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Life Cycle of Chicken Pox (Varicella)

Chickenpox is caused by the varicella zoster virus (VZV), also known as human herpes virus 3 (HHV-3), is one of the eight herpes virus known to affect humans.

The life cycle of VZV causes it to be very contagious. The virus is usually acquired by inhaling airborne droplets from the respiration of an infected person, but it can also be acquired from direct contact with an infected vesicle. The virus then infects the conjunctivae or the mucosae of the upper respiratory tract, and 2-4 days after infection, begins to proliferate in the regional lymph nodes of the upper respiratory tract. Viremia, or infection of the bloodstream, soon follows. About 14-16 days after infection, secondary viremia causes a second round of replication, this time mainly in the body's internal organs (mostly liver and spleen). This secondary viremia also is characterized by viral invasion of capillary endothelial cells and the epidermis, resulting in the characteristic vesicles of chickenpox. After primary infection of VZV, the virus spreads from mucosal and epidermal cells to nerve cells, especially the dorsal root ganglia, where it remains latent until reactivation later in life.

Left image shows overall structure of Varicella zoster virus. VZV has a genome made of linear double stranded DNA contained in an icosahedral nucleocapsid.  The capsid is surrounded by a protein tegument and a lipid envelope.  The envelope incorporates major glycoproteins which are also expressed on the surfaces of virus infected cells (see chart right and below).  Right image shows naked capsids of Varicella zoster virus.

The virus particle lands on a cell and docks with cell surface proteins. The viral envelope then fuses with the plasma membrane of the cell and the viral capsid containg the viral genome and tegument proteins enter the cytoplasm. The capsid then travels along a microtubule towards the nucleus where it docks with a nuclear pore. The viral DNA enters the nucleus through the pore and circularises before replication. New viral capsids assemble in the nucleus and daughter genomes are taken into them. The capsids bud through the inner nuclear envelope gaining a temporary envelope that surrounds them during their stay in the perinuclear space. This envelope then fuses with the outer nuclear envelope and the now naked capsids progress through the cytoplasm until they bud into Golgi vesicles laden with viral proteins. This budding into the vesicle furnishes the developing virion with tegument proteins, an envelope and surface projections. The vesicle delivers the contained virion to the cell surface. The vesicle fuses with the plasma membrane and the new virus particle is free to infect another cell.


A. Viral glycoproteins allow the virus to attach and enter the cell. B. The envelope and cell membrane fuse the viral capsid is released into the cytoplasmViral DNA enters the nucleus and the capside is discarded.  C.  Host enzymes catalyze the early transcription, and viral mRNA directs the production of viral enzymes.  D.  These enzymes facilitate the replication of viral DNA.  E.  Late transcription produces the mRNA encoding the production of glycoproteins and capsid elements.  F.  The capsid components return to the nucleus and the DNA is packaged. G.  The glycoproteins fix themselves to the nuclear membrane and the DNA filled capsid acquires this coat as it buds out of the nucleus.  H.  The virus is released from the cell by unknown mechanisms.

MPRs play an important role in the VZV life cycle:

-The envelope of VZV contains the unusual sugar mannose 6-phosphate (Man 6-P).

-VZV exiting from cells accumulates in late endosomes due to their M 6-P (MPRs). Most virus is inactivated there.

-M 6-P receptors facilitate VZV entry into cells and divert newly assembled virions to acid-containing late endosomes. Cell free virus enters cells, but cell-associated virus does not exit in infectious form. With one exception...the skin.