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Rhinovirus Infection 

  • Author: Michael Rajnik, MD; Chief Editor: Burke A Cunha, MD   more...
 
Updated: Sep 13, 2012
 

Background

Rhinoviruses (RVs) are members of the Picornaviridae family, which includes the human pathogens enterovirus and hepatovirus (notably, hepatitis A virus). More than 100 different subtypes exist in 3 major groups, categorized according to receptor specificity: intercellular adhesion molecule-1 (ICAM-1), low-density lipoprotein (LDL) receptors, and sialoprotein cell receptors.

RV infections are chiefly limited to the upper respiratory tract but may cause otitis media and sinusitis; they may also exacerbate asthma, cystic fibrosis, chronic bronchitis, and serious lower respiratory tract illness in infants, elderly persons, and immunocompromised persons.[1, 2] Although infections occur year-round, the incidence is highest in the fall and the spring. Of persons exposed to the virus, 70-80% have symptomatic disease. Most cases are mild and self-limited.

The common cold is an acute respiratory tract infection (ARTI) characterized by mild coryzal symptoms, rhinorrhea, nasal obstruction, and sneezing. Although the list of agents that cause the common cold is large, 66-75% of cases are due to 200 antigenically distinct viruses from 8 different genera. RVs are the most common of these (25-80% of cases), followed by coronaviruses (10-20%), influenza viruses (10-15%), and adenoviruses (5%).

Although the incidence of ARTI cannot be clearly defined, because of seasonal and locational variability, it is estimated to range from 3-6 cases per person per year in the United States. Children younger than 1 year have experienced an average of 6-8 episodes of ARTI. This figure decreases to 3-4 episodes per year by adulthood.

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Pathophysiology

Viral transmission

RV possesses various transmission modes and can infect a huge population at any given time. Most commonly, RVs are transmitted to susceptible individuals through direct contact or via aerosol particles. The primary site of inoculation is the nasal mucosa, though the conjunctiva may be involved to a lesser extent. RV attaches to respiratory epithelium and spreads locally. The major human RV receptor is ICAM-1 (found in high quantities in the posterior nasopharynx).[3, 4]

Highly contagious behavior includes nose blowing, sneezing, and physically transferring infected secretions onto environmental surfaces or paper tissue. Contrary to popular belief, behaviors such as kissing, talking, coughing, or even drooling do not contribute substantially to the spread of disease.

Infection rates approximate 50% within the household and range from 0% to 50% within schools, indicating that transmission requires long-term contact with infected individuals. Brief exposures to others in places such as movie theaters, shopping malls, friends’ houses, or doctors’ offices are associated with a low risk of transmission. Because children produce antibodies to fewer serotypes, those who attend school are the most common reservoirs of RV infection.

Pathogenesis of infection

The natural response of the human defense system to injury involves ICAM-1, which aids the binding between endothelial cells and leukocytes. RV takes advantage of ICAM-1 by using it as a receptor for attachment. In addition, it uses ICAM-1 for subsequent viral uncoating during cell invasion. Some RV serotypes also upregulate ICAM-1 expression on human epithelial cells to increase susceptibility to infection.

Few cells are actually infected by RV, and the infection involves only a small portion of the epithelium. Symptoms develop 1-2 days after viral infection, peaking 2-4 days after inoculation, though reports have described symptoms as early as 2 hours after inoculation with primary symptoms 8-16 hours later.[5] Viremia is uncommon.

A local inflammatory response to RV in the respiratory tract can lead to nasal discharge, nasal congestion, sneezing, and throat irritation. The nasal epithelium is not damaged.[6, 7] Various polymorphisms in cytokine genes have been shown to impact the severity of rhinovirus infection, suggesting a genetic predisposition.[8] Detectable histopathology causing the associated nasal obstruction, rhinorrhea, and sneezing is lacking, which leads to the hypothesis that the host immune response plays a major role in the pathogenesis.

