Porcine Reproductive and Respiratory Syndrome (PRRS) Virus


Clinical outbreaks characterized by severe reproductive losses, respiratory disease, reduced growth, and increased mortality appeared in the United States in 1987 and then Europe in 1990. In 1991, researchers in the Netherlands determined the cause to be a previously unrecognized virus which they named “porcine reproductive and respiratory syndrome virus” (PRRSV) (Terpstra et al., 1991; Wensvoort et al., 1991).


Today, PRRSV is present in most swine-producing regions of the world. PRRSV typically enters herds by the introduction of infected animals, virus-contaminated semen, aerosol spread, or breaks in biosecurity. Once infected, PRRSV tends to circulate in the herd indefinitely. This process is driven by persistent PRRSV infections (carrier animals) and the availability of susceptible animals introduced into the population through birth or purchase. In Europe and North America, the cost of PRRSV was estimated at $6.25 to $15.25 USD per pig marketed (Holtkamp et al. 2013; Nathues et al. 2017). Thus, PRRSV has a major impact on swine health and productivity, but consistent control in the field is difficult.


  • Review the virus, clinical signs, and pathology
  • Provide an overview of PRRSV diagnostics
  • PRRSV immunity, control, and eradication

The cause

PRRSV consists of two species (PRRSV-1 and PRRSV-2) of enveloped RNA viruses in the family Arteriviridae (Zimmerman et al., 2019). Characteristics shared by PRRSV and other arteriviruses include continual genetic mutation and recombination, a requirement to replicate in macrophages, and an ineffective immune response that results in long-term infection (carrier animals).  While PRRSV-1 and PRRSV-2 are genetically distinct, there are no meaningful clinical differences between the two species and the information provided here applies to both.


In North America, PRRSV-2 is more prevalent than PRRSV-1, but both species are present and both may circulate concurrently in the same herd. PRRSV is highly genetically diverse, but a simple, accurate method of characterizing viral diversity and naming PRRSV variants has not yet been developed. Most commonly, virus variants are named on the basis of restriction fragment length polymorphism (RFLP) typing of the ORF 5 region of the genome, despite the fact that this approach has major weaknesses: (1) RFLP types do not reflect genetic relationships, are not associated with virulence, and do not predict cross-protection among PRRSV isolates, (2) RFLP patterns are not stable and change during replication in pigs, and (3) the RFLP identification terminology is increasing complex as new variants are identified.


PRRSV cannot infect humans and does not pose a risk for human health. Likewise, cats, dogs, guinea pigs, mice, opossums, raccoons, rats, and skunks are not susceptible to PRRSV (Hooper et al. 1994; Wills et al. 2000). Swine can be infected with PRRSV by intranasal, intramuscular, or oral exposure, and in sows by intrauterine and vaginal routes of exposure. Introducing the virus through breaks in the skin is an extremely efficient mode of transmission. This includes bites and lacerations from fighting between infected and susceptible pigs when animals are mixed, e.g., at weaning, and the use of PRRSV-contaminated instruments or contaminated needles, syringes, medications, and biologics. Pigs shed virus in saliva and to a much lesser extent, in blood, urine and feces. In the environment, PRRS virus is inactivated by heat, drying, and at pH below 6 or above 7.5, but will remain infectious for some time in cold, moist environments, and almost indefinitely when frozen. Jacobs et al. (2010) estimated the virus half-life (time to inactivate 1/2 of the virus) of 155 hours at 4°C (39°F), 84.5 hours at 10°C (50°F), 27.4 hours at 20°C (68°F), and 1.6 hours at 30°C (86°F). These inactivation parameters should be considered when cleaning and disinfecting facilities or equipment.


The most important epidemiological feature of PRRSV is its ability to continue replicating in tonsil or other lymphoid tissues over time (“chronic persistent infection”). The virus is eventually cleared from the infected animal, but infectious PRRSV is typically present for 3-to-5 months after infection and even longer in some animals (Fangman et al. 2007; Horter et al. 2002; Wills et al. 1997b). Carriers represent a real threat to PRRSV control and/or elimination projects because carrier animals can transmit virus to other pigs in the herd. At present, there are no tests able to differentiate carriers from animals that have successfully cleared the virus.

