January 2014

Influenza is common and almost all patients recover fully; how is it that 1% develop smell loss?

There are about 30 million patients in the United States who develop influenza-like symptoms yearly. Almost all of these patients recover fully from this illness. However, about 1% of these patients develop chronic smell and/or taste dysfunction subsequent to recovery from this illness. What is the mechanism that makes these 1% of patients (i.e., 310,000 yearly) develop these sensory dysfunctions?

1. The Primary Illness. Patients who develop a flu-like syndrome exhibit an acute viremia usually with upper respiratory symptoms. Most patients with an intact immunological system neutralize this virus, killing the virus and recover completely from this viral attack. This is a common occurrence among most people and all of us have had this type of illness in our lifetime. The influenza virus attacks the body usually following entry into the upper respiratory system. This is manifested usually by pharyngitis (sore throat), rhinorrhea (running nose), acute rhinitis (infectious nasal symptoms), nasal congestion and eventually leading to symptoms related to the lower respiratory system including cough and bronchitis. After the viremia is attacked by the intact immune system the virus is inhibited and these symptoms are inhibited.

2. The Secondary Illness. While the systemic viremia is inhibited in most patients the virus can establish a latent reservoir in the parotid glands in the mouth and in the serous glands in the nose. This latent reservoir is not eliminated by conventional anti viral drugs or by the body's conventional immune system response although the upper and lower respiratory symptoms may have been eliminated. This latent viral reservoir acts to inhibit secretion of growth factors from these glands which would act normally on stem cells in the taste buds in the mouth and on olfactory receptor cells in the nose to promote growth and development of these receptors. Thus, this viral reservoir acts to inhibit formation and secretion of these growth factors and causes taste and smell loss since these stem cells are not being stimulated by growth factors (which are inhibited) and patients develop loss of taste and smell acuity.

This scenario is the cause of the most common loss of smell and taste function. Subsequent to these losses there can also be changes in brain function by which taste and smell distortions can occur similar to changes which cause phantom limb symptoms. These distortions occur in about 60% of these patients who lost smell and taste acuity.

These symptoms have been discussed previously in some detail.

1. Henkin RI, Levy LM, Fordyce A. Taste and smell function in chronic disease: A review of clinical and biochemical evaluation of taste and smell dysfunction in over 5000 patients at The Taste and Smell Clinic in Washington, DC. Am J Otolaryngol. 2013;34(5):477-489.
   
2. Henkin RI, Potolicchio SJ, Levy LM. Olfactory hallucinations without clinical motor activity: a comparison of unirhinal with birhinal phantosmia. Brain Sci. 2013;3(4):1483-1553.
   
3. Henkin RI, Larson AL, Powell RD. Hypogeusia, dysgeusia, hyposmia and dysosmia following influenza-like infection. Ann Otol Rhin Laryngol. 1975;84:672-682.