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Herpes simplex virus replication
----------------------------------------------------
Herpesviruses are large double-stranded DNA animal viruses with
the distinguishing ability to establish latent, life-long infections. To
date, eight human herpesviruses that exhibit distinct biological and
corresponding pathological/clinical properties have been identified.
During their life cycles, herpesviruses execute an intricate chain of
events geared towards optimizing their replication. This sets an
interesting paradigm to study fundamental biological processes. This
review summarizes recent developments in herpesvirus research with
emphasis on genome transactions, particularly with respect to the
prototypic herpes simplex virus type-1.
Icosahedral capsid. Enveloped, linear dsDNA viruses. Very large (120-200nm in diameter) - 2nd in size only to poxviruses.
Envelope derived by budding from the nuclear membrane (not a cytoplasmic membrane) because assembly occurs in the nucleus.
HSV-1, HSV-2, and VZV → MNGCs (multinucleated giant cells) with intranuclear inclusion bodies on Tzanck smear of a swab of vesicular skin lesions.
[Note: MNGCs are also seen in retroviruses, paramyxoviridae (RSV, parainfluenza virus, mumps, and measles) due to the F (fusion) protein on the surface of all members of the paramyxovirus family]
Latent infections:
----------------------------
HSV-1: Latent in the trigeminal nerve ganglion
HSV-2: Latent in sacral nerve ganglia
VZV: Latent in any sensory ganglia
EBV: Latent in B-cells
CMV: Latent in leukocytes
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