Genetic Control of Immune Response to Pseudorabies and Atrophic Rhinitis Vaccines: II: Comparison of Additive Direct and Maternal Genetic Effects

Meeker, David; Rothschild, Max F.; Christian, L. L.; Warner, Carol M.; Hill, Howard T.

doi:10.2527/jas1987.642414x

Cited by 14 publications

(12 citation statements)

References 20 publications

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“…Heritability was estimated at 0.18. Similar antibody heritabilities were estimated for pure‐bred pigs immunized with two different vaccines 22 . Here low heritabilities of 0.18 ± 0.09 and 0.15 ± 0.07 were recorded for immune response to a modified‐live pseudorabies vaccine and an inactivated bacterial bacterin, respectively, both measured 56 days after inoculation (however, it was 0.52 ± 0.15 for the bacterin after 119 days).…”

Section: Heritable Variation and Contraception Resistancesupporting

confidence: 69%

Immunocontraception for population control: Will resistance evolve?

et al. 2003

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SummaryThe prospect for successful biocontrol using immunocontraception is threatened if there is adaptation to the vaccine through natural selection of individuals that are genetically resistant to the contraceptive agent. To assess this possibility we examined the literature and found that little relevant data are available for any species on the appropriate trait, fertility variation among immunized individuals, or about appropriate population and genetic parameters influencing the likelihood of a selection response. Some data are available on variation in antibody response to immunocontraceptives, but the relationship between antibody response and fertility levels is poorly documented. The antibody response data indicate low heritability for this trait suggesting that fertility levels of contraceptive-resistant individuals will also have a low heritability. Slow evolution of contraception resistance might therefore be anticipated. The absence of information about relevant parameters makes the construction of quantitative models premature. We discuss factors in particular need of investigation if predictions about resistance evolution are to be made. These include: 1. the genetic basis of fertility retention, 2. the proportion of the population resistant to the contraceptive agent and how this is affected by gene flow from refuge populations, 3. the geneticallybased fitness tradeoffs of resistant individuals that often accompany selection, 4. cross-generation effects that can thwart the effects of selection, and 5. the efficiency of delivery of the contraceptive agent. An understanding of the above for particular species, and the development of appropriate divergently acting multiple vaccines that can be used in temporal rotation or in mixtures, should facilitate the development of management options to minimize resistance evolution.

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Section: Heritable Variation and Contraception Resistancesupporting

confidence: 69%

Immunocontraception for population control: Will resistance evolve?

et al. 2003

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“…The breed rankings differed in Rothschild et al (1984a) and Rothschild et al (1984b) using different antigens. Meeker et al (1987b) estimated the heritability of response to pseudorabies vaccine to be .18 measured at 56 d of age, and the heritabilities of response to B. bronchiseptica vaccine to be .15 and .52 measured at 56 and 119 d of age, respectively. Meeker et al (1987a) showed no evidence for nonadditive genetic control (heterosis) of immune response to pseudorabies or B. bronchiseptica vaccines, but did observe additive genetic control and breed differences similar to Rothschild et al (1984a).…”

Section: Disease Resistance and Immune Responsementioning

confidence: 99%

“…Huang (1977) and Takahashi et al (1984) indicate that larger than trace amounts of specific maternal antibody interfere with active immunity. Immune colostrum interference with active antibody production in pigs for about the first 3 wk reduces the importance of the genetics of a pig in the early stage of immunity development (Hoerlein, 1957;Segre and Kaeberle, 1962a,b;Perry and Watson, 1967;Rothschild et al, 1984a,b;Meeker et al, 1987b).…”

Section: Genetic Control Of Immune Response--the Major Histocompatibimentioning

confidence: 99%

Genetic Control of Immune Responsiveness: A Review of Its use as a Tool for Selection for Disease Resistance1

Warner

Meeker

Rothschild

1987

Journal of Animal Science

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Disease resistance and immune responsiveness have been traits generally ignored by animal breeders. Recent advances in immunology and molecular biology have opened new avenues towards our understanding of genetic control of these traits. The major histocompatibility gene complex (MHC) appears to play a central role in all immune functions and disease resistance. The need to understand the relationship between immune responsiveness, disease resistance and production traits is discussed in this review. Antagonistic relationships might prevent simultaneous improvement of all of these traits by conventional breeding methods. It is suggested that genetic engineering methods may allow the simultaneous improvement of disease resistance and production traits in domestic animals. Genes of the MHC will be especially good candidates for genetic engineering experiments to improve domestic species.

