Porcine Reproductive and Respiratory Syndrome: Key Insights

Porcine Reproductive and Respiratory Syndrome (PRRS) is one of the most economically significant diseases affecting pig production worldwide. It leads to reproductive failure in sows and severe respiratory illness in piglets, resulting in considerable financial losses for farmers. Despite extensive research, controlling PRRS remains a challenge due to its ability to evade immune defenses.

Basic Characteristics Of The Virus

Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) belongs to the family Arteriviridae and the genus Betaarterivirus. It is an enveloped, single-stranded, positive-sense RNA virus, highly prone to genetic mutations and recombination. The viral genome is approximately 15 kilobases long and encodes structural and non-structural proteins essential for replication, host interaction, and pathogenesis. The glycoproteins GP2, GP3, and GP4 contribute to viral entry, while GP5, the most abundant envelope protein, plays a role in receptor binding and immune evasion. The nucleocapsid protein (N) forms the core of the virion and aids in genome packaging.

PRRSV persists in infected pigs due to its high mutation rate and genetic diversity. The error-prone RNA-dependent RNA polymerase lacks proofreading capability, leading to a quasispecies—a population of closely related but genetically distinct viral variants within a single host. This genetic plasticity complicates vaccine development, as immune responses to one strain may not protect against others. PRRSV is divided into two major species: Betaarterivirus suid 1 (formerly PRRSV-1), predominant in Europe, and Betaarterivirus suid 2 (formerly PRRSV-2), more common in North America and Asia. These species exhibit significant genetic and antigenic differences, further complicating control efforts.

The virus primarily targets macrophages, particularly in the lungs and lymphoid tissues, where it replicates efficiently. The primary receptor for PRRSV entry is CD163, a scavenger receptor on porcine macrophages. The virus also utilizes heparan sulfate and sialoadhesin (CD169) as attachment factors. Once inside the host cell, PRRSV undergoes endocytosis, uncoating, and genome replication in the cytoplasm. Newly synthesized virions are assembled and released via exocytosis, spreading the infection. This macrophage tropism allows PRRSV to evade rapid clearance and maintain long-term circulation within a herd.

Transmission Pathways Among Swine

PRRSV spreads through multiple routes, making containment difficult. Direct contact between infected and susceptible pigs is a primary mode of transmission, as the virus is shed in respiratory secretions, saliva, urine, semen, and feces. In high-density farming environments, close interaction facilitates rapid spread, with infected pigs remaining viremic for weeks.

Aerosolized transmission is another significant concern, particularly in intensive pig farming regions. Studies have detected viable PRRSV particles up to 9.1 kilometers from an infected source. Factors like temperature, humidity, and wind direction influence airborne spread. Filtration systems, including high-efficiency particulate air (HEPA) filters, have been implemented in swine facilities to reduce this risk.

Semen-mediated transmission is particularly relevant in breeding operations. Infected boars can shed the virus in semen for extended periods, even without clinical signs. Artificial insemination with contaminated semen accelerates PRRSV spread across distant herds. Stringent testing protocols, including reverse transcription polymerase chain reaction (RT-PCR) assays, are used to screen semen before distribution.

Fomites, including contaminated equipment, clothing, and transport vehicles, also contribute to PRRSV dissemination. The virus can persist on surfaces, particularly in cold and humid conditions. Research indicates PRRSV remains viable on boots and gloves for up to 48 hours. Effective disinfectants include quaternary ammonium compounds, peroxides, and phenolics. Transport biosecurity measures, such as heated disinfection chambers and downtime protocols, help mitigate the risk of virus introduction into naïve herds.

Clinical Manifestations

PRRS symptoms vary based on the age of affected pigs, strain virulence, and concurrent infections. In breeding herds, reproductive failures include late-term abortions, stillbirths, and weak-born piglets with high pre-weaning mortality. Affected sows may experience irregular estrous cycles and reduced conception rates. The virus crosses the placenta in the third trimester, leading to mummified piglets or neonates with severe respiratory distress, lethargy, cyanosis, and failure to thrive.

