Novel entry pathway of bovine herpesvirus 1 and 5.

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. The fusion area is proposed to function as an axis for driving the virus particle into an invagination that is concomitantly formed close to the fusion site. The virus particle enters the cytoplasm through the opened tip of the invagination, and the viral envelope defuses from the plasma membrane. There is strong evidence that the intact virus particle is then transported to the nuclear region.

The genome of caprine herpesvirus 1: genome structure and relatedness to bovine herpesvirus 1.

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.

The genome of bovine herpesvirus 1 (BHV-1) strains exhibiting a neuropathogenic potential compared to known BHV-1 strains by restriction site mapping and cross-hybridization.

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-1.2 (a/b) and BHV-1.3 (a/b). BHV-1.1 and BHV-1.2 correspond to the well known 'common' BHV-1 strains, whereas BHV-1.3 has only recently been recognized and exhibits a neuropathogenic potential. In the present paper we describe the structural genome characteristics of BHV-1.3 compared to those of the other BHV-1 strains, examined by means of restriction site mapping, electron microscopy and cross-hybridization. Our results also confirm and complete data concerning BHV-1.1 and BHV-1.2 published by other authors. The following main conclusions can be drawn from our investigations: BHV-1.1 and BHV-1.2 differences are restricted to distinct genomic regions, characterized by loss or gain of restriction sites. BHV-1.3, however, differs from the other BHV-1 strains in restriction site alterations throughout the whole genome. Electron microscopy showed the typical BHV-1 DNA structure for BHV-1.3. Genetic homology between BHV-1.1 and BHV-1.2, reported to be about 95%, was confirmed by cross-hybridization, and a similar high base sequence homology for BHV-1.3 could be shown.