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admin 28.07.2014

Varicella zoster virus is an alpha herpes virus that has been described in a previous post as having  remarkable capabilities and a very complex lifestyle—the ability to travel up and down axons in a neuron, to move in and out of several different types of cells, to travel and multiply in T cells, to fool several different nuclear pore complexes, to commandeer microtubule motors, and to alter its own behavior pattern in different settings.
The infection begins in upper respiratory mucosa cells, spreads to the lymph and the tonsils, and, then, is carried by T cells in the blood to the skin where it causes a widespread skin rash. The outer layer is a lipid membrane envelope with the fusion complex that allows it to grab onto and fuse with human cell’s membranes. Inside the envelope there is a layer of proteins, called tegument, which the virus uses for regulation of its linear double stranded DNA.
The first entry into the cell is not totally understood, but varicella uses five distinct receptors to fuse with the skin cell’s membrane, allowing DNA to enter the cell. One major protein that is released when the coat is removed is IE62 (immediate early protein 62), which is a transcription factor to activate viral material in the nucleus. The harder protein capsid, beneath the membrane-like envelop and the tegument, docks by the nuclear pore at the cell’s membrane.
The surface molecules are so similar to the human cell surface that in this process some human cells combine into a syncytium, which includes the material from many cells with multiple nuclei. Varicella’s DNA includes at least 71 active regions, which can make proteins, with many promotor regions associated with each. Specific T cells are essential to clear a primary infection and avoid reactivation from latency. However, varicella is able to fool the very intelligent T cells and multiply inside of them. Remarkably, the virus induces specific signals and factors that keep the T cells alive and gives them time to transport the virus. Because of these varicella stimulated factors, the T cells do not fuse together, which means that each T cell is infected individually. Varicella is able to suppress the innate response to allow skin lesions with many live viruses for transmission to other humans. A very significant anti nuclear viral protein PML is usually stimulated by the immune factor IFN. The virus can spread without fusion of cells, but in the skin it uses this fusion to spread. In T cells and skin cells there are adaptive immune responses, but there aren’t any in neuron infection. A very unusual action of the virus is to stimulate neurons and satellite cells (the cells that surround peripheral neurons) to fuse in the same way as skin cells. When the herpes virus rides on the dynein motor travelling on the microtubule transportation system in the neuron’s axon, it doesn’t passively take the ride. Varicella exhibits an enormous amount of intelligent actions, including many very complex signals to induce fusion of skin cells, neurons and satellite cells, and to avoid fusion of T cells. Varicella uses five distinct receptors to fuse with the skin cell’s membrane when entering the cell.
This entry was posted in Blog, Human Brain, Microbes and tagged Varicella commandeers the dynein motor on axon microtubules, varicella commandeers the dynein motor on the microtubule in the axon, Varicella creates syncytium in skin cells and neurons, Varicella fools the T cell and travels inside of it, Varicella sends signals to calm neuron, Varicella sends signals to control T cells, Varicella signal to cause fusion of skin cells and neurons, varicella signals to avoid cell death in T cells, Varicella tricks multiple nuclear pores, Varicella uses five receptors to fuse with skin cell's membrane. Yes, like a self-driving car could be considered intelligent for its ability to navigate different streets under different conditions.
The complex molecular mechanisms for each behavior of the remarkable intelligent varicella virus are just now being discovered. The virus is, also, able to enter sensory neurons, take over transport motors and travel to the ganglion cell bodies.


