Viral transmission

Rhinovirus possesses various transmission modes and can infect a huge population at any given time. Most commonly, they 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. The virus attaches to respiratory epithelium and spreads locally. Rhinovirus species A and B bind to the major human rhinovirus receptor, ICAM-1 (found in high quantities in the posterior nasopharynx). [3, 4, 5] Rhinovirus C (RV-C) binds to cadherin-related family member 3 receptor (CHDR-3). Viral particles are usually transmitted via inoculation into the eye or the nose from contact with the fingers that harbor the virus, especially since rhinoviruses are capable of surviving on hands for hours. [6, 7, 8]

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 rhinovirus infection.

Pathogenesis of rhinovirus infection

The attachment of the virus to its receptors (ICAM-1, CHDR-3, low-density lipoprotein receptor [LDLR]) in susceptible individuals elicits an innate immune response leading to airway inflammation and remodeling.

Few cells are actually infected by rhinovirus, 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. [9] Viremia is uncommon.

A local inflammatory response to rhinovirus in the respiratory tract can lead to nasal discharge, nasal congestion, sneezing, and throat irritation. The nasal epithelium is not damaged. [10, 11] Various polymorphisms in cytokine genes have been shown to impact the severity of infection, suggesting a genetic predisposition. [12] 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 (PMN) leukocytes. 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 rhinovirus 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. Rhinovirus 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.