Adult macaques do not develop disease after infection with a nef deletion mutant of the simian immunodeficiency virus (SIV) and are protected against challenge with pathogenic virus. This finding led to the proposal to use nef-deleted viruses as live, attenuated vaccines to prevent human acquired immunodeficiency syndrome (AIDS). In contrast, neonatal macaques developed persistently high levels of viremia after oral exposure to and SIV nef, vpr, and negative regulatory element (NRE) deletion mutant. Severe hemolytic anemia, thrombocytopenia, and CD4+ T cell depletion were observed, indicating that neither nef nor vpr determine pathogenicity in neonates. Because such constructs have retained their pathogenic potential, they should not be used as candidate live, attenuated virus vaccines against human AIDS.

The clinical, ultrasonographic and, when available, histopathologic findings of gastric ulceration in 7 dogs were reviewed. The most common clinical signs were vomiting, hematemesis, melena, weight loss and anemia. Ultrasonographic features of gastric ulcer included local thickening of the gastric wall, possible loss of the 5-layer structure, the presence of a wall defect or "crater," fluid accumulation in the stomach and diminished gastric motility. The localized gastric thickening varied from 9 to 16 mm. The ulcer crater was often located in the center of the thickened site and appeared as a mucosal defect associated with persistent accumulation of small echoes, most likely representing microbubbles. In this preliminary study, there was no definitive ultrasonographic distinction between benign and malignant ulcers.

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