRRSV is a small, single-stranded, positive-sense, enveloped RNA virus. The 15 kb genome consists of one linear, single stranded RNA molecule consisting of a 5′ untranslated region (UTR), ten open reading frames (ORFs 1a-1b-2a-2b-3-4-5-5a-6-7) and a 3′ UTR followed by a polyadenylation tail.
Two large ORFs (1a and 1b) comprise 75% of the viral genome. They are translated and processed into 14 non-structural proteins including four proteases and the RNA-dependent RNA polymerase. A PRRSV particle is composed of eight viral structural proteins encoded by ORFs 2-7. They consist of envelope proteins (GP2a, E, GP3, GP4, GP5, ORF5a and M) and the nucleocapsid (N) protein. The most conserved proteins within the whole family of Arteriviridae and PRRSV, in particular, are nsp9 (RNA-dependent RNA polymerase) and nucleocapsid (N) protein. Similarity analysis demonstrates the presence of hyper-variable regions in nsp2 and GP4. An assembled PRRSV virion appears as a spherical particle with a mean diameter of 56 nm. The particles display a very smooth outline of the lipid bilayer of the envelope with few protruding features represented by the two major envelope protein complexes: M-GP5 and GP2-GP3-GP4. These complexes interact with the well-characterized receptors CD169 (sialoadhesin) and CD163, respectively.
Genetic variability
PRRSV is subdivided in two major types, the European (also known as Type 1) and the North American (also known as type 2). Prototype sequences for each PRRSV type have been defined. For the European PRRSV, this is the Lelystad virus (LV), while for the North American PRRSV, this is the VR-2332. The European and North American PRRSV strains cause similar clinical symptoms, but represent two distinct viral genotypes whose genomes diverge by approximately 40%, thus creating a veil of mystery about the origin of this virus. It was suggested that the emergence of these distant types of PRRSV was a result of two independent evolutionary events. To accommodate the clear divergence of the Type 1 and Type 2 PRRSV, they were split into two separate viruses. The genetic variation among the viruses isolated from different places increases the difficulty of developing vaccines against it. Similarly, maintaining diagnostic PCR detection assays is difficult due to the high mutation rate of this virus. In Europe, a geographical demarcation exists between areas of low (Western and Central Europe) and high (Eastern Europe) PRRSV1 diversity. Current genetic classification based on the size of open reading frame (ORF) 7 revealed the existence of three different subtypes within PRRSV1 strains: subtype 1, with Lelystad virus as prototype, is present in Europe and Russia, subtype 2 in Russia and Lithuania and subtype 3 in Belarus. Besides known subtypes, a recent study showed non-subtypeable PRRSV1 isolates.
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