Rhinovirus (RV) is the most important etiological agent of common cold in humans, accounting for approximately 25-50% of respiratory tract infections annually, leading to considerable economic burdens related to medical visits and school and work absence. RV infections occur year-round and are usually associated with upper respiratory tract illness, otitis media, and sinusitis. In recent years, the increasing implementation of molecular diagnostic assays for respiratory virus detection in clinical laboratories has facilitated the recognition of RV as a lower respiratory tract pathogen, particularly in patients with asthma, infants, elderly patients, and immunocompromised hosts. RVs are now implicated in exacerbations of chronic pulmonary disease, asthma development, severe bronchiolitis in infants and children as well as fatal pneumonia in elderly and immunocompromised adults. There are currently no approved antiviral medications or vaccines for RV infection, and treatment remains primarily supportive.


RVs have a positive-sense, single-stranded-RNA (ssRNA) genome of approximately 7,200 bp  and are members of the  genus Enterovirus of the family Picornaviridae .

The genomic RNA has a highly structured 5’untranslated region (UTR) of about 600-1200 bases long that is important in translation, virulence and possibly encapsidation and a short 3’ untranslated region of 50-100 bases that is instrumental in (-) strand synthesis. The 5′ UTR contains a ‘clover-leaf’ secondary structure known as the Internal Ribosome Entry Site (IRES) while the rest of the genome encodes a single polyprotein that is cleaved by viral proteases to produce 11 proteins. Both ends of the genomes are modified: basic protein VPg is covalently attached at the 5′ end and there is a poly(A) tract at the 3′ end. The viral RNA genome is enclosed within the viral capsid that consists of four proteins, VP1, VP2, VP3, and VP4. Variations within capsid proteins VP1, VP2 and VP3 are responsible for the antigenic diversity among the viruses, while VP4 anchors the RNA core to the capsid. There are 60 copies each of the four capsid proteins, giving the virion an icosahedral structure, with a canyon in VP1 that serves as the site of attachment to cell. The remaining nonstructural proteins are involved in viral genome replication and assembly.


Currently there are 160 RV types identified and classified into three genetically distinct species; RV-A (containing 76 types), RV-B (29 types) and RV-C (55 types) based on VP4/VP2 and VP1 phylogenetic sequence criteria (Picornavirus Study Group http://www.picornastudygroup.com/). RV-C viruses do not grow in standard cell culture, therefore the genetically based classification system is currently used for rhinovirus typing.


Approximately 90% of the 100 established RV-A and RV-B serotypes, designated as the “major receptor group”, utilize the cell surface receptor intercellular adhesion molecule 1 (ICAM-1), while the “minor group” attaches to and enters cells via the low-density lipoprotein receptor (LDLR). Some of the major-group RVs also use heparan sulfate as an additional receptor The cadherin-related family member 3 protein (CDHR3) was recently identified as the cellular receptor for RV-C viruses).

DDL offers the following Rhinovirus analyses:

  • Detection and quantification of rhinovirus by qRT-PCR, aimed at the 5’-UTR region
  • Subtyping of Rhinovirus A, B, and C
  • Target specific sequencing by next generation sequencing (Illumina)


  • Nasal, nasopharyngeal or oropharyngeal swabs
  • Lavages/sputum
  • Cultured strains.

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