RHINOVIRUSES
المؤلف:
Stefan Riedel, Jeffery A. Hobden, Steve Miller, Stephen A. Morse, Timothy A. Mietzner, Barbara Detrick, Thomas G. Mitchell, Judy A. Sakanari, Peter Hotez, Rojelio Mejia
المصدر:
Jawetz, Melnick, & Adelberg’s Medical Microbiology
الجزء والصفحة:
28e , p541-543
2025-12-08
55
Rhinoviruses are the common cold viruses. They are the most commonly recovered agents from people with mild upper respiratory illnesses. They are usually isolated from nasopharyngeal secretions but may also be found in throat and oral secretions. These viruses—as well as coronaviruses, adenoviruses, enteroviruses, parainfluenza viruses, and influenza viruses—cause upper respiratory tract infections, including the common cold syndrome. Rhinoviruses are also responsible for about half of asthma exacerbations.
Classification
Human rhinovirus isolates are numbered sequentially. More than 150 types are known. Isolates within a type share more than 70% sequence identity within certain protein-coding regions.
Human rhinoviruses can be divided into major and minor receptor groups. Viruses of the major group use inter cellular adhesion molecule-1 (ICAM-1) as receptor, and those of the minor group bind members of the low-density lipoprotein receptor (LDLR) family.
Properties of the Virus
A. General Properties
Rhinoviruses share many properties with other enteroviruses but differ from HEV A–D in having a buoyant density in cesium chloride of 1.40 g/mL and in being acid labile. Virions are unstable below a pH of 5.0–6.0, and complete inactivation occurs at a pH of 3.0. Rhinoviruses are more thermostable than other enteroviruses and may survive for hours on environmental surfaces.
Nucleotide sequence identity over the entire genome is more than 50% among all rhinoviruses and between enteroviruses and rhinoviruses. There is greater or less identity for particular genomic regions.
In 2009, the genomes of all known strains of rhinovirus were sequenced, defining conserved and divergent regions. This information will facilitate new understanding of pathogenic potential and the design of antiviral drugs and vaccines.
B. Animal Susceptibility and Growth of Virus
These viruses are infectious only for humans, gibbons, and chimpanzees. They can be grown in a number of human cell lines, including the WI-38 and MRC-5 lines. Organ cultures of ferret and human tracheal epithelium may be necessary for some fastidious strains. Most grow better at 33°C, which is similar to the temperature of the nasopharynx in humans, than at 37°C.
C. Antigenic Properties
More than 150 serotypes are known. New serotypes are based on the absence of cross-reactivity in neutralization tests using polyclonal antisera. Human rhinovirus 87 is reclassified as human enterovirus 68.
Pathogenesis and Pathology
The virus enters via the upper respiratory tract. High titers of virus in nasal secretions—which can be found as early as 2–4 days after exposure—are associated with maximal ill ness. Thereafter, viral titers fall, although illness persists. In some instances, virus may remain detectable for 3 weeks. There is a direct correlation between the amount of virus in secretions and the severity of illness.
Replication is limited to the surface epithelium of the nasal mucosa. Biopsies have shown that histopathologic changes are limited to the submucosa and surface epithelium. These include edema and mild cellular infiltration. Nasal secretion increases in quantity and in protein concentration.
Rhinoviruses rarely cause lower respiratory tract disease in healthy individuals, although they are associated with the majority of acute asthma exacerbations. Experiments under controlled conditions have shown that chilling, including the wearing of wet clothes, does not produce a cold or increase susceptibility to the virus. Chilliness is an early symptom of the common cold.
Clinical Findings
The incubation period is brief—from 2 to 4 days—and the acute illness usually lasts for 7 days, although a nonproductive cough may persist for 2–3 weeks. The average adult has one or two attacks each year. Usual symptoms in adults include sneezing, nasal obstruction, nasal discharge, and sore throat; other symptoms may include headache, mild cough, malaise, and a chilly sensation. There is little or no fever. The nasal and nasopharyngeal mucosa become red and swollen. There are no distinctive clinical findings that permit an etiologic diagnosis of colds caused by rhinoviruses versus colds caused by other viruses. Secondary bacterial infection may produce acute otitis media, sinusitis, bronchitis, or pneumonitis, especially in children.
Immunity
Neutralizing antibody to the infecting virus develops in serum and secretions of most persons. Depending on the test used, estimates of the frequency of response have ranged from 37% to greater than 90%.
Antibody develops 7–21 days after infection; the time of appearance of neutralizing antibody in nasal secretions parallels that of serum antibodies. Because recovery from ill ness usually precedes appearance of antibody, it seems that recovery is not dependent on antibody. However, antibody may accomplish final clearance of infection. Serum antibody persists for years but decreases in titer.
Epidemiology
The disease occurs throughout the world. In the temperate zones, the attack rates are highest in early fall and late spring. Prevalence rates are lowest in summer. Members of isolated communities form highly susceptible groups.
The virus is believed to be transmitted through close contact by means of virus-contaminated respiratory secretions. The fingers of a person with a cold are usually contaminated, and transmission to susceptible persons then occurs by hand-to-hand, hand-to-eye, or hand-to-object-to-hand (eg, doorknob) contamination. Rhinoviruses can survive for hours on contaminated environmental surfaces. Self-inoculation after hand contamination may be a more important mode of spread than that by airborne particles.
Infection rates are highest among infants and children and decrease with increasing age. The family unit is a major site of spread of rhinoviruses. Introduction of virus is generally attributable to preschool-aged and school-aged children. Secondary attack rates in a family vary from 30% to 70%. Infections in young children are symptomatic, but infections in adults are often asymptomatic.
In a single community, multiple rhinovirus serotypes cause outbreaks of disease in a single season, and different serotypes predominate during different respiratory disease seasons. There are usually a limited number of serotypes causing disease at any given time.
Treatment and Control
No specific prevention method or treatment is available. The development of a potent rhinovirus vaccine is unlikely because of the difficulty in growing rhinoviruses to high titer in culture, the fleeting immunity, and the multiplicity of serotypes causing colds.
Antiviral drugs are thought to be a more likely control measure for rhinoviruses because of the problems with vac cine development. Many compounds effective in vitro have failed to be effective clinically.
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