Clinical signs

Clinical disease is variable and dependent upon numerous factors including strain virulence, presence and consistency of strain-specific immunity in the herd, age at infection, presence of other co-infections, and management practices. Notably, the absence of clinical signs does not mean that a herd is free of PRRSV; this must be established by testing. In sows and boars, clinical signs may include anorexia, fever, depression, and less often generalized redness of the skin or light blue discoloration of skin on ears, nose and legs, labored breathing, vomiting or nervous signs that may include tremors, head tilt or seizures. Reproductive losses are often the most obvious signs and manifest as poor semen quality, reduced conception rates, decreased farrowing rates, premature farrowing, abortions, stillbirths, weak born piglets, and mummified fetuses. Pre-weaning mortality can be very high following PRRSV infection and suckling piglets may have labored breathing, fever, diarrhea, poor growth and swelling around the eyes.  Growing and finishing pigs often exhibit fever, labored breathing, redness of the skin, blue/dark red ears, poor growth and rough hair coats. Secondary bacterial infections, particularly caused by Streptococcus suis, Glaesserella (Haemophilus) parasuis, Mycoplasma hyorhinis are commonly observed. Clinical signs of these pathogens are often observed together with those of PRRSV and may include nervous signs such as head-tilt, lateral recumbency and paddling, swollen joints and lameness, labored breathing and rough hair coats. There is little that can be done to reduce the clinical effects of a PRRSV outbreak, but anti-inflammatories may be administered to control fever and antibiotics may be used to manage secondary bacterial infections.


PRRSV appears in the blood (viremia) within 24-to-48 hours of exposure. Viremia, the presence of the virus circulating in the blood, typically lasts 3-to-4 weeks. This allows the virus to disseminate to multiple organs, including the uterus and fetuses of pregnant females. PRRSV prefers cells of the immune system, including macrophages – the primary target cell for viral infection and replication (Lunney et al., 2016). The porcine cell receptor CD163 is the major receptor that mediates viral internalization in infected macrophages. PRRSV infection also results in a reduction in skeletal muscle synthesis in growing pigs as amino acids are reallocated toward the immune system, thus contributing to the poor growth often observed in PRRSV infected pigs (Helm et al., 2016).  Recovered animals are resistant to reinfection when exposed to the same or closely related strains of PRRSV, but may show clinical signs if re-infected with genetically different strains. Whole genome sequencing may be required to identify these genetically different strains.


Similar lesions are described in all ages of pigs with PRRSV infection, but the severity and distribution of lesions varies with the virulence of the infecting virus. To the naked eye, the lungs often appear mottled purple or tan, moist, firm-to-meaty, and fail to collapse; however, lesions are highly variable depending upon strain and stage of infection. Lymph nodes are frequently systemically enlarged, pale tan, and edematous. In reproductive outbreaks, aborted litters contain variable combinations of normal appearing fetuses, smaller fetuses with reddened skin, fetuses that are flaccid with brown skin and variably sunken eyes, and fully mummified fetuses.


Initially, PRRSV infection induces a strong immunosuppressive response in the pig that weakens the adaptive immune response and contributes to chronic persistent PRRSV infection (Lunney et al., 2016). In addition to the interstitial pneumonia that develops as a direct result of infection, destruction of alveolar macrophages compromises pulmonary clearance mechanisms, which may then lead to severe secondary bacterial pneumonia. Generalized destruction of macrophages also renders pigs more susceptible to systemic infection and severe disease by bacteria that usually reside in the tonsils and nasal cavity of healthy pigs. In general, resistance to infection increases with age, i.e., sows are more resistant than weaned pigs to viral replication and disease (Klinge et al. 2009).


Over the long run, PRRSV infection induces an immune response that will slowly control and eliminate the virus from the body. Likewise, infection will produce immunological memory that is protective against similar PRRS viruses but not against dissimilar viruses. The exact viral characteristics that determine the degree of cross-protection are not known at this time. In the field, the degree of cross-protection provided by one strain against clinical disease induced by infection with a second strain is a concern, particularly for reproductive PRRSV, because outbreaks have been reported in herds with regular vaccination or live virus inoculation programs.


Clinical signs, particularly in the case of reproductive disease, may strongly suggest PRRSV, but any presumptive clinical diagnosis must be confirmed by detection of the virus. Microscopic lung lesions are often suggestive of PRRSV infection, but are not definitive.  A definitive diagnosis is achieved by confirmation of PRRSV in the tissues or fluids of pigs with characteristic clinical signs and lesions, typically using polymerase chain reaction (PCR) tests. Antibody detection tests are also available and can provide evidence of infection when PRRSV RNA is not readily detectable. Samples for PCR testing should be collected from pigs with clinical signs consistent with acute PRRSV infection, immediately chilled, and transported on ice to a laboratory for testing. The best specimens include lung, lymphoid tissues (lymph nodes, spleen, tonsil), serum, processing fluids,  or oral fluids. A positive test result suggests PRRSV as cause of the observed disease, but this finding must be put into context before its role in disease can be confirmed. For example, many commercial pigs receive modified live (MLV) PRRSV vaccines and vaccine virus is easily detected by standard diagnostic PRRSV PCR tests. Thus, a positive test must correlate to typical gross and microscopic lesions of PRRSV to be considered diagnostic for PRRS. Additional more sophisticated testing to differentiate field (wild-type) strains from MLV vaccine strains may be appropriate in certain circumstances. In cases of suspected PRRSV reproductive failure, PCR testing should be performed on tissues recovered from aborted fetuses from several litters and processing fluids collected from neonatal liveborn pigs within the same farrowing groups as aborted litters. In addition, serum from fevering off-feed or aborted sows can be PCR tested. Sequencing of entire or partial genomes of detected PRRSV can determine if the virus is a wild-type or MLV vaccine-like strain and can be used to compare the current virus with historical strains from a given population to determine relatedness over time.

