Virus-host interaction for defence and transmission
The classification of herpes viruses has recently been updated [1, http://www. ictvonline.org]. Morphologically, herpes viruses are distinct from all other viruses. A linear, double-stranded DNA genome of 125–290 kbp is contained within a T = 16 icosahedr
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2.1 The virus The classification of herpes viruses has recently been updated [1, http://www. ictvonline.org]. Morphologically, herpes viruses are distinct from all other viruses. A linear, double-stranded DNA genome of 125–290 kbp is contained within a T = 16 icosahedral capsid, which is surrounded by a proteinaceous matrix, dubbed the tegument, and then by a lipid envelope containing membraneassociated proteins. Genetically, herpes viruses fall into three distinct groupings that are related only tenuously to each other. These groupings consist of viruses of mammals, birds and reptiles, viruses of fish and frogs, and a single virus of bivalves [1]. In the order Herpesvirales, the cytomegalovirus (also named as the human herpes virus 5) belongs to the family of Herpesviridae and the subfamily of Betaherpesvirinae. In the human cytomegalovirus 71 viral and more than 70 host proteins have been detected by mass spectrometric analyses of extracellular virions [2]. In addition to these structural proteins, the massive CMV genome, which is approximately 50 % larger than the genome of herpes simplex, encodes an undefined number of non-structural proteins (some authors mention that the CMV genome encodes over 200 proteins). The genome itself is organised into long and short unique regions, each flanked by inverted repeats [3, 4]. The replication of CMV is slow compared with other herpes viruses. CMV lytic gene expression, like that of the other herpes viruses, occurs in a temporally ordered cascade. Virus entry begins with virion attachment to the ubiquitously expressed heparin sulphate proteoglycans at the cell surface, followed by binding of the viral glycoproteins gB and gH to one or more cellular receptor(s), including the integrin heterodimers α2β1, α6β1 and αvβ3, the plateletderived growth factor-α receptor and the epidermal growth factor receptor, whose role in CMV entry is still debated [5]. Subsequent delivery of capsids into the cytoplasm requires fusion of the virus envelope with the cellular membranes. This fusion appears to be mediated either by the gH/gL/UL128-131A complex and/or the gH/gL/gO complex. Thereafter, the de-enveloped capsids must be transported towards the nucleus. This trafficking must be active, be-
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2 Virus-host interaction for defence and transmission
cause passive diffusion would take >200 years for 1 cm of cytoplasm. The reason for this is the crowded cytoplasm, which has a protein density of approximately 300 mg/ml, analogous to the viscosity of wet sand [6]. To overcome this problem, the virus acts like a pirate. The docking and boarding of the virus, which is initiated by the coordinated interaction of viral glycoproteins (the core fusion machinery) with host receptors, induce a cytoskeletal rearrangement inside the cell [6]. Thus, the virus can move along the microtubule highways by using molecular motor proteins (i. e. dynein). Using this cellular cargo transport via the microtubular highway it takes in fibroblasts only a few hours for the virus to reach the perinuclear sites [7]. Once th
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