Latent infection and subsequent reactivation of pseudorabies virus in swine exposed to pseudorabies virus while nursing immune dams

作者
William Lloyd Mengeling
出处
期刊:American Journal of Veterinary Research [American Veterinary Medical Association]
卷期号:50 (10): 1658-1666 被引量:24
标识
DOI:10.2460/ajvr.1989.50.10.1658
摘要

SUMMARY The ability of pseudorabies virus (prv) to infect and establish latency in pigs with passively acquired (maternal) antibody for prv was tested by exposing such pigs to the virus and subsequently attempting to reactivate latent virus by administering large doses of dexamethasone. Pigs of each of 4 litters that had nursed gilts with relatively high (512, gilts 1 and 2), moderate (32, gilt 3), and no (< 2, gilt 4) serum titers of virus-neutralizing (vn) antibodies for prv were allotted to 3 treatment groups (A, B, C) when they were 2 weeks old. Group-A pigs were separated from littermates and dam and thereafter kept in isolation; group-B pigs were experimentally exposed oronasally to prv and 1 hour later returned to their dam; group-C pigs were kept with their dam and potentially exposed to prv by contact with littermates of group B. Sera obtained from pigs at selected intervals until they were 17 weeks old were tested for vn activity and for precipitating activity for radiolabeled viral proteins. All group-A pigs remained clinically normal throughout the experiment. Depending on the initial amount of passively acquired antibody, little or no serum vn or precipitating activity remained by the time these pigs were 17 weeks old. Group-B and -C pigs, with relatively high amounts of passively acquired antibody when exposed to prv, also remained clinically normal. However, most became latently infected as subsequently evidenced by either dexamethasone-induced or noninduced virus reactivation. Noninduced reactivation may have been initiated by weaning the pigs when they were about 8 weeks old. Group-B and -C pigs, with no or moderate amounts of passively acquired antibody when exposed to prv, had severe clinical signs. These pigs either died or recovered but remained stunted in growth. Virus was reactivated in all of the recovered pigs by treatment with dexamethasone. Quantitative and qualitative changes in serum precipitating activity, especially for viral proteins of relatively low molecular weight (< 46,000), were a more consistent indication of virus reactivation than were either increased vn titers or virus isolation. Results with litters 1 and 2 clearly indicate that latent infection of young pigs with highly virulent prv can develop in the absence of clinical signs.

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