Venezuelan equine encephalomyelitis: research needs and criteria for selecting research components.
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Biomedical subjects
Publications and source records attributed to P D DeLay.
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Pigs were inoculated with a modified isolate of African swine fever virus (ASFV). Complement-fixing (CF) and agar gel diffusion precipitin (AGDP) antibodies could be detected in the serums of most pigs from 14-days postinoculation (DPI) until their immunity was challenged with virulent ASFV at 117 DPI. Reductive cleavage with 2-mercaptoethanol showed that serums collected at 14 to 35 DPI contained 19S antibody, but that the 7S antibody was dominant at 35 and 117 DPI. This distribution of antibody was confirmed by sucrose-gradient centrifugation. Nearly all of the early serums also contained 7S antibodies which fixed complement and reacted in the AGDP test. Pigs whose serums contained both CF and AGDP antibodies at time of challenge failed to develop acute disease while pigs without CF antibodies were usually not protected. Pigs surviving challenge with virulent virus showed no increase in antibody titers, or reversion to 19S antibody.
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The clinical response to Teschen disease and the excretion and rate of virus distribution in tissues of colostrum-deprived, specific pathogenfree pigs was determined. Severe, mild, and clinically inapparent responses to the disease were noticed following simultaneous intracranial and intranasal infections. Fourteen-day-old pigs reacted more severely to infection than 21-day-old pigs. The virus was detected in feces 2-3 days following infection but not in stools of surviving pigs 30 days after infection. The highest concentration of virus occurred during the incubation period and before onset of paralysis; the lowest concentrations were found during terminal disease stages. In tissues collected before or immediately after death of pigs, Teschen disease virus was found in several visceral organs but not in blood, urine or urinary bladder tissue. Virus yield was highest in brain and spinal cord tissues. Highest virus concentration was found in the cervical thoracic portions of the spinal cord, thalamus and cerebellum. Other aspects of the clinical disease are discussed.
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