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Rhinovirus
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<h2 id="history">History</h2> <p>In 1953, when a cluster of nurses developed a mild respiratory illness, <a href="/facts/Winston_Price/5LShK8fo">Winston Price</a>, from <a href="/facts/Johns_Hopkins_University/56US0mHw">Johns Hopkins University</a>, took nasal passage samples and isolated the first rhinovirus, which he called the JH virus, named after <a href="/facts/Johns_Hopkins/DvdDT6TQ">Johns Hopkins</a>.<a class="footnote-ref" id="fnref:10" href="#fn:10"><sup>10</sup></a><a class="footnote-ref" id="fnref:11" href="#fn:11"><sup>11</sup></a> His findings were published in 1956.<a class="footnote-ref" id="fnref:12" href="#fn:12"><sup>12</sup></a> </p><p>In 2006, advancements in molecular testing techniques for identifying rhinoviruses in clinical specimens led to the discovery of rhinovirus C species in samples from Queensland, Australia and New York City, United States. The <a href="/facts/International_Committee_on_Taxonomy_of_Viruses/M71khRCo">ICTV</a> formally designated RV-C as a separate species in 2009.<a class="footnote-ref" id="fnref:13" href="#fn:13"><sup>13</sup></a> </p> <h2 id="transmission">Transmission</h2> <p>Rhinoviruses may be spread via airborne <a href="/facts/Aerosols/X1jXFLp2">aerosols</a>, <a href="/facts/Respiratory_droplet/oMugYAEa">respiratory droplets</a> and from <a href="/facts/Fomite/0sTjFaIR">fomites</a> (contaminated surfaces), including direct person-to-person contact.<a class="footnote-ref" id="fnref:14" href="#fn:14"><sup>14</sup></a> Rhinoviruses can survive on surfaces such as stainless steel or plastic for several hours. <a href="/facts/Airborne_transmission/hpm1oR83"> Airborne precautions</a><a class="footnote-ref" id="fnref:15" href="#fn:15"><sup>15</sup></a> are likely effective in reducing transmission, while other precautions such as hand-washing or cleaning surfaces with disinfectants are known effective in preventing rhinovirus transmission.<a class="footnote-ref" id="fnref:16" href="#fn:16"><sup>16</sup></a> </p> <h2 id="signs-and-symptoms">Signs and symptoms</h2> <p class="note">Main article: <a href="/facts/Common_cold/fP9A03U9">Common cold</a></p><p>Rhinoviruses are the primary cause of the <a href="/facts/Common_cold/fP9A03U9">common cold</a>. <a href="/facts/Symptom/BzP6MrTN">Symptoms</a> include <a href="/facts/Pharyngitis/PF8tKu39">sore throat</a>, <a href="/facts/Rhinitis/VYf2UR8U">runny nose</a>, <a href="/facts/Nasal_congestion/xClWzxrg">nasal congestion</a>, <a href="/facts/Sneeze/Nxj3dJbc">sneezing</a> and <a href="/facts/Cough/mqyhR6zj">cough</a>; sometimes accompanied by <a href="/facts/Myalgia/AbVybHB8">muscle aches</a>, <a href="/facts/Fatigue_(medical)/C2oo4Hvg">fatigue</a>, <a href="/facts/Malaise/vdb5DxAU">malaise</a>, <a href="/facts/Headache/mdmmC9DP">headache</a>, <a href="/facts/Muscle_weakness/H5FEnEBF">muscle weakness</a>, or <a href="/facts/Anorexia_(symptom)/G7RsaXp9">loss of appetite</a>. <a href="/facts/Fever/waVxR2Ac">Fever</a> and extreme <a href="/facts/Fatigue_(medical)/C2oo4Hvg">exhaustion</a> are less common in rhinovirus infection compared to <a href="/facts/Influenza/nWuFzh6L">influenza</a>, but rhinovirus can cause lower respiratory tract infection<a class="footnote-ref" id="fnref:17" href="#fn:17"><sup>17</sup></a><a class="footnote-ref" id="fnref:18" href="#fn:18"><sup>18</sup></a> and the pneumonia can, in young children, be fatal.