The next layer is the tegument with many essential proteins including the critical IE immediate early release protein. The virus inserts a large number of glycoproteins into the membranes—the glycoproteins are manufactured using the host cell’s machinery. This is assumed to be through fusion with the cell’s membrane or by a sac that is brought into the cell.
The T cell populations CD3, CD4 and CD8 and the dual CD4CD8 allow varicella to travel and multiply inside. The virus controls the T cell fusion in order to maintain them as transport in and out of the tissues. These factors stop the T cell from killing itself (since it normally would if infected) and counteract other cytokines like IFN, which might stop the infection. During latency up to 10 varicella are present in 4% of the neurons in the dorsal route ganglion, but protein factors are not produced during this residence.
This occurs because varicella specifically silences genes in the neurons with interfering RNAi. Critical to this silencing of neurons is that varicella’s capsid can be collected and sequestered by PML bodies in the neuron and satellite cells’ nucleus.
In keeping with its general intelligence, it commandeers the dynein motor and alters the ATP energy mechanism. How does this small virus with DNA for 70 proteins know how to orchestrate this complex lifestyle? How can such a simple organism, which is basically just a small piece of DNA with protein covers, take control of multiple large complex cells, such as human T cells, neurons and skin cells? The hard capsid beneath is an icosahedron with 20 triangular faces, 30 edges and 12 vertices, which is about 100 nm in diameter.
There are many complex glycoproteins that interact with the cell surface and allow this fusion. Manufacturing more virus depends upon the virus transcription factors that act on both the human DNA and the viral DNA. This capsid fuses with the nuclear membranes and awaits a new virus from the nucleus where it disengages from the nuclear membrane, covers the virus and travels to the outside cell membrane. The ability to infect so many T cells allows the widespread skin lesions. In the skin because of varicella stimulation, cells do fuse together to form a syncytium with a large amount of the virus present—this allows increased spread of the virus throughout the skin region.
A critical component of the virus action on T cells decreases the expression of MHC1, which is the primary way that other cells would know the T cell was infected.
They appear near hair follicles where skin cells have fused together into a syncytium with many nuclei and many viruses. Complex immune factors and cytokines are involved in the reaction. PML usually forms an important structure in the nucleus called the PML nuclear body for this purpose.
When the virus is activated, 25% of the neurons are involved with the production of many measurable protein factors.
Cages of the PML fibers contain virus and newly forming virions in the neurons that are infected. This fusion spreads the virus further in the ganglion, which, also, increases the area of skin that is involved in the painful lesions.
In this process it, actually, speeds up the motor transport to arrive much more quickly at the nucleus in one trip and then later the second trip back to the skin.
It stimulates specific signals that maintain the T cell and stop the cell’s possible fusion in order for varicella to continue to travel.


It will appear again to recognize weakness in host immune barrier, and it give severe skin disorder. When it awakens, varicella, again, travels on the axon microtubule transport system to the skin to cause the painful zoster rash in the region that neurons innervate. The virus coated with the capsid goes to the cell’s Golgi, where it is dressed with its original protein layer and a membrane envelop for its journey. These changes do not reverse easily, which is a source of ongoing pain after zoster infection.
It foils the complex nuclear pore mechanisms while entering the nucleus of each type of cell.
The virus is plentiful in the skin lesions and through contact with other humans continues its journey to other people. The IE62 molecule combines with many human molecules to form a large complex that regulates the process. The entire virus is then released from the cell as if it were a sac filled with neurotransmitters. Of these 71 regions, 40 genes, including 8 glycoproteins, appear to be critical for all herpes viruses; these 40 genes are involved in DNA copying, DNA cutting and packaging, metabolism of nucleic acids, and capsid building.
The T cells with varicella are attracted specifically to skin cells because of the signaling proteins and receptors on the T cells. The major reaction is innate and not adaptive, which allows for an infection that is not catastrophic and allows the long-term existence of the virus in the tissues.
A special section of the virus genome appears to affect both T cells and skin cells at the same time in these very different complex ways. Using very complex machinery it forms circular DNA and uses the cell’s genetic process to reproduce. Proteins for replication include RNA reductase, DNA polymerase, DNA binding protein, DNA replication origin binding protein, protein kinases, as well as other DNA related proteins.
Varicella spreads near hair follicles because of the many small blood vessels around the follicles.
Varicella uses another tricky technique to keep the cell alive longer by stimulating autophagosomes that compete with cell death pathways. In the skin cell it uses complex signaling to cause a skin cell syncytium and to stop programmed cell death. By competing with the cell death pathways it maintains the longevity of the cell and, therefore, the longevity of varicella in the cell.
It hijacks the complex dynein transport motor, taking it over, accelerating it and directing it the long way up the axon to the neuron’s cell body and nucleus. It manufactures specific molecules that stop further activity in the neuron’s nucleus so as not to kill the neuron.
At some time it awakens and leaves the nucleus, again travelling back on the microtubule machinery along the long axon. It, then, leaves the neuron, enters skin cells where it reproduces and uses this vantage point to jump to another person.




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