The Reproductive Strategy Of Varicella Zoster Virus Biology Essay
Cellular tropism is the ability of a pathogen to infect a host cell as well as the host cell’s susceptibility to that pathogen. Varicella zoster exhibits tropism for a wide variety of human cells including T-cells, in particular tonsil T cells, epithelial cells, and neurons. (1, 2) Tropism is important in the first step in the replication cycle of VZV: attachment and entry into the host cell. VZV is easily acquired through virus-containing respiratory droplets. (2) According to studies, tonsil T cells are highly receptive to the VZV glycoprotein VZV-gB located on the viral envelope, a main factor in VZV infection. (3) Entry into the host cell is facilitated by gB and other glycoproteins such as gD, gH, and gL. (3,4) It is believed that after the virus enters the tonsil T cells, the T cells bring the virus to the lymph system where VZV infects CD4 + T cells containing specialized skin markers, thus establishing viremia and enabling the virus to be transported directly to epithelial cells. (1,2)
After attachment and entry into a host cell, VZV particles are uncoated, though the exact methods by which are no very well known. Once uncoated, tegument proteins are released and migrate toward the nucleus of the host cell where transcription and replication occurs. (2) Viral transcription involves the conversion of DNA to RNA. Transcription of viral genes depend on the fact that promoter regions on VZV genes are have two binding sites with high affinity for the host cell’s transcriptional factor, Sp1. (5) As a result, host DNA transcription is inhibited while viral protein transcription takes place. (5) After transcription, the new viral mRNA is transported out of the nucleus to the cytoplasm where translation into infectious and structural proteins occurs. Transcription and translation of VZV consists of an intermediate early (IE), early, and late phase. IE genes, namely IE62, are involved in the induction of transcription of early and late genes. (1) Early genes are involved with the actual infection of the host. The early gene IE63 aids in the inhibition of interferon activation by the host’s immune system, thus promoting infection by preventing viral replication and apoptosis. (1,6) Late genes are involved with structural development and assembly of the viral capsid before the virus egresses. Late phase capsid proteins are developed and assembled within the nucleus. (4) The newly assembled capsid is filled with newly replicated DNA and migrates out of the nucleus, through the cytoplasm, and out of the cell.
Viral replication occurs within the nucleus. Several viral proteins are important for the replication of the VZV genome. (7) Some of these proteins include the virus’ own DNA dependent DNA polymerase (Pol), the UL9 and ICP8 proteins used to bind to the replication origin, and a helicase primase complex involved in the rolling circle mechanism of replication. (7) The linear DNA circularizes and the DNA Dependent DNA Polymerase knicks the strand, and the helicase primase complex separates the two DNA strands. (8) At this point, the internal strand is copied and new strand of DNA is formed. (8)
After transcription and translation of proteins and replication of the genome are completed, assembly of the new viral particle happens in the nucleus. Late proteins assemble into a capsid and the newly replicated DNA strand is inserted into it. Though it is not entirely understood, it is speculated that the virus buds from the nucleus to the ER, gaining an envelope from the plasma membrane of the nucleus along the way. (4) When the viral particle exits the ER, it loses the newly obtained envelope. (4) Then, before the viral particle actually egresses from the cell, the particle obtains its actual envelope by entering into another membrane compartment in the cytoplasm, possibly the Golgi. (4)
The final step of the reproductive cycle of Varicella zoster is egress of the viral particle from the host cell. It has been discovered that the same glycoprotein, gB, that was involved with attachment and entry is also essential to viral egress. (4) The appearance of syncytia is an indication of viral egress. (4) The gB glycoprotein is also associated with the latent VZV phase. After VZV infection of epithelial cells resulting in chicken pox, the VZV- gB protein attaches to neural cells through receptor cell-mediation involving myelin-associated glycoproteins expressed on the surface of sensory ganglion neurons. (1, 3) The virus becomes latent in the neurons for years and reemerges as shingles in immunocompromised and elderly patients.
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