Lymphoreticular and myeloid pathogenesis of Venezuelan equine encephalitis in hamsters.

Abstract

Ultrastructural, histopathologic, and virologic studies of adult hamsters infected with virulent Venezuelan equine encelphalomyelitis (VEE) virus (Subtype I-B) demonstrated precise chronologic and topographic progression of lesions and viral replication in extraneural sites. Thymus contained the earliest lesions and the highest initial and subsequent viral titers. No particular cytotropism was observed as highly efficient viral replication and severe cytonecrosis proceded. Early cortical necrosis of splenic periarteriolar lymphocytic sheath was followed by lymphoblastoid repopulation of the peripheral zone. Massive bone marrow necrosis was accompained by ultrastructural evidence of VEE viral particle production in reticulum cells, rubricytes, myeloid cells, lymphoblastoid cells, and megakaryocytes. Speed, efficiency, destructiveness, and relative sensitivity of virtually all lymphoreticular and hematopoetic cells were hallmarks of virulent VEE infection in the hamster.

Full text

PDF

• 351
• 352
• 353
• 354
• 355
• …
• 370
• Next

Images in this article

Figure 8
on p.366

Figure 9
on p.366

Figure 1
on p.363

Figure 2
on p.363

Figure 3
on p.363

Figure 10
on p.367

Figure 11
on p.367

Figure 4
on p.364

Figure 5
on p.364

Figure 6
on p.364

Figure 12A and B
on p.368

Figure 13
on p.368

Figure 7
on p.365

Figure 14
on p.369

Figure 15
on p.369

Figure 16
on p.369

Figure 17
on p.370

Figure 18
on p.370