HCVM Is Capable of Infecting Cells in Vivo Essay

HCVM Is Capable of Infecting Cells in Vivo Essay

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HCMV is capable of infecting an extensive range of cell types in vivo. According to Compton (2004), the infection of a fibroblast begins with an initial tethering of a virion to cell surface - heparan sulfate proteoglycans. Then the HCMV glycoprotein, gB, is directly fused to cellular receptors such as epidermal growth factor receptor (EGFR) and cellular integrins occurs at neutral pH (Compton, 1992). The fusion with the envelope is followed by attachment of the virion and release into the cytoplasm (Roizman & Pellet, 2001). HCMV entry into epithelial and endothelial cells occurs through endocytosis in a low-pH condition (Ryckman et al., 2006) using the viral glycoproteins UL131-128 (Hahn et al., 2004). Infected cells show several characteristics which are nuclear swelling, chromatin margination and the formation of both intra-nuclear and intra-cytoplasmic inclusions (Pass, 2001). Once the HCMV enter the cell, the tegument proteins remain associated with the capsid which is transported along microtubules to the nucleus (Kalejta, 2008).

In HCMV there are three phases of gene expression sequence which are immediate early (IE), early (E), and late (L). The IE phase is short and its products are derived from three major genes which are IE1, IE2, and IE3 (Keil et al., 1987). The expression of both E and L genes need the prior expression of one or more IE gene products which function as transcriptional activators (Messerle et al., 1992). Generally the IE genes are responsible for regulating the production of host cell products, the E genes control the production of daughter virions, and the L genes are involved in the synthesis of proteins that form the structural components of the virion (Griffiths & Grundy, 1987). The process of HCM...


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...teins (Gibson, 1996). In the maturation process, the nuclear lamina is dissolved to generate delaminated infoldings of the inner nuclear membrane that form long intranuclear tubules (Buser et al., 2007). Nucleocapsids attach to the membranes and obtain a putative primary tegument and a temporary membrane. Then these virions are transported along the intranuclear tubules to the nuclear periphery where it fuses with the outer nuclear membrane (Buser et al., 2007). The primary membrane is later lost throughout de-envelopment at the outer nuclear membrane resulting in the release of a naked nucleocapsid into the cytoplasm. The final phase of maturation occurs in the trans-Golgi membrane where the capsid obtains a secondary tegument and undergoes a second envelopment process (Buser et al., 2007). The mature virions are then transported to the plasma membrane for release.

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