Cell-mediated immune responses of suckling pigs inoculated with attenuated or virulent transmissible gastroenteritis virus

Two litters of suckling pigs seronegative for transmissible gastroenteritis (TGE) virus were orally inoculated with live attenuated (P115) or virulent (M5C) strains of TGE virus. A third seronegative litter (controls) was given cell culture fluids from uninfected cells. Lymphocytes were collected from blood, spleen, mesenteric lymph nodes, and Peyer patches of euthanatized pigs at 0 day and approximately weekly until 26 days after exposure and at approximately 45 days after exposure. Sera were tested for virus-neutralizing antibody titers by use of plaque reduction. Lymphocytes were tested in a lymphocyte proliferation assay for uptake of [3H]thymidine after incubation with the homologous or the heterologous strain of inactivated TGE virus or uninfected cell culture fluids. Only pigs inoculated with virulent TGE virus developed clinical signs of TGE and shed virus. However, all pigs inoculated with TGE virus seroconverted at 6 days after exposure. Responses of lymphocytes from all sources from TGE virus-inoculated pigs peaked between 6 and 14 days after exposure. Pigs inoculated with virulent TGE virus had higher lymphocyte proliferative responses and neutralizing antibody titers than did pigs inoculated with attenuated TGE virus. Cessation of virus shedding coincided with the peak of lymphocyte proliferative responses. The highest responses were with intestinal lymphocytes (mesenteric lymph nodes and Peyer patches) from pigs inoculated with virulent TGE virus. The responses of intestinal lymphocytes from pigs inoculated with attenuated virus were not significantly different from those of pigs inoculated with cell culture fluid. Lymphocytes collected from all sources, except blood from M5C-inoculated pigs, had significantly (P less than 0.05) higher responses to the homologous than to the heterologous TGE virus stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Leukocyte-aggregation assay for transmissible gastroenteritis of swine.

An in vitro leukocyte-aggregation assay was developed to detect the exposure of swine to transmissible gastroenteritis virus. Leukocytes in heparinized blood samples aggregated when mixed with test antigen prepared from transmissible gastroenteritis-infected swine testicle cell cultures. Twenty-two of 23 swine exposed 3 days or more were positive or suspects in the assay; 6 nonexposed swine were negative. Aggregation was shown as early as 3 days postexposure in 1 sow and persisted for as long as 14 months in another. Persistence of the assay was proved by repeated evaluations on 2 experimentally exposed swine.     

Patterns of alveolar macrophage activation upon attenuated and virulent African swine fever viruses in vitro

The pattern of porcine alveolar macrophage (AM) activation upon classical stimuli of two strains of African swine fever (ASF) viruses, an attenuated ASFV-BA71V and virulent ASFV-Georgia2007 were investigated. In an in vitro experiment ASFV-Georgia2007-infected AM showed M1 polarization pattern different from the one induced by classical stimuli. Altered morphology, appearance of binuclear cells, decreased synthesis of IFN-alpha as well as IFN-epsilon was observed compared with attenuated ASFV-BA71V, and decreased synthesis of IFN-omega compared with intact cells. However, CD68 level did not significantly differ between alveolar macrophage populations infected by ASFV-Georgia2007 and control group, while both LPS/IFN-gamma stimulation and non-pathogenic ASFV-BA71V virus increased the level of CD68 soluble receptor.AM infection with ASFV-Georgia2007 resulted in remarkable DNA proliferation whereas LPS/IFN-gamma and ASFV-BA71V induced less expressed DNA proliferation in activated cells. The higher value of nitric oxide was obvious in the cells infected with ASFV-BA71V, compared to ASFV-Georgia2007 and LPS/IFN-gamma activated cells.In conclusion, pattern of activation of alveolar macrophages induced by ASFV-Georgia2007 virus differs from the one expressed in LPS/IFN-gamma- and ASFV-BA71V-activated cells. ASFV-BA71V and LPS/IFN-gamma share similar antiviral response of porcine AM. Therefore we assume that wild type virulent ASFV can partially down regulate antiviral response of AM and conclude that evolutionary decrease of virulence in ASFV is related to alterations of control of the host cell antiviral response.     

Intrafetal inoculation of swine with transmissible gastroenteritis virus.

Fetuses in 3 sows were inoculated (intramuscularly) with transmissible gastroenteritis (TGE) virus on 95th, 77th, and 74th days of the gestation. At 15, 14, and 37 days later (or days when pigs were obtained by hysterectomy), there was evidence of intestinal localization of virus, with villous atrophy and subsequent repair. All intrafetal-inoculated pigs became serologic-positive for TGE. A noninoculated pig shown to be seropositive for TGE at 15 days of age (after hysterectomy) was resistant to challenge exposure with virulent TGE virus given on the 32nd day, in contrast to 3 seronegative littermates that developed typical disease when challenge exposed.     

猪传染性胃肠炎的流行特点与综合防制技术

猪传染性胃肠炎是由冠状病毒科中的猪传染性胃肠炎病毒，引起的一种高度接触性肠道传染病。本文就该病的流行特点、致病因素与综合防制方面进行了专门探讨，且取得了明显的诊疗效果。以供同仁共同商榷。     

Risk factors associated with transmissible gastroenteritis in swine.

Commercial production data base records from 2 Illinois farms, on which epizootic or enzootic transmissible gastroenteritis (TGE) was experienced, were accessed for an epidemiologic study. Risk factors investigated were sow parity, source of sows, location of farrowing crates, and breeding practices. At farm 1, an epizootic was experienced; at farm 2, an epizootic of TGE followed by enzootic TGE was experienced. Initially, crude risk ratios were calculated for these risk factors, and the crude risk ratios were subsequently adjusted for confounders and interactions, using multiple logistic regression techniques. After adjustment, parity-3 sows were 2.3 times more likely to have litters with TGE than were sows of all other parities on farm 1, and parity-1 sows were 2.6 times more likely to have litters that experienced TGE than were sows of all other parities on farm 2. A single boar on each farm was linked to increased likelihood of a sow's litter contracting epizootic TGE on each farm. Enzootic TGE was maintained by the periodic influx of outside-source gilts on farm 2; these gilts were 2.2 times more likely to have litters with TGE than were sows derived from farm 2. Sows housed in farrowing crates located under the cold air inlet of farm 2 were 1.7 times as likely as sows located in other rows to have litters with enzootic TGE.