How Viruses Inhibit Taste and Smell Function
With any viral cold we experience a type of viremia. Viruses travel from the inoculation site through the blood system into all body tissues. That is why we experience malaise muscle and joint aches and pains with influenza-like illness. These symptoms usually stop after 2-3 days because our antiviral and immune systems kill the virus, but at this time we may begin to recognize that we have lost taste and smell function. How does this happen?
Although the viruses in our blood and tissues have been killed, viral particles have entered the cells of the parotid glands in the mouth and the nasal serous glands in the nose. The viral DNA in these particles, the “viral program,” has become part of the program by which the cells of these glands secrete a variety of proteins, including the growth factors that stimulate the stem cells of both taste buds and olfactory epithelial cells to initiate growth and maturation of taste buds and olfactory epithelial cells. This program either inhibits synthesis of these proteins or alters their production in such a manner that these proteins no longer perform their normal functions. This causes both taste buds and olfactory epithelium to undergo cellular atrophy or apoptosis, which inhibits taste and smell function.
We know this can happen because recent studies of gene delivery systems indicate that viral DNA can be delivered into cells by “prying open” cellular pores for DNA entry. Indeed, this is a newly developing area of biotechnology, applicable for deciphering gene structure, function, and regeneration. Techniques using substances called Nucleofection or TransFectin, substances composed of cationic lipids and a colipid called DOPE (1,a-dioleophosphatidylethanolamine) interact with DNA in solution to form positively charged micelles or liposomes that fuse with cellular membranes, become internalized in the cell, and are subsequently expressed.
These biotechnology products are one example of how DNA from a cold or influenza enters a cell to alter the cell’s function. This is how we hypothesize the viral DNA enters the cells of the glands that support taste bud and olfactory epithelial cell function and inhibit their function, causing taste and smell loss.
What Can Be Done About This?
We can correct this series of events and restore normal taste and smell function by inhibiting the action of this viral DNA. This can be accomplished by the use of small interfering RNAs (siRNA), which can knock out the function of these viral DNAs and inhibit this genetic activity. While this technique is scientifically logical and plausible, it is not yet clinically or medically practical. However, this concept offers a positive future approach for the restoration of smell function in those many millions of patients who develop the most common form of loss of taste and smell, that which follows an influenza or viral-type coryza.
Our present treatment strategies are limited by our inability to convince drug companies to take these problems seriously. Our present treatment strategies do not attack the viral cellular function abnormalities directly but rather indirectly by attempting to enhance cellular function, by inhibiting the metabolism of the small amount of normal growth factor activity that the virus itself did not inhibit. This therapy requires significant time and dosage of a medication that functions in response to the viral action only in a peripheral manner. These drugs are effective in most patients, but they do not attack the major pathology we have defined above. Hopefully, the future will allow for more effective therapy for this pathology, which alters the quality of life for many millions of patients.
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