Previous studies have suggested that the UL17 gene of herpes simplex virus type 1 (HSV-1) is essential for virus replication. Due to the partly overlapping clinical manifestations of infection with HSV-1 and its closest relative among herpesviruses, HSV-2, diagnostic methods are required to discriminate between infections with these two viruses. The UL20 mutant genes could be broadly categorized into four main groups: Group I UL20 mutant genes complemented for both virus production and virus-induced cell fusion; Group II UL20 mutant genes did not complement for either virus-induced cell fusion or infectious virus production; Group III UL20 mutant genes complemented for virus-induced cell fusion to variable extents but exhibited substantially decreased ability to complement UL20-null infectious virus production; Group IV mutant genes complemented for infectious virus production but had variable effects on virus-induced cell fusion; this group included two mutants that efficiently complemented for gBsyn3, but not for gKsyn1, virus-induced cell fusion. The lytic HSV-1 life cycle takes ∼18 hours and the steps include: 1) attachment to heparan sulfate and cell-surface receptors; 2) fusion of the virion envelope with the plasma membrane; 3) release of the capsid … Expression of the ICP0 and ICP27 reporter transgenes was present in anatomically distinct subsets of neurons in the absence of viral proteins. The ability of wild-type ICP27 expressed from a cloned gene to complement tsY46 and tsLG4 constitutes additional evidence that these mutants are defective in an ICP27-associated function. Additionally, we demonstrated that ORF38 transcription overlaps ORF39 and the products presumably share the same poly(A) signal.
(26, 37, 42, 43). ΔgKhpd-1 and ΔgKhpd-2 viruses produced lower yields and smaller plaques than ΔgK. RNA interference (RNAi) is now the term used to describe the mechanism of RNA-inducible gene silencing. The high proportion of such transcripts suggests that the alpha27 gene plays a major role in the early decline in cellular gene expression so characteristic of HSV infection.