Abstract
UL21 of herpes simplex virus type 1 (HSV-1) is an accessory gene that encodes a component of the tegument. Homologs of this protein have been identified in the alpha, beta, and gamma herpesvirus subfamilies, although their functions are unclear. To clarify the functions of UL21, we generated a UL21-null HSV-1 mutant. Growth analysis showed that the synthesis of infectious UL21-null HSV-1 in glial cells was delayed and that the overall yield was low. The plaque sizes of the UL21-null mutant were smaller than those of wild-type HSV-1. We identified several candidate UL21-interacting proteins, including intermediate filaments, by yeast two-hybrid screening. The distribution of glial fibrillary acidic protein (GFAP), which is the main component of intermediate filaments, was altered in UL21-null mutant-infected glial cells compared to wild-type virus-infected cells. These results will help clarify the function of UL21 and broaden our understanding of the life cycle of HSV.
Highlights
Herpes simplex virus type 1 (HSV-1) is an enveloped, large DNA virus with a genome consisting of approximately 80 genes that encode transcriptional regulatory proteins, capsid proteins, enveloped glycoproteins, viral DNA replication proteins, and proteins involved in the cleavage/packaging of viral DNA
Viral DNA from UL21D and UL21R were used to amplify the manipulated area by PCR; sequencing of the products showed that the desired genetic manipulations had been made
The product of UL21 was not expressed in UL21D-infected cells, but it was detected in both wild-typeand UL21R-infected cells (Figure 1)
Summary
Herpes simplex virus type 1 (HSV-1) is an enveloped, large DNA virus with a genome consisting of approximately 80 genes that encode transcriptional regulatory proteins, capsid proteins, enveloped glycoproteins, viral DNA replication proteins, and proteins involved in the cleavage/packaging of viral DNA. UL21 of HSV-1 is an accessory gene that encodes a 535-amino acid component of the tegument (Baines et al, 1994). Homologs of this protein have been identified in the alpha, beta, and gamma herpesvirus subfamilies (Baer et al, 1984; Davison and Scott, 1986; Chee et al, 1990). Absence of UL21 results in a delay early in the HSV-1 replication (Mbong et al, 2012), while processing of newly replicated viral DNA is impaired in UL21-null pseudorabies virus (de Wind et al, 1992).
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