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PubMed1992

[Chemoprophylaxis and chemotherapy of common colds caused by rhinoviruses: overview and outlook].

Rhinoviruses are the main etiologic agents of infectious common colds, which represent about 40% of the acute respiratory infections in man. The antigenic diversity of rhinoviruses precludes any prevention by vaccination. Within the last 20 years, efforts have therefore concentrated on chemoprophylaxis or chemotherapy with antiviral agents. Interferons (alpha and beta) administered intranasally at high doses, exerted a significant prophylactic activity in volunteers inoculated with rhinoviruses or in the course of epidemics in families. By contrast, the therapeutic activity of interferons is almost nonexistent, which greatly limits their practical interest. Various synthetic chemicals exert a marked and selective inhibitory effect on the replication of various serotypes of rhinoviruses in cell cultures. In the absence of an animal model of rhinovirus infection, in vivo studies of these molecules have been performed in human volunteers, chiefly at the Common Cold Research Unit in Salisbury (Great Britain). 3 synthetic compounds (an imidazothiazole, a benzimidazole derivative and a piperazinyl-pyridazine) have exerted a significant prophylactic activity, especially marked with the latter. None of these compounds, however, was active when administered after the infectious challenge. The search for selective anti-rhinovirus compounds is still going on; it will probably be facilitated through a combination of structural studies of rhinovirus capsids (or of their cellular receptors) with computer-assisted design of synthetic molecules. The recent observation of the influence of psychological factors on the propensity of rhinovirus-infected subjects to develop clinically apparent common cold must be taken into account in future studies.

Antiviral Agents↗
PubMed1998

Low grade rhinovirus infection induces a prolonged release of IL-8 in pulmonary epithelium.

Rhinoviruses are important respiratory pathogens implicated in asthma exacerbations. The mechanisms by which rhinoviruses trigger inflammatory responses in the lower airway are poorly understood, in particular their ability to infect the lower airway. Bronchial inflammatory cell (lymphocyte and eosinophil) recruitment has been demonstrated. IL-8 is a potent proinflammatory chemokine that is chemotactic for neutrophils, lymphocytes, eosinophils, and monocytes and may be important in the pathogenesis of virus-induced asthma. Increased levels of IL-8 have been found in nasal samples in natural and experimental rhinovirus infections. In these studies we therefore examine the ability of rhinovirus to infect a transformed lower airway epithelial cell line (A549) and to induce IL-8 protein release and mRNA induction. We observed that rhinovirus type 9 is able to undergo full viral replication in A549 cells, and peak viral titers were found 24 h after inoculation. Rhinovirus infection induced a dose- and time-dependent IL-8 release up to 5 days after infection and an increase in IL-8 mRNA expression that was maximal between 3 and 24 h after infection. UV inactivation of the virus completely inhibited replication, but only reduced IL-8 protein production and mRNA induction by half, while prevention of virus-receptor binding completely inhibited virus-induced IL-8 release, suggesting that part of the observed effects was due to viral replication and part was due to virus-receptor binding. These studies demonstrate that rhinoviruses are capable of infecting a pulmonary epithelial cell line and inducing IL-8 release. These findings may be important in understanding the pathogenesis of rhinovirus-induced asthma exacerbations.

Cells, Cultured↗
PubMed1991

Rhinovirus induces natural killer-like cytotoxic cells and interferon alpha in mononuclear leukocytes.

Natural killer-like cellular cytotoxicity was augmented by incubation of human rhinovirus serotype 2 with peripheral blood mononuclear leukocytes collected from healthy donors. The production of alpha interferon but not gamma interferon was identified in the same cell cultures. A specific interaction of conformationally intact rhinovirus with peripheral blood mononuclear leukocytes was required for induction of the response, since the response was extinguished at reduced quantities of infectious rhinovirus, and acid inactivated rhinovirus did not augment cellular cytotoxicity. Productive replication of rhinovirus was not observed in cultures of peripheral blood mononuclear leukocytes. The replicative failure was not related merely to interferon production, since the rate of disappearance of rhinovirus was similar to that observed in cell free medium. The findings suggest that natural killer cells should be considered as a potential component of the local nasopharyngeal pathophysiology of rhinovirus infection.

Cytotoxicity, Immunologic↗
PubMed1999

Rhinovirus identification by BglI digestion of picornavirus RT-PCR amplicons.

