Balb/C weanling mice were inoculated intraperitoneally with a myocarditic variant of coxsackie-virus B3, with the aim of characterizing more fully the cell damage induced in the heart as well as in other organs. During the first week postinfection (pi), all animals developed acinar pancreatitis, followed by focal myocarditis. In accordance with the increasing infectivity titers, such progressive histopathological changes correlated with local viral replication. From day 4 pi, acinar degeneration accompanied by diffuse inflammatory exudate was observed in the pancreas, followed by fatty tissue replacement by day 8. In the heart, focal necrosis rather than inflammatory reaction first appeared at 4 days pi and became widespread by 6-8 days pi. Necrotic foci usually presented calcium deposits, with absence of myofibrils in the affected fibers. The fact that both periodic acid Schiff (PAS) and Best carmine staining remained positive even after diastase treatment ruled out basophilic necrosis. In summary, the pancreas appeared to be the site of primary viral replication leading to viremia.

The ultrastructure of the hydatid cyst germinal membrane was studied. It was divided into 3 regions, the tegument, the tegumental cell region, and the innermost area bordering the cyst cavity. The morphology of tegumental, muscular, flame, duct, and glycogen-containing cells and cells containing lysosomal-like bodies is described. The significance of these findings is discussed in terms of the possible function of these structures and present knowledge on the penetration of macromolecules into hydatid cysts.

Peroxidase-antiperoxidase technique and histology were employed to elucidate the peripheral routes involved in HSV-2 progression from vagina towards the central nervous system in mice. 12 week-old female Balb/c mice were intravaginally infected with 5 X 10(5)LD50 of HSV-2. Sixty per cent of animals developed vulvovaginitis, perigenital alopecia and hind-limb paresia. Death occurred at 9-11 days post-infection. Colon dilatation and urinary bladder distention were observed in all cases. Complete transversal sections from vulva to kidneys were obtained of each animal, including the spinal cord in situ. Herpes antigen were regularly detected in vulvovaginal epithelium, intramural, perigenital and perivesical small nerves. Besides, their invariable presence in Auerbach's plexus and sympathetic ganglia, strongly suggests preferential autonomic nervous system involvement in the progression of HSV-2 intravaginal infection towards the spinal cord.

The progress of an experimental infection with Herpesvirus hominis type 1 was studied in newborn mice inoculated into the foot pad of the hind leg. To trace the viral antigen, the unlabeled antibody enzyme PAP (peroxidase/antiperoxidase) method was employed. The virus antigen appeared first in the epidermal and connective tissue cells of the inoculation site, and then progressed along the sciatic nerve. This nerve was studied by electron microscopy and showed active multiplication within the Schwann cells, with the production of virions, some of which were found in the intercellular spaces. No intra-axonal particles were observed. The infection then spread to the spinal ganglia and to the spinal cord. In this progression, the pia mater appeared to play an important role. From the spinal cord, the infection spread to the encephalon. The present study supports a mixed route for the neural transport of herpes simplex virus: a) by cell-to-cell transmission (Schwann and connective tissue cells in the sciatic nerve; meningeal cells, neurons and glial cells in the CNS); b) by a passive motion of the virions along the intercellular spaces. The inoculated virus also gave rise to viremia with viral multiplication in several viscera.

Intracerebral inoculation of strain XJ Clon 3 of Junín virus into 1-2-day-old mice resulted in the appearance of viral antigen, detectable by means of the peroxidase antiperoxidase (PAP) technique, within the cytoplasm of the neurons of the cerebral cortex, the basal nuclei, cerebellum, pons, medulla, spinal cord, and spinal ganglia; Junín antigen was likewise observed, although to a lesser extent, in the cytoplasm of astrocytes. The viral antigen was found in highest concentration at the cytoplasmic periphery, near the cell membrane, where complete virions are formed by budding. In some cells a "tigroid" distribution of the antigen was observed, suggestive of its production and concentration within the granular endoplasmic reticulum. In spite of the heavy infection of the neural structures, the neurons did not always show major alterations. By immunolabeling of the glial fibrillary acidic protein (GFAP) by the PAP method, a severe glial response could be seen in infected mice, featuring hyperplasia, hypertrophy, and shape distortion of the astrocytes. This easy labeling was not observed in normal mice of the same age, and suggests the accelerated maturation of the astrocytes and the increased GFAP synthesis by direct action of the virus upon such cells. In view of its specificity, use of the PAP technique for GFAP immunolabeling will most likely replace the traditional metal impregnation methods in the study of the astrocytes. Its utilization would be indicated whenever astroglial changes are suspected in any CNS pathologic condition.