Acute viral nasopharyngitis pathophysiology: Difference between revisions
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==Pathogenesis== | ==Pathogenesis== | ||
Viruses undergo frequent changes in their antigenic coat. This helps the viruses to evade the immune system and enables them to cause recurrent infections. | * Viruses undergo frequent changes in their antigenic coat. This helps the viruses to evade the immune system and enables them to cause recurrent infections. | ||
* Rhinovirus binds to ICAM-1 receptors on epithelial cells. Binding to ICAM-1 receptors releases inflammatory cytokines but does not cause damage to epithelial cells. | |||
Rhinovirus binds to ICAM-1 receptors on epithelial cells. Binding to ICAM-1 receptors releases inflammatory cytokines but does not cause damage to epithelial cells. | * Respiratory syncytial virus does not cause release of cytokines. Instead, it replicates in the nose and pharynx. In many occasions, it can spread to the lower respiratory tract. | ||
* Human parainfluenza virus causes inflammation of the tract and subsequently, parainfluenza infection is much more severe than other viruses. | |||
Respiratory syncytial virus does not cause release of cytokines. Instead, it replicates in the nose and pharynx. In many occasions, it can spread to the lower respiratory tract. | * The body responds using both humoral immunity (IgA in the epithelium) and cellular immunity (different inflammatory cells in the adenoids and tonsils) to fight the offending virus. | ||
* Normal flora inhabitants in the nasopharynx also play an important role in eliminating the infection. | |||
Human parainfluenza virus causes inflammation of the tract and subsequently, parainfluenza infection is much more severe than other viruses. | |||
The body responds using both humoral immunity (IgA in the epithelium) and cellular immunity (different inflammatory cells in the adenoids and tonsils) to fight the offending virus. | |||
Normal flora inhabitants in the nasopharynx also play an important role in eliminating the infection. | |||
==References== | ==References== |
Revision as of 14:44, 21 June 2017
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Ahmed Younes M.B.B.CH [2]
Overview
Pathophysiology
Virus
Common colds are most often caused by infection by one of the more than 100 serotypes of rhinovirus, a type of picornavirus. Other viruses causing colds are coronavirus, human parainfluenza viruses, human respiratory syncytial virus, adenoviruses, enteroviruses, or metapneumovirus.[1][2]
Transmission
The common cold virus is transmitted between people by one of two ways:
- In aerosol form generated by coughing, sneezing, or
- From contact with the saliva or nasal secretions of an infected person, either directly or from contaminated surfaces.
- Symptoms are not necessary for viral shedding or transmission, as a percentage of asymptomatic subjects exhibit viruses in nasal swabs.[3]
- The infectious period (time during which an infected person can infect others) begins about one day before symptoms begin, and continues for the first five days of the illness.
- The virus enters the cells of the lining of the nasopharynx (the area between the nose and throat) and rapidly multiplies.
- The major entry point is normally the nose, but can also be the eyes (in this case drainage into the nasopharynx would occur through the Nasolacrimal duct).
Pathogenesis
- Viruses undergo frequent changes in their antigenic coat. This helps the viruses to evade the immune system and enables them to cause recurrent infections.
- Rhinovirus binds to ICAM-1 receptors on epithelial cells. Binding to ICAM-1 receptors releases inflammatory cytokines but does not cause damage to epithelial cells.
- Respiratory syncytial virus does not cause release of cytokines. Instead, it replicates in the nose and pharynx. In many occasions, it can spread to the lower respiratory tract.
- Human parainfluenza virus causes inflammation of the tract and subsequently, parainfluenza infection is much more severe than other viruses.
- The body responds using both humoral immunity (IgA in the epithelium) and cellular immunity (different inflammatory cells in the adenoids and tonsils) to fight the offending virus.
- Normal flora inhabitants in the nasopharynx also play an important role in eliminating the infection.
References
- ↑ "Common Cold (Upper Respiratory Infection)". The Merck Manual Online. Merck & Co. November 2005.
- ↑ CKS (2007). "Common Cold (Topic Review)". Clinical Knowledge Summaries Service.
- ↑ "Common Cold" (PDF) (pdf). Department of Health, Government of South Australia. 2005.