Control and Eradication

Implementing measures that reduce the probability of PRRSV entering negative herds or new PRRSV variants into positive herds is mandatory for control. Every premises is different, so the first step is to identify site-specific biosecurity weaknesses. Once infected, herds are best managed through pig flow strategies, such as McREBEL management in the farrowing house, batch farrowing, and all-in / all-out animal flow to reduce viral circulation (McCaw, 2000). The use of MLV PRRSV vaccines has been shown to reduce losses and the shedding of wild-type virus (Linhares et al., 2012). Proper sanitation and disinfection of facilities between groups is important in reducing the exposure of incoming groups of healthy pigs. The presence of an “envelope” on the exterior of PRRSV increases the virus’ susceptibility to inactivation by quaternary ammonium, chlorine-based, and gluteraldehyde-based disinfectants. In addition, as noted previously, PRRSV is readily inactivated by heat and desiccation.


PRRSV elimination is justified by expected improvements in pig health and productivity, but elimination is difficult to achieve and maintain, particularly in “swine dense” regions. The most common method of PRRSV elimination is “herd closure”, i.e., exposure of all animals to live PRRSV or vaccine followed temporarily stopping the introduction of replacement animals while herd immunity builds. Herd closure is based on the fact that, although PRRSV is a chronic persistent infection, the immune system will eventually clear the virus.


Whether the choice is to maintain PRRSV-negative status, “live with” PRRSV, or eliminate the virus, it is important to perform routine surveillance to track the virus and measure success (or failure). Surveillance based on oral fluid and/or neonatal processing fluid samples is both better and less expensive than serum-based testing. However, PRRSV sequencing is best performed on serum and or tissue samples from viremic groups of pigs. 


Thirty years after its discovery, PRRSV continues to impose major losses on swine health and productivity. The clinical signs associated with PRRSV are highly variable and may range from inapparent to severe, but the most consistent clinical picture is reproductive disease characterized by abortions and early farrowing of litters containing a mixture of clinically normal, weak, and/or stillborn pigs and respiratory disease in growing pigs. Clinical signs, if present, cannot be differentiated from those caused by other pathogens of swine. Therefore, a definitive diagnosis of PRRSV requires laboratory confirmation based on detection of virus, viral products, and/or antibodies. PRRSV circulates in the pigs’ blood stream (viremia) for 2-to-5 weeks after the initiation of the infection, but live virus may be recovered from lymphoid tissues, for example tonsils, for 2-to-5 months. These carrier animals are a source of virus to susceptible animals and act to maintain the virus in the herds. Elimination of PRRSV is the optimal solution, but has proven to be difficult to achieve and maintain. All herds should implement routine PRRSV surveillance using processing fluids or oral fluids for the purpose of verifying herd status and tracking changes.

References and Citations

Fangman, T. J., Kleiboeker, S. B., and Coleman, M. 2007. Tonsillar crypt exudate to evaluate shedding and transmission of porcine reproductive and respiratory syndrome virus after inoculation with live field virus or vaccination with modified live virus vaccine. J. Swine Health Prod. 15:219-223.


Helm, E. T., Curry, S. M., De Mille, C. M., Schweer, W. P., Burrough, E. R., Zuber, E. A., Lonergan, S. M., and Gabler, N. K. 2019. Impact of porcine reproductive and respiratory syndrome virus on muscle metabolism of growing pigs. J. Anim. Sci. 97:3213-3227.


Holtkamp, D. J., Kliebenstein, J. B., Neumann, E. J., Zimmerman, J. J., Rotto, H. F., Yoder, T. K., Wang, C., Yeske, P. E., Mowrer, C. L., and Haley, C. A. 2013. Assessment of the economic impact of porcine reproductive and respiratory syndrome virus on United States pork producers. 2013. J. Swine Health Prod. 21:72–84.