Rhinoviruses are the main cause of the common cold and precipitate the majority of asthma exacerbations. RT-PCR followed by internal probe hybridisation or Southern blotting, or nested PCRs are currently the most sensitive methods for their identification. However, none of the published techniques can differentiate satisfactorily rhinoviruses from other picornaviruses. Examination of the restriction maps of sequenced rhinoviruses, revealed a highly conserved BglI restriction site (GCCnnnnnGGC), located exactly in the middle of the 380-bp amplicon generated with the OL26-OL27 primer pair, which has been used extensively in the past to identify picornaviruses. Such a site was either not present, or positioned differently in other picornaviruses of known sequence. It was, therefore, considered that digestion of rhinovirus amplicons with this enzyme would result in two equal length fragments, generating a single 190-bp band in gel electrophoresis. In contrast, either one undigested 380-bp band or a double-band pattern would appear in amplicons from other picornaviruses. To test this hypothesis, Bgl digestions of OL26-OL27 amplicons from cultured and wild-type rhinoviruses, whose identity was confirmed by acid lability, as well as from echo, polio and coxsackie viruses were carried out. All rhinovirus samples were digested successfully generating single bands. Among the other picornaviruses, only 6.6% presented a single band pattern, while the rest were as predicted from the model. With a sensitivity of 100% and a specificity over 90%, the method described, which is rapid and remarkably easy to perform, can be used to distinguish rhinoviruses from other picornaviruses to a considerable extent.

Deoxyribonucleases, Type II Site-Specific↗
PubMed1998

Serious respiratory illness associated with rhinovirus infection in a pediatric population.

BACKGROUND: Rhinoviruses have long been associated with mild upper respiratory illness in both adults and children. However, the role of rhinoviruses as lower respiratory tract pathogens has not been fully characterized. Previous data suggests that rhinoviruses may cause severe lower respiratory illness in young children or infants. OBJECTIVES: The present study describes the clinical presentations, severity of illness and outcomes for a large cohort of pediatric patients with documented rhinovirus infections. SUBJECTS AND METHODS: A retrospective chart review was done on 93 pediatric patients from whom 101 nasopharyngeal or endotracheal specimens were positive by viral culture for a rhinovirus. All patients were hospitalized or seen in the pediatric emergency department at The Children's Hospital of Philadelphia between 1 January, 1990 and 31 May, 1996. RESULTS: Of the 93 patients, 52 were male and 41 female. The age range was 0 days to 18 years with 25 (27%) less than 3 months, 42 (45%) between 3 and 12 months and 26 (28%) over the age of 12 months. Clinical presentations on evaluation in the emergency department or admission included 78 (84%) patients with acute respiratory illness, 13 (17%) with fever and suspected sepsis and 11 (12%) with other complaints. Reported physical findings on examination included one or more lower respiratory symptoms or signs of acute distress and fever greater than or equal to 38.1 degrees C. A total of 64 (69%) children were noted to have significant past medical histories, including 28 (44%) with prematurity or complicated neonatal courses, 11 (17%) with prior reactive airways, 8 (12%) with congenital cardiac disease and 7 (11%) with neurologic disorders. Of the patients, 29 (31%) were considered to be otherwise healthy children with no underlying dysfunctions. The mean duration of hospitalization for 69 patients admitted with respiratory illness who did not develop subsequent unrelated complications was 3.7 days. No significant bacterial or fungal pathogens were identified in 91% of the cases. CONCLUSIONS: This study shows that rhinoviruses were associated with severe lower respiratory illness and hospitalization in a large pediatric population and that rhinovirus infection was a complicating factor in those patients with underlying or predisposing conditions.

Adolescent↗
PubMed1997

The refined structure of human rhinovirus 16 at 2.15 A resolution: implications for the viral life cycle.

