Biomedical subjects

J M Harb

Publications and source records attributed to J M Harb.

At least 37 records · Page 2Linked to original sources

PubMed1979

Lesions induced by encephalomyocarditis virus and coxsackievirus B in newborn mice.

Electron microscopic studies of various tissues from virus-infected newborn mice disclosed a consistent form of viral cytonecrotic ultrastructural lesion in divergent types of cells (myocardial, valvular fibroblastic, aortic, exocrine and endocrine pancreatic, and hepatic cells) due to three different picornaviruses (coxsackieviruses B4 and B1 and encephalomyocarditis virus). The lesion is characterized by numerous membrane-vesicle complexes, margination of nuclear chromatin or nuclear pyknosis, dilation of rough endoplasmic reticulum, inflammation, and, at times, mitochondrial swelling. It seems apparent that the finding of this ultrastructural type of cytonecrosis is characteristic of a picornaviral infection regardless of the tissue involved and the offending member of the picornavirus group.

Animals↗

PubMed1975

Encephalomyocarditis (EMC) virus infection of the femoral vein of newborn mice.

The EMC virus was found to infect and injure the femoral veins of newborn mice. EMC viral crystals were found in the advential fibroblasts of these veins. In view of the extensive damage observed in the extremely small amount of tissue examined electron microscopically, the extent of the viral phlebitis must have been considerable. The relationship of these findings to the pathogenesis of thrombophlebitis in man provokes interesting speculations.

Animals↗

PubMed1975

Spherical aggregates of coxsackie B4 virus particles in mouse pancreas.

A high titer culture of Coxsackie B4 virus was used to induce pancreatitis in newborn mice. In animals sacrificed 1 or 2 days after intraperitoneal inoculation, we observed cytonecrosis consistent with picornaviral infection as well as necrosis indicative of pancreatitis. In addition, we observed aggregates of particles which seem to be Coxsackie B4 virus particles, some arranged in the typical picornaviral crystalloid lattice formation and others arranged into spherical masses approximately 102 nm in diameter. Depending upon the depth and orientation of section through the spherical aggregates, the particles were arranged into two patterns which were readily distinguishable. When the plane of section was through the center of the sphere, 10 particles circularly arranged around a dense particle core were observed. When the sphere was cut tangentially, the particles were arranged in a zig-zag pattern so that there were two concentric layers of at least 6 particles per layer, with no central core. Both crystalloid and spherical aggregates were observed free within acinocyte cytoplasm, and within autophagic vacuoles, cytosegresomes, and fine granular bodies of acinocytes, and within phagocytic vacuoles of macrophages. We conclude that the spherical aggregates represent a distinct crystalloid form of Coxsackie B4 virus during its replicative cycle, which may eventually develop into the more typical picornaviral crystalloid lattice configuration and that the spherical aggregates are located in foci of viral synthesis. Marked pathogenicity of Coxsackie B4 virus in the newborn mouse pancreas should be considered a factor in the observations noted.

Animals↗

PubMed1975

Coxsackie viral infection of human myocardium.

The myocardiu m of a young patient who had clinically established cardiomyopathy and suspected Coxsackie virus B4 infection was studied. Coxsackie B4 viral antigen was found in the ventricular and atrial myocardium by specific immunofluorescent antibody staining. Histologic examination revealed varying degrees of myocardial damage. Interstitial fibrosis and edema, swelling and deterioration of hypertrophic muscle fibers, connective tissue proliferation, stasis of small coronary blood vessels, atrophy of myocardial fibers with pyknosis of nuclei, and lytic deterioration were observed. Electron microscopic examination showed portions of the Z bands to be either widened or displaced into the sarcomere. Adjacent cell membranes in the region of the intercalated disc in the myocardium of both the ventricle and the atrium were separated, forming large gaps. Morphologic changes were most pronounced in the atrium adjacent to the mitral valve, in which the mitochondria were grossly swollen, and large vesicles were present in the sarcoplasm. The pathologic changes found in the myocardium of all chambers of the heart apparently were due to Coxsackie B4 viral infection.

Adult↗

PubMed1975

Coxsackie B4 virus crystal formation in mouse pancreas.

For the first time, Coxsackie B4 virus crystals are demonstrated in tissues of animals inoculated with the virus. Until this report, Coxsackie B4 virus had never been found to form crystalline aggregates in tissues of any kind. The viral crystals which were located in the pancreas of newborn mice were associated with ultrastructural damage to the pancreas not observed in control animals, thereby indicating that viruses directly invade and damage these tissues. Thus, this virus must be considered among etiologic factors in pancreatic disease.

Animals↗

PubMed1975