Below are answers to some commonly asked questions about influenza A virus in swine (IAV-S), its impact, and prevention.


  • What is influenza A virus (IAV)?

    Influenza A virus (IAV) is an orthomyxovirus.1 The genetic material of the virus is made up of 8 segments of RNA containing 8-11 genes, which code for different attributes of the virus (e.g., attachment, replication).2 Influenza A virus in swine (IAV-S) identifies the influenza viruses that have become adapted to swine as the primary host.

  • How does the disease differ between pigs and other species?

    In mammals, including pigs, the virus has an affinity for respiratory mucosa only,3,4 and causes respiratory disease with fever, going off feed, and lethargy.4,5 In birds, influenza A causes a systemic disease capable of entering the bloodstream and affecting multiple organ systems.1

  • Do humans get IAV from other animals?

    Yes, humans can get IAV from other animals, but they can transmit influenza to other species as well. IAV is zoonotic, meaning it is a disease that transmits between animals and humans or vice-versa. IAV is capable of being transmitted to humans from pigs and birds, as well as from humans to pigs and other species (i.e., companion animals, when in close contact).1 Swine have been considered a 'mixing vessel' for IAV in the past because they have receptors for both avian and human IAV.6 Research, however, has determined pigs are not unique, and humans also have receptors for both human and avian IAV.5

  • Why does IAV change?

    Although viruses are not 'alive', they behave like all other pathogens—their existence is based on 'survival'. To that end, IAV can withstand many genetic changes. Although these changes can be random, selection pressure due to host immunity, environmental conditions, or the presence of new susceptible hosts can lead to viable genetic changes that improve the fitness of the virus (genetic drift).7,8

    In addition, if an animal becomes co-infected with different IAV-S subtypes, then the viral gene segments within host cells can recombine (i.e., genetic shift) into novel virus progeny.8,10 With the abundant animal movements common in swine production, it is possible that pigs can become exposed to and infected by multiple subtypes of IAV-S.9–11

  • How is the virus able to continue to circulate in pig populations (i.e., become endemic)?

    IAV-S survives in a pig population because of the presence of non-immune animals. Thus, sow farms, in particular, can become endemic because of replacement animals and the birth of naive pigs.12

    Replacement animals enter frequently and can either be a new source of IAV-S or a new susceptible population unexposed to 'resident IAV-S'.12,13 In the US, IAV-S is an endemic disease in most production systems.12 It maintains endemicity within the farrowing house (where pigs, people, and fomites are frequently moved between rooms, potentially moving IAV-S from infected to susceptible piglets), as well as continuous flow nurseries, which have similar management practices.10

  • Is there a 'flu season' for pigs?

    IAV-S is present in farms all year. In northern regions, clinical IAV-S tends to be associated with the fall/winter and spring seasons. The reasons include cooler temperatures, increased humidity, and indoor environments with limited ventilation.7

  • What is the impact of IAV-S in contemporary pig production?

    Pigs infected with influenza display a host of clinical signs, including coughing, discharge from the eyes and/or nose, sneezing, depression, anorexia, fever, and lethargy. IAV-S can last for 1 week in an individual pig, but may seem to be present for multiple weeks in modern swine barns since the virus moves among susceptible animals within the population.13 The disease reduces weight gain. Young pigs have less robust immunity, which allows IAV to have a prolonged impact and makes the pigs susceptible to more secondary infections. Growing pigs can also be hit hard with acute IAV-S, through reduced feed consumption and increased mortality.13

    However, pigs seldom succumb to IAV-S alone. As a pig grows, there may be other viral and bacterial diseases present in the environment, which are significant cofactors of poor performance caused by porcine respiratory disease complex (PRDC).14,15 IAV-S removes the physical mucosal barrier in the respiratory tract,4 which allows other respiratory pathogens to have enhanced infectivity.

    In one study, a herd with endemic IAV-S in nurseries that also tested positive for other respiratory pathogens* had 2.9% higher combined mortality than another herd testing positive for the same pathogens but without endemic IAV-S.16

    In another study, pigs with IAV-S and Mycoplasma hyopneumoniae (Mhp) or porcine reproductive and respiratory syndrome virus (PRRSV) experienced productivity losses of $10.12 and $10.41, respectively.17 Thus, preventing IAV-S can reduce the impact of these infections on health and productivity.5,14,17

    * PRRSV, Mhp, Haemophilus parasuis, and Streptococcus suis

  • How common is IAV-S in pigs in the US?

