Herpes Zoster Essay

Introduction Herpes Zoster (HZ) virus, also known as shingles, refers to a localized infection which is identifiable by a unilateral vesicular eruption within the dermatome that is supplied by a cranial sensory or single dorsal root ganglion. Clinical manifestations of this disease include painful blistering eruptions on the skin. Herpes Zoster is caused by the Varicella Zoster Virus (HVZ) which has been dormant inside the sensory ganglia, often since the host’s childhood when the host was infected by chicken pox. In this essay, the cellular and molecular pathogenicity of the virus, the bodies repose to the virus, medical ways to fight the infection and the uses of potential vaccines against Varicella Zoster virus will be discussed.
The virus is highly contagious and can easily be transmitted through direct contact of infected cells. The life cycle of the VZV begins with viral entry into the host. While the mechanism of this is yet to be fully understood, it is believed that the virus enters the host either through endocytosis or with direct fusion of particles with the plasma membrane (Zerboni et. al, 2014). It is predicted that viral envelope proteins interact with cell surface receptor such as manose-6-phosphate. After entry into the host cell the viron undergoes uncoating and protein 62 is produced. This protein is regarded as a transcription factor, therefore it must be produced and released before new protein synthesis can occur (Zerboni et. al, 2014). The virus codes for 3 immediate-early (IE) proteins that also play a role in regulating viral transcription by inhibiting the activity of interferon-alpha (Cohen, 2010). These immediate early regulatory proteins are encoded by alpha genes and help regulate beta genes, are present in open reading frames 4, 61, 62 and 63 (Ancton, 2012). These beta genes encode proteins which make enzymes that are used in DNA
In addition, VZV contain open reading frames 18 and 19 which small and large subunits of ribonucleotide reductase whose function is to convert ribonucleotides into deoxyribonuclotides (Cohen, 2010). VZV differentiates from other herpes viruses due to the fact that their reassembly is highly cell mediated. It takes roughly 9-12 hours after infection to see prodigy viron (Zerboni et. al, 2014). After the formation of DNA, late gamma genes are transcribed to make structural proteins. The cytoplasm functions to create these proteins and then transports them to the location of capsid development (Ancton, 2012). After the capsid is formed around the virus it is released into the extracellular space and escape to the sensory nerve endings. After reaching the sensory nerves, the virons can move to cranial sensory and dorsal root ganglia where they become dormant (Ancton, 2012). This is the latent form of VZV.