BACKGROUND: Rhinoviruses belong to the picornavirus family and are small, icosahedral, non-enveloped viruses containing one positive RNA strand. Human rhinovirus 16 (HRV16) belongs to the major receptor group of rhinoviruses, for which the cellular receptor is intercellular adhesion molecule-1 (ICAM-1). In many rhinoviruses, one of the viral coat proteins (VP1) contains a hydrophobic pocket which is occupied by a fatty acid-like molecule, or so-called 'pocket factor'. Antiviral agents have been shown to bind to the hydrophobic pocket in VP1, replacing the pocket factor. The presence of the antiviral compound blocks uncoating of the virus and in some cases inhibits receptor attachment. A refined, high-resolution structure would be expected to provide further information on the nature of the pocket factor and other features previously not clearly identified. RESULTS: The structure of native HRV16 has been refined to a resolution of 2.15 A. The hydrophobic pocket in VP1 is observed in two alternative conformations. In one of these, the pocket is filled by a pocket factor and the protein structure is similar to virus-antiviral compound complexes. In the other conformation, the hydrophobic pocket is collapsed and empty. RNA bases stack against both a tryptophan and a phenylalanine residue on the internal surface of the viral capsid. Site-directed mutagenesis of the tryptophan, which is conserved across the picornaviruses, to nonconservative residues results in non-viable virus. Five symmetry-related N termini of coat protein VP4 form a ten-stranded, antiparallel beta barrel around the base of the icosahedral fivefold axis. The N termini of VP1 are amphipathic alpha helices, which stack on the outside of this beta barrel. The N termini of VP1 and VP4 have not been observed previously in rhinovirus structures. CONCLUSIONS: The observation of a partially occupied hydrophobic pocket in HRV16 forms a missing link between HRV14, which is always observed with no pocket factor in the native form, and rhinovirus 1A and other picornaviruses (e.g. poliovirus, coxsackievirus) which contain pocket factors. The pocket factor molecules probably regulate viral entry, uncoating and assembly. Picornavirus assembly is known to proceed via pentamers, therefore, the interaction of RNA with the conserved tryptophan residues across twofold axes between pentamers may play a role in picornavirus assembly. The positioning of a cation on the icosahedral fivefold axes and the structure of the N termini of VP4 and VP1 around these axes suggest a mechanism for the uncoating of rhinoviruses.

Amino Acid Sequence↗
PubMed2003

Predominance of rhinovirus in the nose of symptomatic and asymptomatic infants.

Respiratory infections in infancy may protect against developing Th2-mediated allergic disease (hygiene hypothesis). To estimate the relative contribution of particular viruses to the development of the immune system and allergic disease, we investigated longitudinally the prevalence of respiratory viral infections in infants. One hundred and twenty-six healthy infants were included in this prospective birth cohort study in their first year of life. Physical examination was performed and nasal brush samples were taken during routine visits every 6 months and during an upper respiratory tract infection (URTI) (sick visits). The prevalence of respiratory viral infections in infants with URTI, infants with rhinitis without general malaise and infants without nasal symptoms was studied. Rhinovirus was the most prevalent pathogen during URTI and rhinitis in 0- to 2-year-old infants ( approximately 40%). During URTI, also respiratory syncytial virus ( approximately 20%) and coronavirus ( approximately 10%) infections were found, which were rarely detected in infants with rhinitis. Surprisingly, in 20% of infants who did not present with nasal symptoms, rhinovirus infections were also detected. During routine visits at 12 months, a higher prevalence of rhinovirus infections was found in infants who attended day-care compared with those who did not. We did not observe a relation between breast-feeding or smoking by one or both parents and the prevalence of rhinovirus infections. The parental history of atopy was not related to the prevalence of rhinovirus infection, indicating that the genetic risk of allergic disease does not seem to increase the chance of rhinovirus infections. In conclusion, rhinovirus infection is the most prevalent respiratory viral infection in infants. It may therefore affect the maturation of the immune system and the development of allergic disease considerably.

Age Factors↗
PubMed2002

Effects of rhinovirus-induced common colds on granulocyte activity in allergic rhinitis.

OBJECTIVE: To explore the activities of mast cells, eosinophils, and neutrophils in patients with allergic rhinitis developing common colds and increased responsiveness to allergen following nasal rhinovirus inoculation. METHODS: We have revisited a nasal lavage material obtained from 17 patients who were successfully inoculated with rhinovirus outside the pollen season and received nasal allergen challenges before and after inoculation. We have examined indices of mast cell activity (tryptase), eosinophil degranulation (eosinophil peroxidase; EPO), and neutrophil activation (myeloperoxidase; MPO). RESULTS: Allergen challenges performed before rhinovirus inoculation increased the nasal output of EPO. Notably, this response was significantly greater after rhinovirus inoculation (cf. before inoculation). The output of MPO was also increased following allergen challenge after, but not before, rhinovirus inoculation. Nasal lavage fluid levels of tryptase were increased following allergen challenge similarly before and after rhinovirus inoculation. Also, the viral infection did not affect the baseline levels of tryptase. CONCLUSIONS: The present data demonstrate that rhinovirus infections activate both eosinophils and neutrophils, but that they may not affect mast cell activity. We suggest that common colds in part through stimulation of granulocyte activity potentiate the airway inflammation in allergic diseases.

Administration, Intranasal↗
PubMed1997

Rhinoviruses induce interleukin-8 mRNA and protein production in human monocytes.

