Essentials of Diagnosis
Rhinoviruses are the most frequent cause of the common cold. One hundred two serotypes have been identified by neutralization with specific antisera, and additional strains have been isolated but are not yet typed.
Rhinoviruses produce clinical illness in only half of those infected, and thus many asymptomatic individuals are capable of spreading the virus. Rhinovirus “colds” affect people in temperate climates most frequently in the early fall, which may reflect the return to school rather than any change in the virus itself. Rates of infection are highest in infants and children, who are also the primary vector introducing colds into family units. Secondary infections occur in ~50% of family members, especially other children.
Although many different rhinovirus serotypes may be found in a given community, only a few predominate during a specific cold season. They tend to be the newly categorized serotypes, suggesting that a gradual antigenic drift occurs.
At least 80% of the rhinoviruses share a common receptor, ICAM-1, which is a member of the immunoglobulin family and is expressed on epithelial, fibroblast, and lymphoblastoid cells.
Secretory and serum antibodies are generated in response to the rhinovirus and can be detected within a week of infection. No antigen is common to all rhinoviruses. Although secretory immunoglobulin A (IgA) is probably more important than serum antibody in preventing and controlling infection, its half-life is brief. A better correlate of immunity is the level of serum antibody that begins to wane ~18 months after infection.
Interferon, generated in response to the infection, may both limit the progression of the infection and contribute to the symptoms. The release of cytokines during inflammation can promote the spread of the virus by enhancing the expression of viral receptors. Cell-mediated immunity does not appear to play an important role in controlling rhinovirus infections.
Infection can be initiated by as little as one infectious viral particle. During the peak of illness, titers of 500 to 1,000 infectious virions are reached in nasal secretions. Most viral replication occurs in the nose, and the severity of symptoms correlates with the quantity (titer) of virus in nasal secretions. Biopsies of nasal mucosa taken during a “cold” reveal severe edema of the subepithelial tissue but minimal inflammatory cell response. Infected ciliated epithelial cells may be sloughed from the nasal mucosa.
Nasal washings are the best type of clinical specimen for recovering the virus. Rhinoviruses grow in vitro only in cells of primate origin, with human diploid fibroblast cells (eg, WI-38) as the optimum system. As already stated, these viruses grow best at 33°C, which is not the optimum temperature for any other clinically important viruses. Thus their isolation may require a separate incubator. Isolation in tissue culture occurs 4–5 days on average. The virus is identified by typical cytopathic effects and the demonstration of acid lability. Serotyping is rarely necessary but is done by using pools of specific neutralizing sera.
Serologic testing to document rhinovirus infection is not practical. No antigen is common to all rhinoviruses; thus it would be necessary to have the patient's viral isolate or a prototype of the specific rhinovirus prevalent in the community in order to perform this kind of testing.
BOX 28-1 Rhinovirus Infection
BOX 28-2 Treatment of Rhinovirus Infection
There is no specific therapy for rhinovirus (Box 28-2). Nasal vasoconstrictors may provide relief, but their use may be followed by rebound congestion and worsening symptoms. Antibacterial agents are not beneficial unless a true bacterial infection (eg, sinusitis) occurs. Even when nasal secretions have become purulent, a carefully performed Gram's stain will usually show few if any bacteria. Rigorous studies of vitamin C therapy have not shown efficacy. Topical interferon provides antiviral activity but itself produces upper respiratory symptoms. Drugs that block viral attachment, penetration, or replication have been discovered and are being evaluated in clinical trials.
Because rhinovirus illnesses are usually uncomplicated, the prognosis for recovery is excellent, but as mentioned above in the complications section, exacerbations of chronic lung disease may occur, and fatal illnesses in immunocompromised patients have been reported.
Prevention & Control
There are three potential methods of prevention or control of rhinoviruses: vaccines, antiviral agents (especially interferon), and interruption of transmission (Box 28-3).
BOX 28-3 Control of Rhinovirus Infection
The multiple serotypes and apparent antigenic drift in rhinovirus antigens suggest that successful vaccines are unlikely. Formalin-inactivated, parenterally administered vaccines induce antibody in serum but not in nasal secretions and are not as useful as those given intranasally.
Prophylactic topical interferon is effective but associated with unacceptable side effects. Since transmission is person to person, infection may be reduced by minimizing finger to nose and hand to hand spread as well as by covering coughs and sneezes.
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