    IAV-S is considered endemic in pig herds.12 As of 2012, the USDA reported that > 70% of growing pigs in US swine operations are affected by IAV-S.18


  • How does IAV-S spread/transmit (e.g., droplet, animal/animal)?

    Pigs are exposed to IAV-S mainly through direct pig-to-pig contact (nose-nose) or through droplet or aerosol transmission. Fomites can carry influenza for a short time. The virus is most stable at cooler/cold temperatures, in water, and in environments with mild-to-moderate humidity (where water is able to exist more as a 'droplet'). These conditions promote the transmission of IAV through a swine population.6,19

  • What are the transmission rates and the role of other species?

    IAV-S is transmitted laterally through nose-to-nose contact and through droplets and aerosols over short distances. It is NOT a virus that can be transmitted through the placenta or by colostrum/milk; it is only carried in the respiratory tract of mammals. IAV is highly transmissible and in naive, unprotected animals it has been shown that one infected animal is able to shed the virus and infect 10 additional animals.19 Since IAV is also zoonotic, other species may play a role in infection within a herd, particularly humans and birds.

  • What is the shedding period of natural infection with and without vaccine (individuals and population)?

    When an unvaccinated pig is infected with IAV-S, viral shedding can be readily detected from day 1 post-infection to approximately day 7, as determined by virus isolation.13 Thereafter, IAV-S is difficult to detect from nasal swab samples. However, IAV-S transmission in a population continues to occur if there are naive individuals to infect. IAV-S can be detected in samples from populations for a longer period of time because of this.10,12 In vaccinated pigs, virus is usually detectable from nasal swabs for a shorter period (3–5 days).20 In herds where pigs are vaccinated, the reduced infectivity rate also favors reduced transmission as long as the vaccine protects against that strain of virus.21

  • Can influenza be controlled in a swine herd? If so, how?

    With dedication, strict attention to details, and a focus on preventing IAV-S transmission, IAV-S can be controlled in a swine herd because IAV-S cannot survive long outside of a host, and it does not survive in immune animals. The virus is continuously seeking new, susceptible animals to infect—there is no 'carrier' state. Nevertheless, in a farm, reservoirs or sources of IAV-S may be found in certain locations or areas because of continuous movement of animals into and out of that population. If all animals in a herd gain exposure and then immunity to the resident viruses circulating in the farm, influenza will 'die out'. However, this protocol must also include control of animal movement (in particular, significantly less frequent entry of replacement animals), IAV-S monitoring, and strict attention to biosecurity measures.6,10,22,23



  • Are pigs immune to IAV-S once they have gotten the disease?

    It is known that infections caused naturally initiate robust, long-lasting, and broad protection.19,21 Although a pig may become immune to the IAV-S that it is infected with, pigs can be affected by another IAV-S during their lifetime because IAV is an RNA virus and changes so readily.26

    Live attenuated influenza vaccines (LAIVs) mimic a natural infection without causing clinical disease.