Hooper, C. C., Van Alstine, W. G., Stevenson, G. W., and Kanitz, C. L. 1994. Mice and rats (laboratory and feral) are not a reservoir for PRRS virus.  J. Vet. Diagn. Invest. 6:13-15.


Horter, D. C., Pogranichniy, R. M., Chang, C. C., Evans, R. B., Yoon, K. J., and Zimmerman, J. J. 2002. Characterization of the carrier state in porcine reproductive and respiratory syndrome virus infection. Vet. Microbiol. 86:213-228.


Jacobs, A. C., Hermann, J. R., Muñoz-Zanzi, C., Prickett, J. R., Roof, M. B., Yoon, K.-J., and Zimmerman, J. J. 2010. Stability of porcine reproductive and respiratory syndrome virus at ambient temperatures. J. Vet. Diagn. Invest. 22:257-260.


Klinge, K. L., Vaughn, E. M., Roof, M. B., Bautista, E. M., and Murtaugh, M. P. 2009. Age-dependent resistance to porcine reproductive and respiratory syndrome virus replication in swine. Virol J 6:177.


Linhares, D., Torremorell, M., Cano, J. P., and Dee, S. A. 2012. Effect of modified live porcine reproductive and respiratory syndrome (PRRS) vaccine on the shedding of wild-type virus from an endemically infected population of growing pigs. Vaccine 30:407-413.


Lunney, K. J., Fang, Y., Ladinig, A.,Chen, N., Li, Y., Rowland, B., and Renukaradhya, G. J. 2016.  Porcine reproductive and respiratory syndrome virus (PRRSV): Pathogenesis and interaction with the immune system.  Annu. Rev. Anim. Biosci. 4:129-154.


McCaw, M. B. 2000. Effect of reducing cross-fostering at birth on piglet mortality and performance during an acute outbreak of porcine reproductive and respiratory syndrome. J. Swine Health Prod. 8:15-21


Nathues, H., Alarcon, P., Rushton, J., Jolie, R., Fiebig, K., Jimenez, M., Geurts, V., and Nathues, C. 2017. Cost of porcine reproductive and respiratory syndrome virus at individual farm level – an economic disease model. Prev. Vet. Med. 142:16-29.


Terpstra, C., Wensvoort, G., and Ter Laak, E. A. 1991. The “new” pig disease: laboratory investigations. In: The new pig disease. Porcine reproductive and respiratory syndrome. A report on the seminar/workshop held in Brussels on 29-30 April 1991 and organized by the European Commission Directorate General for Agriculture, pp. 36-45.


Wensvoort, G., Terpstra, C., Pol, J. M. A.,Ter Laak, E. A., Bloemraad, M., De Kluyver, E. P., Kragten, C., Van Buiten, L. D., Den Besten, A., Wagenaar, F., and Broekhuijsen, J. M. 1991. Mystery swine disease in the Netherlands: The isolation of Lelystad virus. Vet. Q. 13:121-130.


Wills, R. W., Osorio, F. A., and Doster, A. R. 2000. Susceptibility of selected non-swine species to infection with PRRS virus. Proceedings of the American Association of Swine Practitioners, pp. 411-413.


Wills, R. W., Zimmerman, J. J., Yoon, K. J., Swenson, S. L., McGinley, M. J., Hill, H. T., Platt, K. B., Christopher-Hennings, J., and Nelson, E. A. 1997.  Porcine reproductive and respiratory syndrome virus: a persistent infection.  Vet Microbiol. 55:231-240.


Zimmerman, J. J., Dee, S. A., Holtkamp, D., Murtaugh, M. P., Stadejek, T., Stevenson, G. W., Torremorell, M., Yang, H., and Zhang, J. 2019. Porcine reproductive and respiratory syndrome viruses (porcine arteriviruses).  In: Zimmerman, J. J., Karriker, L. A., Ramirez, A., Schwartz, K. J., Stevenson, G. W., Zhang, J. (editors).  Diseases of Swine, 11th edition.  John Wiley and Sons, Inc., Hoboken NJ. pp. 685-708.



Reference to products in this publication is not intended to be an endorsement to the exclusion of others which may be similar. Persons using such products assume responsibility for their use in accordance with current directions of the manufacturer. The information represented herein is believed to be accurate but is in no way guaranteed. The authors, reviewers, and publishers assume no liability in connection with any use for the products discussed and make no warranty, expressed or implied, in that respect, nor can it be assumed that all safety measures are indicated herein or that additional measures may be required. The user therefore, must assume full responsibility, both as to persons and as to property, for the use of these materials including any which might be covered by patent. This material may be available in alternative formats.