Abstract
ICP4 is the major transcriptional regulatory protein of herpes simplex virus (HSV). It is expressed in infected cells with immediate early kinetics and is essential for viral growth. ICP4 is also a structural component of the virion tegument layer. Herpesviral tegument proteins exert regulatory functions important for takeover of the host cell. Tegument ICP4 has not been well characterized. We examined the ICP4 present in HSV-1 virions that were either derived from wild type infected cells or from ICP4-expressing (E5) cells infected with ICP4 deletion virus d120. Limited proteolysis demonstrated that virion-associated ICP4 from particles derived from E5 cells was indeed an internal component of the virion. A similar subset of virion structural proteins was detected in viral particles regardless of the cellular origin of ICP4. Genotypically ICP4-negative virions complemented with tegument ICP4 entered cells via a proteasome-dependent, pH-dependent pathway similar to wild type virions. In infected cells, ICP4 was distributed predominantly in intranuclear replication compartments regardless of whether it was expressed from a transgene or from the HSV genome.
Highlights
The herpes simplex virus (HSV) DNA genome is housed in an icosahedral capsid surrounded by an asymmetrical tegument layer and a surface envelope [1]
To determine whether HSV-1 d120 propagated on ICP4-expressing cells is truly complemented with tegument ICP4, the mutant virions were analyzed
Relative to VP5, levels of ICP4 similar to those of wild type KOS virions were found associated with d120 virions and a, 40 kiloDalton ICP4 fragment was detected as reported previously [25]
Summary
The herpes simplex virus (HSV) DNA genome is housed in an icosahedral capsid surrounded by an asymmetrical tegument layer and a surface envelope [1]. Infection of cells with an ICP0 deletion mutant virus yields genotypically null virions that lack tegument ICP0. To determine whether HSV-1 d120 propagated on ICP4-expressing cells is truly complemented with tegument ICP4, the mutant virions were analyzed.
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