Infected cells release interleukin (IL)–8, which is a potent chemoattractant for polymorphonuclear leukocytes (PMNs). Concentrations of IL-8 in secretions correlate proportionally with the severity of common cold symptoms. Inflammatory mediators, such as kinins and prostaglandins, may cause vasodilatation, increased vascular permeability, and exocrine gland secretion. These, together with local parasympathetic nerve-ending stimulation, lead to cold symptoms.

Deficient production of interferon beta by asthmatic bronchial epithelial cells has been proposed as a mechanism for increased susceptibility to RV infections in individuals with asthma.

Viral clearance is associated with the host response and is due in part to the local production of nitric oxide. RV is shed in large amounts, with as many as 1 million infectious virions present per milliliter of nasal washings. Viral shedding can occur a few days before cold symptoms are recognized by the patient, peaks on days 2-7 of the illness, and may last as long as 3-4 weeks.

Serotype-specific neutralizing antibodies are found 7-21 days after infection in 80% of patients. Although these antibodies persist for years, providing long-lasting immunity, recovery from illness is more likely related to cell-mediated immunity. Persistent protection from repeat infection by that serotype appears to be partially attributable to immunoglobulin A (IgA) antibodies in nasal secretions, serum immunoglobulin G (IgG), and, possibly, serum immunoglobulin M (IgM).

Clinical studies indicate sinus involvement in common colds. Abnormal computed tomography (CT) findings (eg, opacification, air-fluid levels, and mucosal thickening) are present in adults with common colds that resolve over 1-2 weeks without antibiotic therapy.

Despite what is reported in folklore, no good clinical evidence suggests that colds are acquired by exposure to cold weather, getting wet, or becoming chilled.

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Etiology

RVs are small, nonenveloped, positive (sense) stranded RNA viruses of the Picornaviridae family. More than 100 different serotypes have been identified, categorized into 3 major groups on the basis of specificity for particular receptors: ICAM-1, LDL receptors, and sialoprotein cell receptors. Their structure is an icosahedral capsid of 12 pentamers containing the 4 viral proteins. A deep cleft is involved in viral attachment. Attachment to cellular receptors can be blocked by a specific antibody.

RV grows efficiently only within a limited temperature range (33-35°C), and it cannot tolerate an acidic environment. Thus, it is rarely found outside the nasopharynx, because of the acidic environment of the stomach and the increased temperature in both the lower respiratory tract and the gastrointestinal (GI) tract.

Transmission of RV occurs with close exposure to infected respiratory secretions, including hand-to-hand contact, self-inoculation of eyes or nose, and, possibly, large- and small-particle aerosolization. The virus has been cultured from the skin after up to 2 hours and after up to 4 days on inanimate objects in ideal conditions. Donors are typically symptomatic with a cold at the time of transmission, and virus is detected on the hands and nasal mucosa.

One study assessed the transfer of virus to surfaces by 15 adults with RV infection; each of the 15 stayed overnight in a hotel room, and afterward, 10 commonly touched sites in each room were tested for viral contamination.[9] The investigators determined that RV could be recovered from 35% of these sites and found that the virus could be transferred back from inanimate objects to fingertips in many cases.

Higher rates of transmission occur in humid, crowded conditions such as are found in nurseries, daycare centers, and schools, especially during cooler months in temperate regions and the rainy season in tropical regions. The likelihood of transmission does not appear to be related to exposure to cold temperatures, fatigue, or sleep deprivation.

