West Nile Virus (Deadly Diseases and Epidemics) 2nd Edition by Jeffrey N. Sfakianos, Alan Hecht

By Jeffrey N. Sfakianos, Alan Hecht

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Sample text

Therefore much smaller than bacteria. Not being able to visualize the virus, Ivanovski never actually identified the cause of the disease and stopped his research. In 1899, the Dutch microbiologist Martinus Beijerinck repeated Ivanovski’s experiments and concluded that the disease was caused by a new form of infectious agent. He even showed that the agent needed living cells to multiply. However, due to the virus’ size, he could never visualize it. Many researchers in several countries continued working with TMV and several other viruses over the years and made numerous discoveries that helped in the understanding of how viruses work.

While genetic material is replicating, the virus will also produce a new glycoprotein coat. Finally, the new copies of the virus are assembled and released from the cell. 29 30 west nile virus Each of these stages of the West Nile virus replication cycle will be described in this chapter. However, before discussing the specifics of the replication cycle, we first need to understand the general structure of the West Nile virus. 2). To give you an idea of how tiny this is, if 2,000 West Nile virus particles were stacked on top of each other, the height of the stack would still be less than the thickness of a single dollar bill.

The molecule is the complementary protein of the West Nile virus E protein. These molecules reach out and bind sugar molecules on the target cell that the virus is going to infect. In particular, the virus binds to sialic acid molecules that are abundant on the surface of most cells. The portion of the molecule that binds to the sialic acid is at the very top of the hemagglutinin molecule. After binding, the influenza virus is internalized by the cell, in a way similar to that described for West Nile virus.

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