Abstract
Alpha (α)-herpesviruses (HSV-1 and HSV-2), like other viruses, are obligate intracellular parasites. They hijack the cellular machinery to survive and replicate through evading the defensive responses by the host. The viral genome of herpes simplex viruses (HSVs) contains viral genes, the products of which are destined to exploit the host apparatus for their own existence. Cellular modulations begin from the entry point itself. The two main gateways that the virus has to penetrate are the cell membrane and the nuclear membrane. Changes in the cell membrane are triggered when the glycoproteins of HSV interact with the surface receptors of the host cell, and from here, the components of the cytoskeleton take over. The rearrangement in the cytoskeleton components help the virus to enter as well as transport to the nucleus and back to the cell membrane to spread out to the other cells. The entire carriage process is also mediated by the motor proteins of the kinesin and dynein superfamily and is directed by the viral tegument proteins. Also, the virus captures the cell’s most efficient cargo carrying system, the endoplasmic reticulum (ER)–Golgi vesicular transport machinery for egress to the cell membrane. For these reasons, the host cell has its own checkpoints where the normal functions are halted once a danger is sensed. However, a cell may be prepared for the adversities from an invading virus, and it is simply commendable that the virus has the antidote to these cellular strategies as well. The HSV viral proteins are capable of limiting the use of the transcriptional and translational tools for the cell itself, so that its own transcription and translation pathways remain unhindered. HSV prefers to constrain any self-destruction process of the cell—be it autophagy in the lysosome or apoptosis by the mitochondria, so that it can continue to parasitize the cell for its own survival. This review gives a detailed account of the significance of compartmentalization during HSV pathogenesis. It also highlights the undiscovered areas in the HSV cell biology research which demand attention for devising improved therapeutics against the infection.
Highlights
Alpha (α)-herpesviruses are DNA viruses belonging to the family Herpesviridae; herpein meaning “to creep.” Their members belong to one of the genera: Iltovirus, Mardivirus, Scutavirus, Simplexvirus, and Varicellovirus
In neuronal cells, where herpes simplex viruses (HSVs) prefers to hide itself from the immune cell attacks from the host, autophagy-enhancing agents can be selected as the appropriate therapeutics for decreasing the HSV infection (Yakoub and Shukla, 2015; Ahmad et al, 2019)
Membrane-bound organelles such as endoplasmic reticulum (ER) and mitochondria are compressed around the nucleus for the proper recruitment and accessibility to the factors required for HSV egress
Summary
Alpha (α)-herpesviruses are DNA viruses belonging to the family Herpesviridae; herpein meaning “to creep.” Their members belong to one of the genera: Iltovirus, Mardivirus, Scutavirus, Simplexvirus, and Varicellovirus. Cell Organelle Exploitation by HSV zoster virus (VZV), have a wide range of vertebrate and invertebrate hosts to infect (Pellett and Roizman, 2013). Infection via HSV can cause direct destruction of the cell via lysis or can hide itself from the attacks of the host immune system by establishing latency (Whitley and Roizman, 2001) in a cell type-specific manner. The outer envelope consists of 16 membrane proteins, out of which 12 are glycoproteins (Campadelli-Fiume et al, 2000; Mettenleiter, 2004; Diefenbach et al, 2008) These glycoproteins (gB, gC, gD, gE, gG, gH, gI, gJ, gK, gL, gM, and gN) mainly assist the entry of the virus into host cells. The review goes about the events that take place at the cell organelles during an HSV infection
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