Risk factors

  • Factors that increase the risk and severity of RV infection include the following:
  • Smoking increases the risk of respiratory infection by approximately 50%
  • Very young or old individuals are at greater risk, possibly because of decreased immunity
  • Exposure to infected contacts increases the risk of infection
  • Touching the conjunctivae or the nose with contaminated fingers or objects increases the risk of infection
  • Crowding leads to increased transmission
  • Men may have a slightly higher risk, but the increase is probably insignificant
  • Breastfeeding has little effect on the incidence of the common cold
  • Underlying chronic medical conditions, including anatomic, metabolic, genetic, and immunologic disorders (eg, tracheoesophageal fistula, congenital heart disease, cystic fibrosis, or immunodeficiency) increase the risk and severity of infection
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Epidemiology

United States statistics

Common colds are most frequent from September to April in temperate climates. RV infections, which are present throughout the year, account for the initial increase in cold incidence during the fall (causing as many as 80% of colds in this period) and for a second incidence peak at the end of spring. Colds that occur from October through March are caused by the successive appearance of numerous viruses (see the image below). Adenovirus infections occur at a constant rate throughout the season.

Seasonal variations in frequency of selected upperSeasonal variations in frequency of selected upper respiratory tract infection pathogens. PIV = parainfluenza virus; RSV = respiratory syncytial virus; MPV = metapneumovirus; Group A Strept = group A streptococcus.

The incidence of the common cold is highest in preschool- and elementary school–aged children. An average of 3-8 colds per year is observed in this age group, and the incidence is even higher in children who attend daycare and preschool. Because of the numerous viral agents involved and the multiple serotypes that several of these agents (especially RV) have, it is not unusual for younger children having new colds every month during the winter. Adults and adolescents typically have 2-4 colds per year.

International statistics

Internationally, RV is a significant cause of respiratory tract infection,[10, 11, 12, 13, 14, 15, 16, 17, 18] as well as a minor cause of bronchiolitis.[19] RVs have been found in all countries, even in remote areas such as the Kaluhi Islands and the Amazon. In Brazil, RVs reportedly cause 46% of ARTIs. A seasonal increase in incidence during the winter months is observed worldwide.

Age-related demographics

Because antibodies to viral serotypes develop over time, the incidence of RV infection is highest in infants and young children and falls as children approach adulthood. Young children are more likely to have the frequent, close, personal contact necessary to transmit RV; they commonly pass the infection to family members after acquiring the virus in nurseries, daycare facilities, and schools. Children may also be more contagious by virtue of having higher virus concentrations in secretions and longer duration of viral shedding.

Sex-related demographics

Some reports indicate a male predominance of infection in children younger than 3 years, which switches to a female predominance in children older than 3 years. In adults, no difference in rates of infection between men and women is apparent.

Race-related demographics

No differences among different races with respect to susceptibility to RV infection or disease course have been described. In general, Native Americans and Eskimos are more likely to develop the common cold and appear to have higher rates of complications such as otitis media. These findings may be explained as much by environmental conditions (eg, poverty and overcrowding) as by ethnicity.

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Prognosis

The prognosis for RV infection is excellent. The most common manifestation of RV infection, the common cold, is mild and self-limited. Complete recovery is usually observed within 7 days for adolescents and adults and within 10-14 days for children. Occasionally, a child’s cough and congestion linger for 2-3 weeks.

Although rarely associated with fatal disease, rhinoviruses are associated with significant morbidity. ARTIs, predominantly RV infections, are estimated to cause 30-50% of time lost from work by adults and 60-80% of time lost from school by children. Severe respiratory disease, including bronchiolitis, asthma exacerbations, and pneumonia ,[20, 21] can occur, particularly in infants and young children.[22] Preterm infants are also at high risk for severe RV infection.[23]

RV is a predominant pathogen in lower respiratory tract infections (LRTI) in very low birth weight infants[17] and shares predominance in LRTI among young infants with respiratory syncytial virus (RSV).[24, 25] RVs may also be involved in LRTIs in elderly persons, persons with cystic fibrosis, and immunosuppressed patients. The true impact of LRTI is not clear. Recovery of RV in these patients may be a marker of an underlying disease process or a precursor to a bacterial infection.

