Photoreceptor cell death by apoptosis in dogs with sudden acquired retinal degeneration syndrome.

OBJECTIVE: To examine the role of apoptosis in retinal photoreceptor degeneration in dogs with sudden acquired retinal degeneration syndrome (SARDS). SAMPLE POPULATION: Retinas from 3 dogs with SARDS and from 2 clinically normal adult dogs. PROCEDURE: Apoptosis was identified by in situ end-labeling and observation of characteristic morphologic changes by light microscopy. RESULTS: The degree of photoreceptor degeneration varied with duration of vision loss in SARDS-affected eyes. The retina of all 3 SARDS-affected eyes had numerous (34, 61, and 70) apoptotic nuclei per section that were overwhelmingly located in the outer nuclear layer. Apoptotic nuclei were not detected, or were rare in similarly sized retinal sections from normal dogs. Inflammation was not an important feature of SARDS. CONCLUSIONS: Apoptosis appears to be at least 1 mechanism of photoreceptor cell death in dogs with SARDS. CLINICAL RELEVANCE: Because apoptosis appears to be a final common pathway in many retinal degeneration syndromes, future treatment strategies that control apoptosis in other diseases may be applicable to dogs with SARDS. Halting this pathway may allow some photoreceptors to survive and, perhaps, preserve vision.

bcl-2 alters influenza virus yield, spread, and hemagglutinin glycosylation.

We previously demonstrated that expression of bcl-2 in Madin-Darby canine kidney (MDCK) cells blocks influenza virus-induced apoptosis and DNA fragmentation. We show here that expression of bcl-2 also reduces the level of infectious virus production and the spread of virus in MDCK cell cultures infected at a low multiplicity of infection. This effect is associated with modified glycosylation of the hemagglutinin protein.