<a class="footnote-ref" id="fnref:19" href="#fn:19"><sup>19</sup></a> </p><h2 id="epidemiology">Epidemiology</h2> <p>Rhinoviruses can be detected year-round; however, the incidence of rhinovirus is higher in the autumn and winter, with most infections occurring between September and April in the northern hemisphere.<a class="footnote-ref" id="fnref:20" href="#fn:20"><sup>20</sup></a> The seasonality may be due to the start of the school year and to people spending more time indoors thereby increasing the chance of transmission of the virus.<a class="footnote-ref" id="fnref:21" href="#fn:21"><sup>21</sup></a> Lower ambient temperatures, especially outdoors, may also be a factor given that rhinoviruses preferentially replicate at 33 °C (91.4 °F) as opposed to 37 °C (98.6 °F).<a class="footnote-ref" id="fnref:22" href="#fn:22"><sup>22</sup></a><a class="footnote-ref" id="fnref:23" href="#fn:23"><sup>23</sup></a> Other climate factors such as humidity may influence rhinovirus seasonality.<a class="footnote-ref" id="fnref:24" href="#fn:24"><sup>24</sup></a> Young children (<5 years old) experience a high rate of infection which can be detected in community surveillance studies of children up to 34% of the year.<a class="footnote-ref" id="fnref:25" href="#fn:25"><sup>25</sup></a> Phylogenetic analysis of rhinovirus strains in Nepalese infants revealed diverse lineages and patterns of virus circulation in low-resource settings.<a class="footnote-ref" id="fnref:26" href="#fn:26"><sup>26</sup></a> Those most affected by rhinoviruses are infants, the elderly, and <a href="/facts/Immunocompromised/CIEujXmc">immunocompromised</a> people.<a class="footnote-ref" id="fnref:27" href="#fn:27"><sup>27</sup></a> </p> <h2 id="pathogenesis">Pathogenesis</h2> <p>The primary route of entry for human rhinoviruses is the upper <a href="/facts/Respiratory_tract/nnG9UEmr">respiratory tract</a> (<a href="/facts/Mouth/WthDlXsC">mouth</a> and <a href="/facts/Nose/Kv0lv34S">nose</a>). Rhinovirus A and B use "major" <a href="/facts/ICAM-1/H2bKaUyN">ICAM-1</a> (Inter-Cellular Adhesion Molecule 1), also known as <a href="/facts/CD54/H2bKaUyN">CD54</a> (Cluster of Differentiation 54), on respiratory epithelial cells, as <a href="/facts/Receptor_(biochemistry)/tjTAC76a">receptors</a> to bind to. Some subgroups under A and B use the "minor" <a href="/facts/LDL_receptor/zsSjTYyb">LDL receptor</a> instead.<a class="footnote-ref" id="fnref:28" href="#fn:28"><sup>28</sup></a> Rhinovirus C uses <a href="/facts/Cadherin_related_family_member_3/KaCKDjxU">cadherin-related family member 3 (CDHR3)</a> to mediate cellular entry.<a class="footnote-ref" id="fnref:29" href="#fn:29"><sup>29</sup></a> As the virus replicates and spreads, infected cells release distress signals known as <a href="/facts/Chemokine/YrySj9eD">chemokines</a> and <a href="/facts/Cytokine/SdWpWABH">cytokines</a> (which in turn activate inflammatory mediators). </p><p>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 <a href="/facts/Incubation_period/cqSwpKPk">incubation period</a> of less than 20 hours, and, at the other extreme, it is expected that 5% of cases would have an <a href="/facts/Incubation_period/cqSwpKPk">incubation period</a> of greater than four and a half days.<a class="footnote-ref" id="fnref:30" href="#fn:30"><sup>30</sup></a> </p><p>Human rhinoviruses preferentially grow at 33 °C (91.4 °F), notably colder than the average human body temperature of 37 °C (98.6 °F), hence the virus's tendency to infect the <a href="/facts/Upper_respiratory_tract/nnG9UEmr">upper respiratory tract</a>, where respiratory airflow is in continual contact with the (colder) extrasomatic environment.