ETIOLOGY OF THE COMMON COLD By R. Steven Davidson, Ph.D. and Charles B. Hensley, Ph.D.
Acute respiratory illness accounts for over one-half of all acute disabling conditions annually, according to national health survey data. In the United States alone, the common cold, which is a viral infection of the superficial columnar cells of the nasal turbinate epithelium, is the most common of identifiable acute respiratory disorders and accounts for about 20 percent of all conditions and ailments and about 40 percent of all respiratory conditions. This includes 110 million disabling colds per year, causing about 300 million days of restricted activity, about 60 million lost days of school, and about 50 million lost days of work. When considering minor, nondisabling respiratory illnesses, common cold represent a higher proportion of respiratory diseases.
Colds are estimated to occur at rates of two to five per person per year. About five percent of the population has a cold at any given time. Over one billion common colds occur in the United States each year. Financial considerations of the common cold are staggering. Over five billion is spent each year on colds in the United States. About $3 billion is spent on professional consultations with about $1.5 billion on remedies and about $1 billion on analgesics.
Over 200 types of viruses induce common colds, with over 113 types of human rhinoviruses causing the majority. Nasal drainage and nasal congestion are primary symptoms of common colds. Malaise, headache, fever, muscle pain, sore throat, scratchy throat, cough and hoarseness are frequently occurring secondary symptoms.
The nose is the body's first line of defense against airborne viruses. The temperature and moisture of the inner nose tend to inhibit growth of some viruses. The nasal turbinates, with their flaplike shape and copious blood supply, assist in warming and moistening the inspired air. The interior of the nose is lined with goblet cells that excrete sticky mucus. The cells lining the respiratory tract also secrete immunoglobulin A (lgA) helping to prevent infections by combining with the surfaces of viruses and bacteria to change their shape into one not allowing attachment. Recently, intercellular adhesion molecule 1 (ICAM-1) has been identified as the molecule that attaches rhinoviruses to cells.
During a cold, viruses have managed to penetrate nasal mucus and invade nasal tissues. Within a few hours, viruses bind to ICAM-1 sites on the surface of the nasal cells and subsequently penetrate them. As cells become infected, they release chemicals initiating several responses from the body's immune system, including responses from immune cells of the nasal mucosa.
Within an hour, prostaglandins are released producing inflammation and attracting infection-fighting white blood cells called neutrophils. These cells attempt to attack an invading virus without damaging infected cells. Neutrophil activity increases inflammation and the infected area becomes swollen and red. Onset of a common cold is thus signaled with symptoms such as sore throat, itchy eyes, a headache, or generalized ill feeling. Tissues and capillaries dilate, while plasma, additional neutrophils and other white blood cells flood the area. Symptoms include increased mucus production, raised temperature, runny nose, sneezing and coughing.
Colds are caused by more than two hundred different viruses that enter the body by binding to receptors on cells lining the nasal cavity. Once the cold virus has entered the nasal cavity, they infect and re-infect the body for several days, eventually overwhelming the body's immune system. Statistics have shown that on an average, the cold lasts about 12 days. In the 1980s it was discovered that the majority of viruses responsible for the common cold used a common entry point into the human body, the nasal cell ICAM-1 receptor. Colds actually start in the nasal cavities. During a cold, viruses manage to penetrate nasal mucus and invade nasal tissues. Viruses bind to ICAM-1 binding sites on the surface of the nasal cells, enter the cells and within a few hours, seize control of cell genetics and force cells to make thousands of copies of invading viruses. The newly formed rhinoviruses then not only enter the systemic circulation, but also are expelled back into the nasal cavity, thereby infecting neighboring nasal epithelial cells. This process of infection and re-infection continues resulting in an extended illness. The key point is that the rhinoviral entry mediated by binding to the ICAM-1 site of the nasal epithelium is a critical first step in the infection process.
Researchers have been working tirelessly to find a drug that would stop or inhibit that entry point. It is hypothesized that if a drug could bind to the viral ICAM binding site, you would eliminate the virus from ever infecting the body. The drug would work like a lock and key mechanism preventing the virus from attaching to the nasal cells.
Conventional drugs have only succeeded in limiting the symptoms of the cold. Look for a new paradigm in the fight against the common cold. New therapeutics are emerging, ones that help shorten the duration of the common cold as well as influence intercellular adhesion molecules. |
