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  • Author or Editor: Peggy A. Weilnau x
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Summary

Five nonneutralizing monoclonal antibodies (MAb) generated to the virulent Miller strain of transmissible gastroenteritis virus (tgev) and specific for the S protein were characterized. Competition assays between purified and biotinylated MAb indicated that MAb 75B10 and 8G11 mapped near a new subsite, designated V and 2 MAb, 44C11 and 45A8, mapped to a previously designated subsite D. A fifth MAb mapped between subsites V and E. These MAb were tested with 3 previously characterized MAb to subsites A, E, and F in fixed-cell ELISA and cell culture immunofluorescent assays against 5 reference and 9 field strains of TGEV and 2 US strains (ISU-1 and ISU- 3) of porcine respiratory coronavirus (prcv). Subsites A, E, and F were conserved on all tgev and prcv strains examined. The 2 MAb to subsite V, 8G11 and 75B10, reacted only with the Miller tgev strains (M5C, M6, and M60), except that 75B10 also recognized field strain U328. The MAb 11H8 did not react with 4 field strains or the Purdue strains of tgev. The 2 MAb to subsite D reacted with all tgev strains examined, but not with 2 US prcv strains, 2 European PRCV strains, 1 feline infectious peritonitis virus strain, and 1 canine coronavirus strain. Because of this specificity for TGEV, but not PRCV, these latter 2 subsite D MAb may be useful for the development of competition ELISA to differentiate serologically between tgev and prcv infections in swine, similar to the currently used European subsite D MAb.

Free access
in American Journal of Veterinary Research

SUMMARY

Monoclonal antibodies (MAB) to subsite A (25C9) and subsite D (44C11) of the S protein of transmissible gastroenteritis virus (tgev) were used in a blocking elisa on fixed tgev-infected swine testis cells to differentiate sera from pigs experimentally inoculated with either tgev or porcine respiratory coronavirus (prcv). Serum samples were obtained from pigs at various intervals from postinoculation day (pid) 0 through at least PID 22 to 40. Eleven-day-old pigs, seronegative for tgev-neutralizing antibodies at the time of inoculation, were inoculated orally and nasally with either the virulent Miller (M5C) strain or the attenuated Purdue (P115) strain of tgev, or with the ISU-1 strain of prcv. Gastroenteritis was observed in 100% of the M5C-tgev-inoculated pigs; but clinical signs of disease were not observed in either the PI 15-tgev- or prcv-inoculated pigs. Virus-neutralization (vn) antibody titer in sera was determined by use of a plaque-reduction assay. Blocking ELISA antibody titer for subsites A and D was determined from the serum dilution that produced 50% reduction in the absorbance values when it competed with biotinylated MAB 25C9 and 44C11, respectively. In sera from the inoculated pigs, the VN antibody titer began to increase by pid 7 and reached maximum by PID 15 to 16. For pigs inoculated with tgev M5C, subsite A and subsite D blocking antibody titers in the serum paralleled the vn antibody titer, began to increase after pid 7, and reached maximum by pid 15 to 16. The blocking antibody titer to sub-sites A and D began to increase in the PI 115- tgev-inoculated pigs after pid 15 to 16 and reached maximum by PID 22 to 26. Blocking antibody titer to subsite A in prcv-inoculated pigs behaved similarly to blocking antibody titer to subsite A in the M5C-tgev-inocuIated pigs, reaching maximum by PID 15 to 16; however, blocking antibody titer was not detected for subsite D up to PID 24 (the latest time point examined) in sera from the prcv-inoculated pigs. Serum antibody responses and clinical signs of disease were monitored in pigs initially inoculated with either M5C-tgev or -prcv and challenge-exposed with M5C-tgev on PID 24. Clinical signs of gastroenteritis were not observed in the M5C-tgev-inoculated pigs after challenge-exposure with M5C-tgev. Low increases in vn antibody titer and in sub-site A or D blocking antibody titer were detected in the M5C-tgev-inoculated and challenge-exposed pigs. Of the 12 pigs initially inoculated with prcv then challenge-exposed with M5C-tgev, 5 pigs developed diarrhea, the vn and subsite A antibody blocking titers began to increase by postchallenge-cxposure day (PCD) 2 and reached maximal titer by PCD 9, increasing approximately 100-fold above the prechallenge-exposure titer. Subsite D antibody-blocking titer began to appear after PCD 9 and, by PCD 12, had reached nearly the same level as that for the primary response to the M5C-tgev inoculation.

Free access
in American Journal of Veterinary Research

Abstract

Objective

To determine the ability of porcine respiratory coronavirus (PRCV) infections to induce passive immunity in suckling pigs to transmissible gastroenteritis virus (TGEV) challenge exposure.

Design and Animals

4 TGEV seronegative sows and their litters (group A) served as controls, whereas 2 other groups (B and C) of sows (also TGEV seronegative) were oronasally inoculated with live PRCV during 1 or 2 subsequent pregnancies, respectively.

Procedure

Effectiveness of passive immunity provided to pigs via colostrum and milk was assessed after TGEV challenge exposure, and TGEV antibody responses in colostrum and milk were analyzed.

Results

Mortality in the 3 groups of young pigs correlated with severity of clinical signs of TGEV infection and was highest in control litters (86% in group-A pigs) and lowest in litters of sows inoculated with PRCV in 2 subsequent pregnancies (14% in group-C pigs). Virus-neutralization and IgA and IgG TGEV antibody titers of milk collected from sows at challenge exposure had significant positive correlation with litter survival. Significantly higher numbers of TGEV-specific IgA and IgG antibody-secreting cells were found in group-A pigs than in group-C pigs, suggesting that high titer of maternal antibodies (induced in group-C sows multiply exposed to PRCV) may interfere with active antibody responses.

Conclusions and Clinical Relevance

Results suggest that, in PRCV-infected pig herds, multiple exposures of pregnant sows are associated with higher IgA and IgG antibody titers to TGEV in milk, and these titers contribute to protection against TGEV infection. (Am J Vet Res 1996; 57:664–671)

Free access
in American Journal of Veterinary Research