<a class="footnote-ref" id="fnref:31" href="#fn:31"><sup>31</sup></a><a class="footnote-ref" id="fnref:32" href="#fn:32"><sup>32</sup></a> </p><p>Rhinovirus A and C species viruses are more strongly associated with significant illness and <a href="/facts/Wheezing/fB5zMcwo">wheezing</a>, while rhinovirus B species are more commonly mild or asymptomatic.<a class="footnote-ref" id="fnref:33" href="#fn:33"><sup>33</sup></a><a class="footnote-ref" id="fnref:34" href="#fn:34"><sup>34</sup></a> </p> <h2 id="taxonomy">Taxonomy</h2> <p>The <a href="/facts/International_Committee_on_Taxonomy_of_Viruses/M71khRCo">International Committee on Taxonomy of Viruses</a> (ICTV) defines rhinoviruses as three species within the genus <i>Enterovirus:</i><a class="footnote-ref" id="fnref:35" href="#fn:35"><sup>35</sup></a> </p> <ul><li><i>Enterovirus alpharhino</i> (<i>Rhinovirus A</i>)</li></ul> <ul><li><i>Enterovirus betarhino</i> (<i>Rhinovirus B</i>)</li> <li><i>Enterovirus cerhino</i> (<i>Rhinovirus C</i>)</li></ul> <h3>Types</h3> <p>Prior to 2020, enteroviruses (including all rhinoviruses) were categorized according to their <a href="/facts/Serotype/fUllA0xY">serotype</a>. In 2020 the ICTV ratified a proposal<a class="footnote-ref" id="fnref:36" href="#fn:36"><sup>36</sup></a> to classify all new types based on the genetic diversity of their VP1 gene. Human rhinovirus type names are of the form RV-<i>Xn</i> where <i>X</i> is the rhinovirus species (A, B, or C) and <i>n</i> is an index number. Species A and B have used the same index up to number 100, while species C has always used a separate index. Valid index numbers are as follows:<a class="footnote-ref" id="fnref:37" href="#fn:37"><sup>37</sup></a> </p> <ul><li>Rhinovirus A: 1, 1B, 2, 7–13, 15, 16, 18–25, 28–34, 36, 38–41, 43–47, 49–51, 53–68, 71, 73–78, 80–82, 85, 88–90, 94–96, 100–108</li> <li>Rhinovirus B: 3–6, 14, 17, 26, 27, 35, 37, 42, 48, 52, 69, 70, 72, 79, 83, 84, 86, 91–93, 97, 99, 100-104</li> <li>Rhinovirus C: 1–57</li></ul> <h2 id="structure">Structure</h2> <p>Rhinoviruses have single-stranded <a href="/facts/Positive-strand_RNA_virus/tEqWffsl">positive sense</a> <a href="/facts/RNA/HxPeNfNj">RNA</a> genomes of between 7200 and 8500 <a href="/facts/Nucleotide/pQKEwlJI">nucleotides</a> in length. At the 5' end of the <a href="/facts/Genome/31Sm08JT">genome</a> is a virus-encoded protein and, as in mammalian mRNA, there is a 3' <a href="/facts/Poly-A_tail/ILnXUBKP">poly-A tail</a>. Structural proteins are encoded in the 5' region of the genome and non structural at the 3' end. This is the same for all <a href="/facts/Picornavirus/QmeWDCDr">picornaviruses</a>. The viral particles themselves are not <a href="/facts/Viral_envelope/5P4eqVHn">enveloped</a> and are <a href="/facts/Dodecahedral/7r519eCl">dodecahedral</a> in structure. </p><p>The viral proteins are translated as a single long <a href="/facts/Polypeptide/C4ltc7UG">polypeptide</a>, which is cleaved into the structural and nonstructural viral proteins.<a class="footnote-ref" id="fnref:38" href="#fn:38"><sup>38</sup></a> </p><p>The structure of the virus was determined in 1985 using <a href="/facts/X-ray_crystallography/WtI0F5DN">x-ray crystallography</a> by researchers at <a href="/facts/Purdue_University/dRuTdltL">Purdue University</a> and the <a href="/facts/University_of_Wisconsin/Rfj54YvS">University of Wisconsin</a> led by <a href="/facts/Michael_Rossmann/5QDkg5nJ">Michael Rossmann</a>. The virus was crystallized forming cubic crystals with four virus particles in each <a href="/facts/Unit_cell/znygJqdx">unit cell</a> (<a href="/facts/Space_group/2XQx0J7M">space group</a> <i>P</i>213, no. 198), similar to a <a href="/facts/Cubic_close-packed/AqL1HUxe">cubic close-packed</a> arrangement.