Publications by authors named "Loepfe E"

Herpesvirus capsids originating in the nucleus overcome the nucleocytoplasmic barrier by budding at the inner nuclear membrane. The fate of the resulting virions is still under debate. The fact that capsids approach Golgi membranes from the cytoplasmic side led to the theory of fusion between the viral envelope and the outer nuclear membrane, resulting in the release of capsids into the cytoplasm.

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Nucleocapsids of herpesviruses originate in the nucleus of host cells and bud through the inner nuclear membrane acquiring tegument and envelope. The release of the enveloped virus particle from the perinuclear space is unknown. Cryobased electron microscopic imaging revealed enveloped virus particles within cisterns associated with the perinuclear space, a pre-Golgi compartment connecting Golgi cisterns to the perinuclear space, and enveloped virus particles in Golgi cisterns where they are packaged into transport vacuoles by membrane fission.

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Herpesviruses enter cells by a yet poorly understood mechanism. We visualized the crucial steps of the entry pathway of bovine herpesvirus 1 (BHV-1) and BHV-5 by transmission and scanning electron microscopy, employing cryotechniques that include time monitoring, ultrarapid freezing, and freeze substitution of cultured cells inoculated with virus. A key step in the entry pathway of both BHV-1 and BHV-5 is a unique fusion of the outer phospholipid layer of the viral envelope with the inner layer of the plasma membrane and vice versa resulting in "crossing" of the fused membranes and in partial insertion of the viral envelope into the plasma membrane.

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Caprine herpesvirus 1 (CapHV-1) DNA was examined by electron microscopy, restriction site mapping and homology studies with bovine herpesvirus 1 (BHV-1) DNA. Although the restriction site maps differed significantly, we showed that the genome structures of CapHV-1 and BHV-1 were identical and that the DNAs shared a high degree of base sequence homology.

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Bovine herpesvirus 1 (BHV-1) strains can be differentiated by their DNA and polypeptide patterns, and by antigenic properties as demonstrated by monoclonal antibodies. We classified the BHV-1 strains according to these data as BHV-1.1, BHV-1.

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