Rhinoviruses are important upper respiratory pathogens that are strongly associated with asthma exacerbations. However, the inflammatory response to rhinovirus infection is poorly understood. Interleukin (IL)-8 has been implicated in the pathogenesis of respiratory viral infections and asthma. Rhinovirus-induced IL-8 release and mRNA induction were examined in peripheral blood mononuclear cells (PBMC). Rhinoviruses induced IL-8 release for up to 7 days after inoculation onto PBMC. This was associated with an increase in IL-8 mRNA expression that peaked 48 h after exposure to the virus. IL-8 protein production was reduced by UV inactivation of the virus and abolished by preventing virus-receptor binding. Although rhinovirus replication was not demonstrated in PBMC, low-grade productive infection was shown in the human monocyte cell line THP-1. Rhinovirus induction of IL-8 in monocytes or airway macrophages may be important in the pathogenesis of rhinovirus-induced asthma exacerbation.

Cells, Cultured↗
PubMed1999

Association of rhinovirus infections with asthma.

Rhinoviruses are the most common cause of the common cold, but they can cause more severe illnesses in people with underlying lung disorders such as asthma, chronic obstructive pulmonary disease, or cystic fibrosis. Epidemiologic studies with sensitive detection methods such as PCR have identified rhinovirus infection as a major source of asthma exacerbations in both children and adults, especially during the spring and fall. Since rhinoviruses cause little tissue destruction, it is presumed that the immune response to the infection may play an important role in the pathogenesis of rhinovirus-induced exacerbations of asthma. This review examines the epidemiologic association between rhinovirus infections and exacerbations of asthma and outlines current information on immune responses to rhinovirus infection and potential connections between antiviral responses and preexisting allergic inflammation. Finally, current and future strategies for treating rhinovirus infections and virus-induced exacerbations of asthma are discussed.

Animals↗
PubMed1999

Improved detection of rhinoviruses in clinical samples by using a newly developed nested reverse transcription-PCR assay.

This paper describes the development and evaluation of a new nested reverse transcription (RT)-PCR for the detection of rhinovirus in clinical samples. The nucleotide sequences of the 5' noncoding regions of 39 rhinoviruses were determined in order to map the most conserved subregions. We designed a set of rhinovirus-specific primers and probes directed to these subregions and developed a new nested RT-PCR. The new assay includes an optimal RNA extraction method and amplicon identification with probe hybridization to discriminate between rhinoviruses and the closely related enteroviruses. It proved to be highly sensitive and specific. When tested on a dilution series of cultured viruses, the new PCR protocol scored positive at 10- to 100-fold-higher dilutions than a previously used nested RT-PCR. When tested on a collection of clinical samples obtained from 1,070 acute respiratory disease patients who had consulted their general practitioners, the new assay demonstrated a rhinovirus in 24% of the specimens, including all culture-positive samples, whereas the previously used PCR assay or virus culture detected a rhinovirus in only 3.5 to 6% of the samples. This new assay should help determine the disease burden associated with rhinovirus infections.

Base Sequence↗
PubMed2006

[Role of rhinovirus in respiratory tract infections in hospitalized children].

BACKGROUND: Rhinovirus is a recognized cause of common cold and has been shown to cause asthma exacerbations in adults and children. The burden of rhinovirus infections in hospitalized children has not been described in Spain. OBJECTIVE: To describe confirmed rhinovirus infections in children hospitalized for respiratory tract infection in a secondary public hospital. PATIENTS AND METHODS: We performed a prospective descriptive study in children admitted to hospital with fever or respiratory tract infection and with a positive isolation of rhinovirus in nasopharyngeal washings between September 2004 and July 2005. Virological diagnosis was made with direct immunofluorescent assay and/or reverse transcription-polymerase chain reaction in specimens obtained from nasopharyngeal washings. The clinical characteristics of the patients were analyzed. RESULTS: There were 76 children with rhinovirus infection, representing 25 % of admissions in 304 children with fever or respiratory tract infection. Rhinovirus was the second most frequent viral agent identified after respiratory syncytial virus (RSV) (29.9 % of admissions). Fifty-four children (71.1 %) were under 2 years of age. The most frequent clinical diagnoses were recurrent wheezing in 60.5 %, bronchiolitis in 23.7 %, pneumonia in 7.9 %, and upper respiratory tract infection in 5.3 %. Fever > 38 degrees C was present in 57.9 % of the patients and radiologic infiltrate was found in 23.7 %. Oxygen saturation less than 95 % was found in 43.4 % of the patients. Of 22 children aged more than 2 years, a diagnosis of asthmatic crisis was made in 21. CONCLUSIONS: Rhinoviruses were frequently identified in hospitalized children with respiratory tract disease and were the second most common viruses after RSV. In our series, it was the most frequent cause of recurrent wheezing in hospitalized children and the second most common cause in infants.