<a class="footnote-ref" id="fnref:39" href="#fn:39"><sup>39</sup></a> </p><p>Human rhinoviruses are composed of a <a href="/facts/Capsid/hm7V6Ewm">capsid</a> that contains four viral <a href="/facts/Proteins/Jxmagu3E">proteins</a>, VP1, VP2, VP3 and VP4.<a class="footnote-ref" id="fnref:40" href="#fn:40"><sup>40</sup></a><a class="footnote-ref" id="fnref:41" href="#fn:41"><sup>41</sup></a> VP1, VP2, and VP3 form the major part of the protein capsid. The much smaller VP4 protein has a more extended structure, and lies at the interface between the capsid and the RNA genome. There are 60 copies of each of these proteins assembled as an <a href="/facts/Icosahedron/wWbpnDYp">icosahedron</a>. Antibodies are a major defense against infection with the <a href="/facts/Epitopes/PL0oBuGh">epitopes</a> lying on the exterior regions of VP1-VP3. </p> <h2 id="novel-antiviral-drugs">Novel antiviral drugs</h2> <p>There are currently no FDA-approved <a href="/facts/Antiviral_drugs/Xgbd2eI2">antiviral drugs</a> to treat rhinovirus infections.<a class="footnote-ref" id="fnref:42" href="#fn:42"><sup>42</sup></a> Several novel antiviral compounds have been tested in clinical trials without sufficient efficacy to progress to FDA approval. Compounds specifically targeted for rhinoviruses, or more broadly, picornaviruses, include the following: </p> <ul><li><a href="/facts/Rupintrivir/U5IIG1ha">Rupintrivir</a> is a <a href="/facts/Peptidomimetic/5fSPtzrw">peptidomimetic</a> drug developed for treatment of rhinovirus infections.<a class="footnote-ref" id="fnref:43" href="#fn:43"><sup>43</sup></a> Rupintrivir inhibits human rhinovirus <a href="/facts/Picornain_3C/tLPQzQMV">3Cprotease</a> and prevents cleavage of the rhinovirus <a href="/facts/Proteolysis/GtQdv6J7">polyprotein</a> following translation, therefore preventing viral assembly and replication. A phase II clinical trial of rupintrivir using <a href="/facts/Human_challenge_study/Lz0IGj25">experimentally induced rhinovirus infection</a> in healthy volunteers demonstrated efficacy in reducing viral load and symptom severity. However, further trials testing rupintrivir in treating natural infections showed minimal benefit, and further clinical development was halted.<a class="footnote-ref" id="fnref:44" href="#fn:44"><sup>44</sup></a></li> <li><a href="/facts/Pleconaril/cPl68pGD">Pleconaril</a> is an orally <a href="/facts/Bioavailable/9l6na9MV">bioavailable</a> antiviral drug developed for the treatment of infections caused by <a href="/facts/Picornaviruses/QmeWDCDr">picornaviruses</a>.<a class="footnote-ref" id="fnref:45" href="#fn:45"><sup>45</sup></a> This drug acts by binding to a hydrophobic pocket in VP1, and stabilizes the protein capsid to such an extent that the virus cannot release its RNA genome into the target cell. Phase III clinical trials showed a slight reduction in symptom duration if taken within 24 hours of symptom onset.<a class="footnote-ref" id="fnref:46" href="#fn:46"><sup>46</sup></a><a class="footnote-ref" id="fnref:47" href="#fn:47"><sup>47</sup></a> However, the FDA denied approval of pleconaril due to concerns about side effects, limited efficacy in non-white participants, and difficulty in treating most patients within a 24 hour window.