In growing and finishing pigs, PRRS primarily presents as a respiratory disease, with affected animals displaying dyspnea, tachypnea, and persistent coughing. Secondary bacterial infections, such as Streptococcus suis, Mycoplasma hyopneumoniae, and Pasteurella multocida, exacerbate bronchopneumonia and increase morbidity. Fever, anorexia, and weight loss impair feed conversion efficiency, prolonging time to market. Mortality rates vary, with some outbreaks causing losses exceeding 10% in nursery and grower pigs.

Boars may not show overt clinical signs but can experience transient fever, lethargy, and reduced semen quality. The virus persists in reproductive tissues, leading to intermittent shedding in semen even after systemic signs resolve. This subclinical persistence complicates disease management in artificial insemination programs, as transmission can occur unnoticed.

Genetic Variability And Strains

PRRSV exhibits extensive genetic diversity, complicating disease management and vaccine development. The virus is classified into two major species: Betaarterivirus suid 1 (PRRSV-1), predominant in Europe, and Betaarterivirus suid 2 (PRRSV-2), more common in North America and Asia. Each species contains numerous genetically distinct strains with varying virulence and antigenicity. Whole-genome sequencing reveals that PRRSV strains can differ by up to 20% at the nucleotide level.

Highly pathogenic variants have emerged, such as HP-PRRSV strains identified in China in 2006, which caused outbreaks with mortality rates exceeding 40%. These strains contain genetic markers linked to increased virulence, including deletions and insertions in non-structural proteins that enhance replication. Similarly, PRRSV-1 has diversified, with subtype 3 strains in Eastern Europe exhibiting heightened pathogenicity. Antigenic drift reduces cross-protection between vaccine strains and circulating field viruses, diminishing vaccine efficacy over time.

Diagnostic Approaches

Accurate PRRSV identification is essential for effective disease management, particularly given its overlapping clinical signs with other swine diseases. Diagnosis relies on molecular, serological, and virological methods.

RT-PCR is the gold standard for PRRSV detection due to its high sensitivity and specificity. It amplifies viral RNA from blood, tissues, or oral fluids, identifying active infections even before symptoms appear. Quantitative RT-PCR (qRT-PCR) provides viral load measurements, useful for monitoring infection dynamics. Whole-genome sequencing helps track viral evolution and inform vaccine selection.

Serological assays, such as enzyme-linked immunosorbent assay (ELISA), detect antibodies against PRRSV, useful for herd-level surveillance. However, ELISA does not differentiate between natural infection and vaccine-induced immunity. Virus isolation, though less common due to its labor-intensive nature, remains useful for characterizing novel or highly virulent strains. Oral fluid sampling is a cost-effective, non-invasive method increasingly used for large-scale herd monitoring.

Gene Editing For Resistant Swine

Gene editing technologies, such as CRISPR-Cas9, offer potential solutions for enhancing PRRSV resistance in pigs. Unlike traditional selective breeding, gene editing enables precise modifications to host genes that the virus exploits.

One promising target is the CD163 receptor, which PRRSV uses for entry. Studies have shown that pigs with a specific deletion of exon 7 in the CD163 gene remain resistant to PRRSV infection while maintaining normal physiological functions. Unlike complete knockouts, which may disrupt immune function, this precise modification selectively removes the viral binding domain. Research from the University of Missouri and Genus PLC has demonstrated that these gene-edited pigs exhibit no signs of PRRSV infection after experimental challenge.

Regulatory approval and commercialization remain hurdles, as gene-edited livestock must navigate ethical, legal, and consumer acceptance challenges. The U.S. Food and Drug Administration (FDA) and the European Food Safety Authority (EFSA) have stringent guidelines for genetically modified animals. If approved, gene editing could revolutionize PRRSV control, reducing reliance on vaccines and antibiotics while improving animal welfare and economic sustainability.