Human rhinoviruses (HRVs) are non-enveloped, positive-sense, single-stranded RNA viruses belonging to the genus Enterovirus within the family Picornaviridae. They are the most frequently identified cause of the common cold and are responsible for the majority of acute upper respiratory tract infections in humans worldwide. Human rhinoviruses are divided into three species, RV-A, RV-B, and RV-C, which together encompass more than 160 recognised types, making them the most diverse group of respiratory viruses currently known.

Human rhinoviruses enter host cells by binding to specific receptors on the surface of epithelial cells lining the upper and lower respiratory tract. The majority of RV-A and all RV-B types use intercellular adhesion molecule 1 (ICAM-1) as their primary receptor, while a minority of RV-A types bind to the low-density lipoprotein receptor (LDLR) family. RV-C, the most recently characterised species, uses cadherin-related family member 3 (CDHR3) for cell entry. Following receptor binding, the virus is internalised by endocytosis, and the acidic environment of the endosome triggers uncoating and release of the viral genome into the cytoplasm. Replication takes place entirely in the cytoplasm, where the positive-sense RNA genome is directly translated to produce a single polyprotein that is processed by viral proteases into the structural and non-structural proteins required for genome replication and assembly of progeny virions.

The rhinovirus genome encodes four capsid proteins, VP1, VP2, VP3, and VP4, and seven non-structural proteins with roles in genome replication, polyprotein processing, and modulation of host innate immune responses. The capsid of major-group rhinoviruses contains a surface depression known as the canyon, which is the site of ICAM-1 receptor binding. Antiviral drug targets have been identified within the canyon and in a hydrophobic pocket beneath it, the latter being the binding site for capsid-binding compounds that inhibit uncoating. Rhinoviruses display extensive genetic diversity and antigenic variability across types, which precludes the development of broadly protective vaccines based on conventional neutralising antibody responses.

Human rhinoviruses are transmitted primarily through direct contact with infectious secretions or contaminated surfaces, followed by inoculation of the nasal mucosa or conjunctiva, and also through inhalation of infectious droplets and aerosols. Infection is established in the ciliated epithelial cells of the nasal cavity and nasopharynx, where viral replication and the resulting inflammatory response produce the typical symptoms of the common cold: nasal congestion, rhinorrhoea, sneezing, sore throat, and cough. Symptoms typically appear one to two days after exposure and resolve within seven to ten days in most individuals, although cough may persist for longer. Rhinoviruses can also infect the lower respiratory tract, and in susceptible individuals are an important trigger for exacerbations of asthma, chronic obstructive pulmonary disease, and other pre-existing respiratory conditions.

Rhinoviruses circulate year-round but show distinct seasonal peaks in early autumn and spring in temperate climates, patterns that correspond to the resumption of school terms and changes in population behaviour rather than to the direct effects of temperature or humidity on the virus itself. All age groups are affected, and most individuals experience multiple rhinovirus infections each year, reflecting both the breadth of circulating types and the limited cross-protective immunity between them. While rhinovirus infections are generally self-limiting and mild in otherwise healthy adults, they carry a disproportionate burden in young children, older adults, and people with underlying lung disease or compromised immune function, in whom lower respiratory tract involvement and hospitalisation are more common.

There are currently no licensed antiviral treatments or vaccines approved for human rhinovirus infection, and clinical management remains largely symptomatic, with over-the-counter remedies used to relieve nasal congestion, fever, and discomfort. Pleconaril, a capsid-binding compound, showed activity against rhinoviruses in clinical trials but was not approved for clinical use. Intranasal interferon-alpha has demonstrated some prophylactic activity but is not in routine clinical use. More recently, compounds targeting the viral 3C protease and the polymerase have been investigated as potential broad-spectrum antivirals, and the development of treatments active across rhinovirus species remains an active area of research, driven in part by the clinical impact of rhinovirus-associated asthma exacerbations.

Overall, human rhinoviruses are the dominant cause of the common cold and represent a significant source of morbidity, healthcare utilisation, and economic cost worldwide, even though individual infections are typically mild. Their extraordinary diversity, the lack of durable cross-protective immunity between types, and the challenge of targeting a positive-sense RNA virus that replicates rapidly in the upper airway continue to make rhinovirus infection a difficult target for antiviral and vaccine development, and a continuing focus for respiratory virology research.