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“…Such an effect has been found in previous generations of our lines (Leitner et ah, 1994). Meeker et al (1987) found a maternal effect on the immune response of young pigs. The maternal effect may have either a random or genetic nature, or both.…”

Section: Discussionmentioning

confidence: 95%

Genetic Differences and Heritability of Antibody Response to Escherichia coli Vaccination in Young Broiler Chicks

Yonash

Leitner²,

Waiman

et al. 1996

Poultry Science

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Broiler chicken lines, selected divergently for high (HC) or low (LC) antibody titer to Escherichia coli vaccination at an early age, were evaluated for antibody response at the S5 and S9 generations of selection. The full-pedigreed populations consisted of about 300 and 400 chicks per line in S5 and S9, respectively. At S5, all chicks were vaccinated at 10 d of age (VA10) and antibody titer was determined twice for each chick, at 8 and 12 d postvaccination (dPV). At S9, each line was divided into two equal groups; in the HC line, one group was vaccinated at 8 d of age (VA8), and the other at 10 d of age (VA10), whereas in the LC line, one group was VA10 and the other was VA12. Antibody titers were determined twice for each chick, 8 and 10 dPV. The effects of line, age at vaccination (VA), and days for antibody development (dPV) were tested, and the heritability of antibody titer was estimated for each line-VA-dPV set of data. The HC and LC lines differed significantly in the maturation process of their immune systems. The percentage of chicks with detectable antibody at 18 d of age (VA10-8 dPV) among HC chicks was significantly higher than among LC chicks (85 vs 48% in S5 and 96 vs 63% in S9). In S9, 90% of the HC chicks had already responded at 16 d of age and 100% at 18 d of age, whereas among the LC chicks, only 62% were positive at 18 d of age, increasing to no more than 98% at 22 d of age. The results demonstrates that selection of antibody titer to E. coli vaccination at 20 d of age actually affects the earliest age of immune response, as the immune system of the HC chicks matures earlier than that of the LC chicks. The HC S9 chicks at 8 dPV exhibited a fourfold higher antibody titer than their LC 8 counterparts. This difference further increased at 10 dPV, indicating that the lines differed not only in the level of antibody at a specific age, but also in their rate of antibody titer development. The highest estimate of heritability was very similar in both lines (0.44 and 0.42 in HC and LC, respectively). However, in the HC line this heritability was exhibited at 18 d of age, and only at 22 d in the LC line. Thus, both lines have a similar amount of genetic variation for early immune response, but in the HC line this variation is fully expressed 4 d earlier than in the LC line. These results suggest that selection for high or low antibody response in young chicks results in early or late antibody production, respectively. To maximize the efficiency of selection for early immune response, one must determine the best vaccination age and timing of antibody evaluation in any given population, and these values must be revalidated and updated as selection proceeds.

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Genetic Control of Immune Response to Pseudorabies and Atrophic Rhinitis Vaccines: II: Comparison of Additive Direct and Maternal Genetic Effects

Cited by 14 publications

References 20 publications

Immunocontraception for population control: Will resistance evolve?

Immunocontraception for population control: Will resistance evolve?

Genetic Control of Immune Responsiveness: A Review of Its use as a Tool for Selection for Disease Resistance1

Genetic Differences and Heritability of Antibody Response to Escherichia coli Vaccination in Young Broiler Chicks

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