Student presentation on

Rhinovirus - "The Common Cold"
by Ryan Michalek

Introduction: Rhinovirus, pictured above, is best known as the common cold. It is a member of the picornaviridae family along with more virulent viruses such as polio and hepatitis A. The viruses of this family are characterized as small (20-30nm genome) positive polarity RNA viruses consisting of one genome segment and a nonenveloped capsid. Unlike the its more lethal relatives, Rhinovirus is designed to attack a host numerous times during their lifetime. It is the perfect pathogen. It is estimated that adults suffer from 2 to 4 infections with the virus each year. The statistics below show the toll that the virus has on the United States Population:

The economic impact of the cold is estimated at 5 billion dollars, but is far greater in indirect costs when considering loss of productivity and school abscence.

Encounter: It is virtually impossible to avoid Rhinovirus encounter because it is one of the few pathogens that is present in the environment year round. There are over 100 serotypes making it unlikely to have antibodies to each strain. It often enters the upper respitory tract via aerosolized droplets coming from an infectious individuals coughing or sneezing. It is also possible to spread the pathogen through saliva. However, studies have proven that contact transmission is the dominant mode of contraction. [9] This is possible because infected individuals can shed the virus 24 hours before symptoms and as long as 2 weeks after symptoms cease. Contrary to popular belief, there is no valid clinical evidence that exposure to cold or moisture will result in infection.

Entry: Primary infection occurs in the nasal mucosa and occasionally the conjunctiva. Once exposed to the epithelial cells, the virus attempts to bind to intracellular adhesion molecule-1 (ICAM1).

ICAM-1 is regularly used by the immune system to bind endothelial cells to leukocytes. However, as the picture above shows, Rhinovirus is able to take advantage of this property and recognizes it with its own receptors. The invasion of the virus can upregulate the immune system and cause more ICAM-1 receptors to become available and increase suseptibility. However, the body has developed natural defenses for dealing with the pathogen.
Rhinovirus is first limited by the number of receptors that are available to it. Sialic acid glycoproteins, normally contained in mucus, are able to can compete with the viral receptors and diminish or prevent the binding of the pathogen. [8] To infect the host, the virus must not be swept away in the mucus, neutralized by IgA, or be destroyed by recruited macrophages. Rhinovirus is also acid labile which means that it is unable to withstand the harsh conditions in the gasterol intestinal tract. The key feature to Rhinovirus is its need for a low temperature environment, about 33 degrees Celsius. The body temperature of 37 degrees Celsius is to extereme for the pathogen. Therefore it is limited to upper respiratory infection and can not become systemic.

Damage: While in the body, Rhinovirus does little or no tissue damage. Below is a picture of Rhinovirus infected cells. Many of the symptoms, such as coryza, sneezing, lacrimation, irritated nasopharynx, headache, sore throat, and chills are a result of the stimulated immune response. The constant cytokines cause inflammation of the respiratory tract. In some cases lyrangitis, tracheitis, and bronchitis can result. More importantly, the Rhinovirus weakens the immune system and allows secondary bacterial infections like sinusitis and in rare cases pneumonitis to take hold.

Human diploid fibroblasts infected with Rhinovirus (100X). Courtesy © Danny L. Wiedbrauk, William Beaumont Hospital, Royal Oak, Michigan USA.

Treatment: The major problem with Rhinovirus is that being infected with one strand will not result in cross immunity to another serotype. There are a few different antiviral drugs on clinical trials for Rhionvirus right now. One such product, being tested by Biota, is designed to block the receptor site on Rhinovirus. It fills the valley where the ICAM-1 binds. However, none of these drugs have yet to make it onto the market. The most common treatment for Rhionvirus is to allow the uman immune response to take its course. This involves plenty of rest, hydration, and for serious symptoms anti-inflammatory medications and nasal decongestants can be utilized. There are no preventative medical precautions, such as vaccines, that can be developed for Rhinovirus due to its broad range of serotypes.

The major health crisis concerning Rhinovirus today is the uneccessary prescription of antibiotics.An estimated 18 million antibiotic prescriptions are written each year in the US for patients suffering from viral respiratory infections including the common cold, but these prescriptions are for antibacterial agents that do nothing to alter the course of the viral respiratory disease.[7] Many doctors feel pressured by the parents of infected children to offer some form of treatment. The problem is that the antibiotics have no effect on the virus and at the same time inflict damage on the patients normal flora. This can lead to colonization by oppurtunistic pathogens and ultimately a more srious helath risk.

Outcome: Contrary to popular belief, there is no valid clinical evidence of Rhinovirus aquired by exposure to cold weather or getting wet. The best method for attempting to avoid Rhinovirus is to wash the hands after coming into contact with various fomites and infected individuals. If infected, cover the mouth when sneezing and discharging other bodily fluids. Make sure to get plenty of rest and stay hydrated. The symptoms should subside within 4-7 days on average. It is virtually impossible to be immune to each serotype, but each infection will produce antibodies to prevent future infection with that specific strain.









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