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== Pathogenesis == The primary route of entry for human rhinoviruses is the upper [[respiratory tract]] ([[mouth]] and [[nose]]). Rhinovirus A and B use "major" [[ICAM-1]] (Inter-Cellular Adhesion Molecule 1), also known as [[CD54]] (Cluster of Differentiation 54), on respiratory epithelial cells, as [[receptor (biochemistry)|receptors]] to bind to. Some subgroups under A and B use the "minor" [[LDL receptor]] instead.<ref name="Palmenberg2009">{{cite journal | vauthors = Palmenberg AC, Spiro D, Kuzmickas R, Wang S, Djikeng A, Rathe JA, Fraser-Liggett CM, Liggett SB | title = Sequencing and analyses of all known human rhinovirus genomes reveal structure and evolution | journal = Science | volume = 324 | issue = 5923 | pages = 55β59 | date = April 2009 | pmid = 19213880 | pmc = 3923423 | doi = 10.1126/science.1165557 | bibcode = 2009Sci...324...55P }}</ref> Rhinovirus C uses [[Cadherin related family member 3|cadherin-related family member 3 (CDHR3)]] to mediate cellular entry.<ref>{{cite journal | vauthors = Bochkov YA, Watters K, Ashraf S, Griggs TF, Devries MK, Jackson DJ, Palmenberg AC, Gern JE | title = Cadherin-related family member 3, a childhood asthma susceptibility gene product, mediates rhinovirus C binding and replication | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 112 | issue = 17 | pages = 5485β5490 | date = April 2015 | pmid = 25848009 | pmc = 4418890 | doi = 10.1073/pnas.1421178112 | doi-access = free | bibcode = 2015PNAS..112.5485B }}</ref> As the virus replicates and spreads, infected cells release distress signals known as [[chemokine]]s and [[cytokine]]s (which in turn activate inflammatory mediators). Infection occurs rapidly, with the virus adhering to surface receptors within 15 minutes of entering the respiratory tract. Just over 50% of individuals will experience symptoms within 2 days of infection. Only about 5% of cases will have an [[incubation period]] of less than 20 hours, and, at the other extreme, it is expected that 5% of cases would have an [[incubation period]] of greater than four and a half days.<ref name=Lessler_2009b>{{cite journal | vauthors = Lessler J, Reich NG, Brookmeyer R, Perl TM, Nelson KE, Cummings DA | title = Incubation periods of acute respiratory viral infections: a systematic review | journal = The Lancet. Infectious Diseases | volume = 9 | issue = 5 | pages = 291β300 | date = May 2009 | pmid = 19393959 | pmc = 4327893 | doi = 10.1016/S1473-3099(09)70069-6 }}</ref> Human rhinoviruses preferentially grow at 33 Β°C (91.4 Β°F), notably colder than the average human body temperature of 37 Β°C (98.6 Β°F), hence the virus's tendency to infect the [[upper respiratory tract]], where respiratory airflow is in continual contact with the (colder) extrasomatic environment.<ref name="Moriyama_2020" /><ref name="Royston_2016" /> Rhinovirus A and C species viruses are more strongly associated with significant illness and [[wheezing]], while rhinovirus B species are more commonly mild or asymptomatic.<ref name="Jacobs Lamson et al 2013" /><ref>{{cite journal | vauthors = Jackson DJ, Gern JE | title = Rhinovirus Infections and Their Roles in Asthma: Etiology and Exacerbations | journal = The Journal of Allergy and Clinical Immunology. In Practice | volume = 10 | issue = 3 | pages = 673β681 | date = March 2022 | pmid = 35074599 | pmc = 10314805 | doi = 10.1016/j.jaip.2022.01.006 }}</ref>
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