<a class="footnote-ref" id="fnref:48" href="#fn:48"><sup>48</sup></a><a class="footnote-ref" id="fnref:49" href="#fn:49"><sup>49</sup></a></li></ul> <p>Other treatments aiming to reduce rhinovirus infection symptoms include immunomodulatory agents. These may promote beneficial antiviral responses or reduce inflammatory responses associated with symptoms. <a href="/facts/Interferon_type_I/jQhMAFA3">Interferon-alpha</a> used intranasally was shown to be effective against human rhinovirus infections. However, volunteers treated with this drug experienced some side effects, such as nasal bleeding and began developing <a href="/facts/Drug_tolerance/EJau9rgm">tolerance</a> to the drug. Subsequently, research into the treatment was abandoned.<a class="footnote-ref" id="fnref:50" href="#fn:50"><sup>50</sup></a> Inhaled <a href="/facts/Budesonide/4p8z8WBy">budesonide</a> has been shown to reduce viral load and pro-inflammatory <a href="/facts/Interleukin_1_beta/tJhf3nRu">IL-1β</a> in mice. <a href="/facts/Omalizumab/EyDGUak5">Omalizumab</a>, which was developed for treatment of severe allergic asthma, has shown evidence in reducing symptom severity of asthma patients infected with rhinovirus.<a class="footnote-ref" id="fnref:51" href="#fn:51"><sup>51</sup></a> </p> <h2 id="vaccine-development">Vaccine development</h2> <p>There are no <a href="/facts/Vaccine/QcXzLug2">vaccines</a> against these viruses as there is little-to-no cross-protection between <a href="/facts/Serotype/fUllA0xY">serotypes</a>. At least 165 types of human rhinoviruses are known.<a class="footnote-ref" id="fnref:52" href="#fn:52"><sup>52</sup></a> However, a study of the VP4 protein has shown it to be highly conserved among many serotypes of human rhinovirus, opening up the potential for a future pan-serotype human rhinovirus vaccine.<a class="footnote-ref" id="fnref:53" href="#fn:53"><sup>53</sup></a> A similar result was obtained with the VP1 protein. Like VP4, VP1 also occasionally "pokes" out of the viral particle, making it available to neutralizing antibodies. Both peptides have been tested on rabbits, resulting in successful generation of cross-serotype antibodies.<a class="footnote-ref" id="fnref:54" href="#fn:54"><sup>54</sup></a> </p><p>Rhinovirus genome has a high rate of variability in human circulation, even occurring with genomic sequences that differ up to 30%.<a class="footnote-ref" id="fnref:55" href="#fn:55"><sup>55</sup></a> Recent studies have identified conserved regions of the rhinovirus genome; this, along with an adjuvanted polyvalent rhinovirus vaccine, shows potential for future development in vaccine treatment.<a class="footnote-ref" id="fnref:56" href="#fn:56"><sup>56</sup></a> </p> <h2 id="prevention">Prevention</h2> <p class="note">Main article: <a href="/facts/Common_cold/fP9A03U9">Common cold § Prevention</a></p> <p>Human rhinovirus can remain infectious for up to three hours outside of a human host. Once the virus is contracted, a person is most contagious within the first three days. Preventative measures such as regular vigorous <a href="/facts/Handwashing/BTgUfoRo">handwashing</a> with soap and water may aid in avoiding infection. Avoiding touching the mouth, eyes, and nose (the most common entry points for rhinovirus) may also assist prevention. Droplet precautions, which take the form of a surgical mask and gloves, are the method used in major hospitals.