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Patient Education

Because spread of secretions by contact with hands is a major route of transmission, encourage parents and patients to wash their hands frequently. In addition, emphasize other environmental measures to control infections, such as avoiding finger-to-eye and finger-to-nose contact and coughing and sneezing into the crook of the elbow.

Reassure families and patients that frequent colds are common at certain times of the year. Inform parents that 6-12 colds per year can be normal for young children, especially if they attend daycare or preschool. Explain that frequent self-limited colds do not indicate a problem with a child’s immune system and do not warrant antibiotic treatment and that patients with common colds need not be excluded from daycare or preschool settings.

Advise patients to return if fever exceeds 102°F, if significant respiratory distress develops, or if symptoms do not resolve in 10-14 days. Remind patients and families that purulent nasal discharge is commonly observed after the first few days of the infection and does not indicate a bacterial infection or the need for antibiotics.

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Contributor Information and Disclosures
Author

Michael Rajnik, MD  Associate Professor, Department of Pediatrics, Program Director, Pediatric Infectious Disease Fellowship Program, Uniformed Services University of the Health Sciences

Michael Rajnik, MD is a member of the following medical societies: American Academy of Pediatrics, Armed Forces Infectious Diseases Society, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Coauthor(s)

Robert W Tolan Jr, MD  Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine

Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility

Disclosure: Novartis Honoraria Speaking and teaching

Chief Editor

Burke A Cunha, MD  Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Additional Contributors

Duane R Hospenthal, MD, PhD Professor of Medicine, Uniformed Services University of the Health Sciences; Physician, Infectious Disease Service, San Antonio Military Medical Center (formerly Brooke Army Medical Center)

Duane R Hospenthal, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Armed Forces Infectious Diseases Society, Association of Military Surgeons of the US, Infectious Diseases Society of America, International Society for Human and Animal Mycology, International Society for Infectious Diseases, International Society of Travel Medicine, and Medical Mycology Society of the Americas

Disclosure: Nothing to disclose.

James D Korb, MD Program Director, Department of Pediatrics, Children's Hospital of Orange County

Disclosure: Nothing to disclose.

Larry I Lutwick, MD Professor of Medicine, State University of New York Downstate Medical School; Director, Infectious Diseases, Veterans Affairs New York Harbor Health Care System, Brooklyn Campus

Larry I Lutwick, MD is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Clinton Murray, MD

Program Director, Infectious Disease Fellowship, San Antonio Uniformed Services Health Education Consortium

Clinton Murray, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Association of Military Surgeons of the US, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Mai Ngoc Nguyen, MD

Staff Physician, Department of Pediatrics, Mattel Children's Hospital, University of California at Los Angeles

Mai Ngoc Nguyen, MD is a member of the following medical societies: American Academy of Pediatrics, and American Medical Association

Disclosure: Nothing to disclose.

José Rafael Romero, MD Director of Pediatric Infectious Diseases Fellowship Program, Associate Professor, Department of Pediatrics, Combined Division of Pediatric Infectious Diseases, Creighton University/University of Nebraska Medical Center

José Rafael Romero, MD is a member of the following medical societies: American Academy of Pediatrics, American Society for Microbiology, Infectious Diseases Society of America, New York Academy of Sciences, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Gregory William Rutecki MD Professor of Medicine, University of South Alabama Medical School

Gregory William Rutecki is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society of Nephrology, National Kidney Foundation, and Society of General Internal Medicine

Disclosure: Nothing to disclose.

Russell W Steele, MD Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Gordon L Woods, MD Consulting Staff, Department of Internal Medicine, University Medical Center

Gordon L Woods, MD is a member of the following medical societies: Society of General Internal Medicine

Disclosure: Nothing to disclose.

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Seasonal variations in frequency of selected upper respiratory tract infection pathogens. PIV = parainfluenza virus; RSV = respiratory syncytial virus; MPV = metapneumovirus; Group A Strept = group A streptococcus.
 
 
 
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