The Rhinosinusitis Initiative was developed by 5 national societies. The current guidance document is an expansion of the 2004 publication, "Rhinosinusitis: Establishing definitions for clinical research and patient care" and provides templates for clinical trials in antimicrobial, anti-inflammatory, and symptom-relieving therapies for the following: (1) acute presumed bacterial rhinosinusitis, (2) chronic rhinosinusitis (CRS) without nasal polyps, (3) CRS with nasal polyps, and (4) classic allergic fungal rhinosinusitis. In addition to the templates for clinical trials and proposed study designs, the Rhinosinusitis Initiative has developed 6 appendices, which address (1) health outcomes, (2) nasal endoscopy and staging of CRS, (3) radiologic imaging, (4) microbiology, (5) laboratory measures, and (6) biostatistical methods.

RT-PCR is more sensitive for rhinovirus detection than cell culture, but healthy controls are frequently rhinovirus (or picornavirus) positive in cross-sectional studies. Fifteen healthy children were followed over at least three seasons of the year with weekly sampling of nasal/nasopharyngeal secretion for RT-PCR testing for picornavirus and daily recording of respiratory symptoms. One sample positive for picornavirus was diagnosed as an infection; consecutive positive weekly samples constituted a single infection. Picornavirus illness was diagnosed if RNA was detected 7 days prior through 21 days after onset. One hundred fifty-five (21%) of 740 weekly samples were picornavirus positive and associated with illness; 37(5%) positives were not associated with illness (P = 0.001). The 192 positive samples occurred in 121 infections, 74 with a single positive and 47 with "runs" of positives in two or more consecutive samples. Forty five (96%) of the 47 runs comprised 2 or 3 consecutive positives. Ninety six (52%) of 185 reported illnesses during 235 child-months were picornavirus positive (0.4/child-month); 25 infections were asymptomatic (0.11/child-month). The infection rate was highest in fall (0.66/child-month); the winter rate (0.44/child-month) was similar to that in spring (0.5) and summer (0.43). Picornavirus infections in healthy children were common (0.51/child-month), episodic, and usually associated with brief illness; one fifth of infections were asymptomatic. The infection rate was highest in fall; infections in winter occurred at the same rate as in spring and summer.

Rhinovirus infection significantly alters the expression of many genes associated with the immune response, including chemokines and antivirals. The data obtained provide insights into the host response to rhinovirus infection and identify potential novel targets for further evaluation.

Tremacamra reduced the severity of experimental rhinovirus colds. Whether tremacamra will be useful clinically will require further study.

To localize the sites and determine the extent of human rhinovirus (HRV) replication in the upper respiratory tract, biopsies of nasal and nasopharyngeal epithelia were collected from 26 HRV- or 7 sham-inoculated volunteers on days 1, 3, and 5 and on days 12, 20, or 33 after inoculation and analyzed by in situ hybridization. HRV-infected cells were detected on at least 1 day in 22 of the 23 HRV-infected subjects and in 1 of the 7 sham-inoculated subjects who developed a cold and had nasal secretions positive for a picornavirus by polymerase chain reaction. Low numbers of in situ hybridization-positive ciliated cells were present in nasal biopsies. In the nasopharynx, most HRV-infected cells were ciliated, but infected nonciliated epithelial cells were also detected. Our results indicate that HRV replicates in a very small proportion of cells in the nasal epithelium and in both ciliated and nonciliated cells in the nasopharynx of experimentally infected humans.