Dear Colleagues,

Herpesviruses are large double-stranded DNA viruses that are disseminated throughout the animal kingdom. Herpesviruses are major human pathogens that cause life-long persistent infections with clinical manifestations that range from a mild cold sore, to lymphoma and angiogenic cancer. Herpesvirus genomes have the coding capacity in excess of 100 genes.

The herpesvirus virion is comprised of four structural components: An icosahedral capsid, which encloses the viral DNA genome; an electron-dense asymmetrically distributed material, which immediately surrounds the capsid and is termed the tegument; and an outer membrane or envelope, which encloses the tegument and capsid and in which are embedded the viral glycoproteins. Capsid assembly, DNA packaging, nuclear exit, and cytoplasmic envelopment involve the participation of a large and diverse set of about 50 proteins. Herpesviruses, like other viruses, hijack the cell machinery for their propagation and morphogenesis. The nuclear lamina is disrupted to facilitate capsid access to the nuclear envelope, the cell cytoskeleton is used to transport capsids and sub-viral structures to sites of maturation in order to facilitate their egress, and the Golgi is modified to create budding sites for production of progeny virions.

Herpesviruses form capsids that possess icosahedral symmetry. Assembly of herpesvirus capsid shells and DNA packaging are all nuclear events. Six proteins form all herpesvirus capsids. The capsid shell is comprised of the major capsid protein, the triplex proteins and the small capsid protein. The scaffold proteins occupy the internal space of the capsid and are required for icosahedral symmetry.  Cleavage of the scaffold proteins by the maturational protease results in the loss of these proteins from the interior of the capsid. This space is subsequently occupied by the viral genome. A complex of six additional proteins are required for the packaging of the viral genome into the interior space of the capsid. Some of these proteins are transiently associated with the capsid during packaging, such as the terminase complex, while others are components of the mature capsid (portal protein) and stabilize the packaged DNA (capsid vertex specific complex proteins).

Initial envelopment of the virion takes place at the inner nuclear membrane. The nuclear egress complex functions to transfer the mature capsid form the site of assembly to the cytosol.  These capsids are then transported to the trans-Golgi compartment or other cytoplasmic organelle (late endosomes) for final envelopment. This cytoplasmic site must accumulate all the different tegument proteins that are incorporated into the mature virion, and also, the lipid membrane that envelopes this particle has to contain the full repertoire of viral glycoproteins. One of the most intriguing aspects of this morphogenesis pathway is the role of the tegument proteins in this dual envelopment process, the cellular localization and movement of tegument proteins prior to their incorporation into the maturing virus, and the viral factors/signals that traffic particles to the maturation compartment.

The tegument is one of the most complex and diverse structures of the virion, both in terms of protein composition and the functions encoded by the constituents of this structure. The viral specified polypeptides that comprise this structure specify a diversity of functions and activities within the infected cell. What has become increasingly evident is the importance of the tegument proteins in the maturation process of the enveloped virus. The mechanisms of how the tegument proteins function in trafficking and virion morphogenesis, and the manner by which protein–protein interactions determine the fate of virus particle formation are actively being discovered.

Dr. Prashant Desai
Guest Editor

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• herpesvirus
• HSV-1/2
• VZV
• HCMV
• KSHV
• EBV
• capsid
• DNA packaging
• tegument
• virion
• nuclear egress
• virus translocation
• cytoplasmic envelopment