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 nuclear membrane (not 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 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 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