Characterization of viral origins of DNA replication in eukaryotic cells has demonstrated that most viral origins consist of two components: an essential core sequence that recruits the origin recognition proteins and specifies the initiation site, and auxiliary regions that modulate the efficiency of replication initiated at the core (for reviews, see references 17 to 19). Whether initiation of DNA replication during reactivation of HSV-1 from neuronal latency also requires OBP is not known. We previously showed that upon infection of antigen-presenting cells, HSV type 1 (HSV-1) rapidly and efficiently downregulates the major histocompatibility complex class I-like antigen-presenting molecule, CD1d, and potently inhibits its recognition by CD1d-restricted natural killer T (NKT) cells. Here, the effect of pseudorabies virus (PRV) gM and the herpes simplex virus type 1 (HSV-1) gM/UL49A complex on the fusion events caused by the HSV-1 glycoproteins gB, gD, gH and gL was investigated. vhs residues 238 to 344 were sufficient for the interaction, and the VP16 acidic transcriptional activation domain was not required. Lateral interaction resulted in coat formation on the membranes. Viruses have developed remarkable strategies to usurp cellular processes for their own needs while maintaining efficient virus production.
Infectious titers were reduced and newly synthesized virion with damaged protein envelopes were observed by electron microscopy.