References: 1. Short KR, Richard M, Verhagen JH, et al. One health, multiple challenges: the inter-species transmission of influenza A virus. One Health. 2015;1:1–13. 2. Taubenberger JK, Kash JC. Influenza virus evolution, host adaptation and pandemic formation. Cell Host Microbe. 2010;7(6):440–451. doi:10.1016/j.chom.2010.05.009. 3. de Graaf M, Fouchier RA. Role of receptor binding specificity in influenza A virus transmission and pathogenesis. EMBO J. 2014;33(8):823–841. 4. Janke BH. Influenza A virus infections in swine: pathogenesis and diagnosis. Vet Pathol. 2014;51(2):410–426. 5. Vincent AL, Lager KM, Anderson TK. A brief introduction to influenza A virus in swine. In: Spackman E, ed. Methods in Molecular Biology: Animal Influenza Virus, Part III. 2014;1161:243–258. 6. Mastin A, Alarcon P, Pfeiffer D, et al. Prevalence and risk factors for swine influenza virus infection in the English pig population. PLoS Curr. 2011;3:RRN1209. 7. Rejmanek D, Hosseini PR, Mazet JAK, Daszak P, Goldstein T. Evolutionary dynamics and global diversity of influenza A virus. J Virol. 2015;89:10993–11001. doi:10.1128/JVI.01573-15. 8. Bouvier NM, Palese B. The biology of influenza viruses. Vaccine. 2008;265:D49–D53. 9. Nelson MI, Viboud C, Vincent AL, et al. Global migration of influenza A viruses in swine. Nat Commun. 2015;6:6696. doi:10.1038/ncomms7696. 10. Pitzer VE, Aguas R, Riley S, Loeffen WLA, Wood JLN, Grenfell BT. High turnover drives prolonged persistence of influenza in managed pig herds. J R Soc Interface. 2016;13:20160138. doi:10.1098/rsif.2016.0138. 11. Allerson MW, Davies PR, Gramer MR, Torremorell M. Infection dynamics of pandemic 2009 H1N1 influenza virus in a two-site swine herd. Transbound Emerg Dis. 2014;61:490–499. 12. Diaz A, Perez A, Sreevatsan S, Davies P, Culhane M, Torremorell M. Association between influenza A virus infection and pigs subpopulations in endemically infected breeding herds. PLoS One. 2015;10(6):e0129213. doi:10.1371/journal.pone.0129213. 13. Corzo CA, Morrison RB, Fitzpatrick AM, Culhane MR. Risk factors for detecting influenza A virus in growing pigs. J Swine Health Prod. 2014;22(4):176–184. 14. Jiménez LFM, Nieto GR, Alfonso VV, Correa JJ. Association of swine influenza H1N1 pandemic virus (SIV-H1N1p) with porcine respiratory disease complex in sows from commercial pig farms in Colombia. Virol Sin. 2014:29:242–249. doi:10.1007/ s12250-014-3471-5. 15. Centers for Disease Control and Prevention. Key facts about swine influenza (swine flu) in pigs. Accessed June 15, 2017. 16. Donovan T. The role of influenza on growing pig performance. System 2. 2005:40-0. 17. Dykhuis Haden C, Painter T, Fangman T, Holtkamp D. Assessing production parameters and economic impact of swine in influenza, PRRS and Mycoplasma hyopneumoniae on finishing pigs in a large production system. In: Proceedings of the 43rd American Association of Swine Veterinarians Annual Meeting; March 10–13, 2012; Denver, CO: 75–76. 18. USDA, APHIS, VS, NAHMS. Swine 2012 Part II: Reference of swine health and health management in the United States, 2012. February 2016. 19. Romagosa A, Allerson M, Gramer M, et al. Vaccination of influenza A virus decreases transmission rates in pigs. Vet Res. 2011;42:120. 20. Hemmink JD, Morgan SB, Aramouni M, et al. Distinct immune responses and virus shedding in pigs following aerosol, intra-nasal and contact infection with pandemic swine influenza A virus, A(H1N1)09. Vet Res. 2016;47:103–117. 21. Sandbulte MR, Spickler AR, Zaabel PK, Roth JA. Optimal use of vaccines for control of influenza SA virus in swine. Vaccines. 2015;3:22–73. 22. Mughini-Gras L, Beato MS, Angeloni G, et al. Control of a reassortment pandemic 2009 H1N1 influenza virus outbreak in an intensive swine breeding farm: effect of vaccination and enhanced farm management practices. PLoS Curr. 2015;7. 23. Torremorell M, Juarez A, Chavez E, Yescas J, Doporto JM, Gramer M. Procedures to eliminate H3N2 swine influenza virus from a pig herd. Vet Rec. 2009;165:74–77. 24. Gerber PF, Dawson L, Strugnell B, Burgess R, Brown H, Opriessnig T. Using oral fluids samples for indirect influenza A virus surveillance in farmed UK pigs. Vet Med Sci. 2017(3):3–12. 25. Kaplan BS, DeBeauchamp J, Stigger-Rosser E, et al. Influenza virus surveillance in coordinated swine production systems, United States. Emerg Infect Dis. 2015;21(10):1834–1836. 26. Vincent AL, Ma W, Lager KM, et al. Live attenuated influenza vaccine provides superior protection from heterologous infection in pigs with maternal antibodies without inducing vaccine-associated enhanced respiratory disease. J Virol. 2012;86(19):10597–10605.