Vaccination against IAV-S

Vaccination against IAV-S, in combination with biosecurity measures and control of animal flow within an operation, is designed to reduce the incidence of disease and the resultant economic losses. Vaccines for IAV-S currently available or in development include killed, vectored, and live attenuated influenza vaccines (LAIVs).1

Killed vaccines

Killed vaccines have until recently been the only type of vaccine available for IAV-S. They are made with viruses that have been inactivated by a chemical process so they are no longer infectious. They are usually administered intramuscularly and combined with an adjuvant, which is a substance designed to enhance the immune response to the vaccine.

Killed IAV-S vaccines are designed to contain strains of the virus most likely to infect pigs, and autogenous IAV-S vaccines are made using specific viral isolates circulating in a production farm or flow. When the match between the IAV isolate in the vaccine is homologous to the strain circulating and causing disease in a population, the vaccine can induce antibody production that protects against the strains present in the herd.

Vector-associated vaccines

Vectored vaccines for influenza ("replicon-based vaccines") are vaccines which use a replication deficient alphavirus with the original internal genes replaced by genes of interest from selected IAV-S strains. IAV-S replicon vaccines have been considered safe since they do not reproduce in the host, and they tend to stimulate a better immune response than killed vaccines, although cross protection against heterologous viruses is still limited.2,3

Live vaccines

Live attenuated influenza vaccines (LAIVs), as their name suggests, are made with attenuated live IAV viruses, which can replicate without being pathogenic. When administered intranasally, at the site of natural infection, LAIVs stimulate robust and broad host immunity.

Because LAIVs are able to replicate in the host, they promote a more complete immune response, which provides better cross-protection than killed vaccines, and without the use of adjuvants.1,4

Clinical studies on intranasal LAIVs have shown them to confer effective immunity without risk of vaccine-associated enhanced respiratory disease (VAERD) unlike killed, intramuscularly administered vaccines.5

Comparative efficacy of vaccine platforms against influenza A virus infection in swine6

Vaccination Options Table

Intranasal vaccines are administered by the route of natural IAV-S infection, which allows the host to develop a localized immune response at the site of IAV-S infection.

Vaccination timing

Sow vaccination

Vaccinating sows using commercially available killed or autogenous IAV vaccines is common practice in the US. Producers vaccinate sows either to protect them from clinical episodes of IAV-S that impact reproduction, or in an attempt to provide maternally derived immunity to piglets that may be exposed to IAV-S at a young age.

Vaccination of sows to mitigate the risk of clinical impact on sow reproductive performance can be useful when strategically implemented, e.g., prior to higher risk times of the year. However, efficacy of vaccinating sows to provide piglets maternally derived immunity is limited and depends on multiple factors:

  • how similar the vaccine IAV strains are to the viruses piglets are exposed to in the field
  • sows may not provide similar and sufficient IAV-S antibodies to pigs depending on parity, IAV-S immune status, or previous IAV-S exposure
  • piglets may not receive sufficient quantities of antibodies depending on how much colostrum they suckle.1,4,7

Because of these factors, IAV-S can continue to circulate among farrowing rooms of endemic sow herds, and piglets become infected and clinical with IAV-S as maternal antibodies decline throughout the nursery phase.

Piglet vaccination

Because of the risk and likelihood of maternal antibody interference, vaccination of piglets with killed vaccines, while appropriate to allow immunization in the individual animal, can only be administered after maternal antibodies (mAb) wane.

Immunity from mAb is inconsistent and declines as the pigs get older, so piglets can quickly become susceptible to circulating strains of IAV-S. Because of this, killed vaccines when administered in the face of maternal antibodies may not adequately stimulate the pig’s immune response. When piglets are unable to develop their own immunity, they remain unprotected and become part of the cycle that perpetuates infection.

With the advancement of an intranasal LAIV, it is now possible to directly stimulate an immune response in the respiratory tract, which is the natural route of infection for IAV-S. Intranasal administration to younger animals protects pigs when they are most vulnerable (e.g., weaning and commingling).8

Additionally, IAV-S strains can change over time, either because of errors during genetic replication or reassortment when an animal is co-infected with multiple IAV-S.9,10 It is known that infections caused naturally or vaccination with an LAIV initiate more robust, long-lasting, and broad protection than killed IAV-S vaccines, whose efficacy depends on how closely they are able to protect against the natural infection.11,12

References: 1. Vincent AL, Ma W, Lager KM, et al. Efficacy of intranasal administration of a truncated NS1 modified live influenza virus vaccine in swine. Vaccine. 2007;25:7999–8009. 2. Rajão DS, Pérez DR. Universal vaccines and vaccine platforms to protect against influenza viruses in humans and agriculture. Front Microbiol. 2018 Feb 6;9:123. doi: 10.3389/fmicb.2018.00123. eCollection 2018. 3. Vander Veen RL1, Harris DL, Kamrud KI. Alphavirus replicon vaccines. Anim Health Res Rev. 2012 Jun;13(1):1-9. doi: 10.1017/S1466252312000011. Epub 2012 Mar 21. 4. Janke BH. Influenza A virus infections in swine: pathogenesis and diagnosis. Vet Pathol. 2014;51(2):410–426. 5. Kale TR, Momin M. Needle free injection technology—an overview. Inov Pharm. 2014;5(1):Article 148. http://pubs.lib.umn.edu/cgi/viewcontent.cgi?article=1152&context=innovations. 6. Vincent AL, Perez DR, Rajao D, et al. Influenza A virus vaccines for swine. Vet Microbiol. 2017;206:35–44. doi:10.1016/j.vetmic.2016.11.026. Epub 2016 Nov 24. 7. Vincent AL, Lager KM, Janke BH, Gramer MR, Richt JA. Failure of protection and enhanced pneumonia with a US H1N2 swine influenza virus in pigs vaccinated with an inactivated classical swine H1N1 vaccine. Vet Microb. 2008;126:310–323. 8. Loeffen WLA, Heinen PP, Bianchi ATJ, et al. Effect of maternally derived antibodies on the clinical signs and immune response in pigs after primary and secondary infection with an influenza H1N1 virus. Vet Immunol Immunopath. 2003;92:23–35. 9. 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. 10. Bouvier NM, Palese B. The biology of influenza viruses. Vaccine. 2008;265:D49–D53. 11. Romagosa A, Allerson M, Gramer M, et al. Vaccination of influenza A virus decreases transmission rates in pigs. Vet Res. 2011;42:120. 12. 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.