<a class="footnote-ref" id="fnref:57" href="#fn:57"><sup>57</sup></a> As with all respiratory pathogens once presumed to transmit via respiratory droplets, it is highly likely to be carried by the aerosols generated during routine breathing, talking, and even singing. In order to prevent airborne transmission, droplet precautions are insufficient, and routine airborne precautions are necessary.<a class="footnote-ref" id="fnref:58" href="#fn:58"><sup>58</sup></a> </p> <h2 id="external-links">External links</h2> <ul><li><a href="https://videos.med.wisc.edu/videos/1691">VIDEO: Rhinoviruses, the Old, the New and the UW</a> James E. Gern, MD, speaks at the University of Wisconsin School of Medicine and Public Health, 2008.</li> <li><a href="http://www.cellsalive.com/howbig.htm">How Big is a Human rhinovirus? (animation)</a></li></ul> <h2 id="references">References</h2> <ol> <li id="fn:1"><p>"Rhinovirus (Common Cold) | Disease Outbreak Control Division". health.hawaii.gov. Retrieved 2024-11-20. <a href="https://health.hawaii.gov/docd/disease_listing/rhinovirus/#:~:text=About%20This%20Disease,children%20may%20have%20even%20more." target="_blank">https://health.hawaii.gov/docd/disease_listing/rhinovirus/#:~:text=About%20This%20Disease,children%20may%20have%20even%20more.</a> <a href="#fnref:1" class="footnote-back-ref">↩</a></p></li> <li id="fn:2"><p>"Genus: Enterovirus | ICTV". ictv.global. Retrieved 2023-12-29. <a href="https://ictv.global/report/chapter/picornaviridae/picornaviridae/enterovirus" target="_blank">https://ictv.global/report/chapter/picornaviridae/picornaviridae/enterovirus</a> <a href="#fnref:2" class="footnote-back-ref">↩</a></p></li> <li id="fn:3"><p>Wang CC, Prather KA, Sznitman J, Jimenez JL, Lakdawala SS, Tufekci Z, et al. (August 2021). "Airborne transmission of respiratory viruses". Science. 373 (6558): eabd9149. doi:10.1126/science.abd9149. PMC 8721651. PMID 34446582. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8721651" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8721651</a> <a href="#fnref:3" class="footnote-back-ref">↩</a></p></li> <li id="fn:4"><p>Jacobs SE, Lamson DM, St George K, Walsh TJ (January 2013). "Human rhinoviruses". Clinical Microbiology Reviews. 26 (1): 135–162. doi:10.1128/CMR.00077-12. PMC 3553670. PMID 23297263. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3553670" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3553670</a> <a href="#fnref:4" class="footnote-back-ref">↩</a></p></li> <li id="fn:5"><p>"Rhinoviruses: Common Colds | CDC". www.cdc.gov. 2023-03-09. Retrieved 2023-12-28. <a href="https://www.cdc.gov/ncird/rhinoviruses-common-cold.html" target="_blank">https://www.cdc.gov/ncird/rhinoviruses-common-cold.html</a> <a href="#fnref:5" class="footnote-back-ref">↩</a></p></li> <li id="fn:6"><p>van Benten I, Koopman L, Niesters B, Hop W, van Middelkoop B, de Waal L, et al. (2003). "Predominance of rhinovirus in the nose of symptomatic and asymptomatic infants". Pediatric Allergy and Immunology. 14 (5): 363–370. doi:10.1034/j.1399-3038.2003.00064.x. PMC 7168036. PMID 14641606. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7168036" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7168036</a> <a href="#fnref:6" class="footnote-back-ref">↩</a></p></li> <li id="fn:7"><p>Auvray C, Perez-Martin S, Schuffenecker I, Pitoiset C, Tarris G, Ambert-Balay K, et al. (2024). "Sudden Infant Death Associated with Rhinovirus Infection". Viruses. 16 (4): 518. doi:10.3390/v16040518. PMC 11054477. 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