Adolescent↗
PubMed1983

Pathogenesis of lower respiratory tract symptoms in experimental rhinovirus infection.

To investigate the pathogenesis of lower respiratory tract symptoms during rhinovirus infection, 19 healthy young adult volunteers were exposed to a currently unnumbered rhinovirus strain (HH). Spirometry and bronchoprovocation with histamine sulfate were performed prior to and on Days 4, 5, and 21 after exposure to the virus. Fiberoptic bronchoscopy for visualization and culture of the tracheobronchial mucosa was done on Day 4 or Day 5. Fourteen of 19 volunteers were infected with rhinovirus; 9 of the 14 had clinical illness. Rhinovirus was isolated from the bronchial brush specimens in 5 of the 13 infected volunteers bronchoscoped, all of whom had clinical illness. Rhinovirus was not isolated at bronchoscopy from any of the 5 infected volunteers without clinical illness (p = 0.025, Fisher's exact test). Spirometry and histamine bronchoprovocation were unchanged during experimental rhinovirus infection. Rhinovirus may invade the lower respiratory tract in symptomatic infections, and thereby cause lower respiratory tract symptoms.

Adult↗
PubMed1995

A rhinovirus outbreak among residents of a long-term care facility.

OBJECTIVE: To describe the epidemiology of and clinical findings associated with a rhinovirus outbreak that occurred among institutionalized elderly persons. DESIGN: Retrospective review of medical records and nursing surveillance reports. SETTING: A 685-bed, long-term care facility for veterans and their spouses. PATIENTS: 33 persons from whom rhinovirus was cultured. MEASUREMENTS: Throat and nasopharyngeal virus culture; review of medical records to determine underlying diseases, signs and symptoms of respiratory illness, illness duration, and interventions during illness; and review of nursing surveillance reports to determine room locations of ill persons. RESULTS: Between 14 August and 2 September 1993, the number of respiratory illnesses increased. Throat and nasopharyngeal virus cultures were taken from 67 ill residents; 33 cultures yielded rhinovirus, and no other respiratory virus was isolated. Geographic clustering of persons infected with rhinovirus was observed. Of those persons with rhinovirus infections, 100% had upper respiratory symptoms, 34% had gastrointestinal symptoms, 71% had systemic symptoms, 66% had lower respiratory symptoms (including productive cough), and 52% had new abnormalities on lung auscultation. The 17 persons with rhinovirus infection who had chronic obstructive pulmonary disease had more severe illnesses: Five (29%) required glucocorticoid or bronchodilator therapy for illness-associated bronchospasm; 2 required transfer out of the facility; 1 developed a radiographically documented infiltrate; and 1 died of respiratory failure. CONCLUSIONS: Rhinovirus may cause epidemic, clinically important respiratory illness in nursing homes residents. A large proportion of residents may become ill, and infection may be severe in persons with underlying lung disease.

Aged↗
PubMed1999

Diagnosis of enterovirus and rhinovirus infections by RT-PCR and time-resolved fluorometry with lanthanide chelate labeled probes.

Detection of enteroviruses and rhinoviruses has traditionally been based on laborious and time-consuming virus isolation. Recently, rapid and sensitive assays for detecting enterovirus and rhinovirus genomic sequences by reverse transcription-polymerase chain reaction (RT-PCR) have been introduced. An RT-PCR assay is described that amplifies both enteroviral and rhinoviral sequences, followed by liquid-phase hybridization carried out in a microtiter plate format. In the hybridization assay, amplicons are identified by enterovirus- or rhinovirus-specific probes carrying lanthanide chelate labels, which can be detected simultaneously by time-resolved fluorometry. The sensitivity and specificity of the RT-PCR-hybridization method were evaluated with a representative collection of enteroviruses and rhinoviruses and tested further its applicability to the clinical setting with cerebrospinal fluid samples and nasopharyngeal aspirates. The RT-PCR assay amplified all enteroviruses and rhinoviruses tested, and all but one amplicon gave a positive result in the subsequent hybridization assay. The RT-PCR-hybridization method was more sensitive than virus isolation for the detection of enteroviruses and rhinoviruses in the clinical samples. High sensitivity, rapidity, and easy performance make the assay suitable for the routine diagnosis of enterovirus and rhinovirus infections.

Animals↗
PubMed1999

Rhinoviruses replicate effectively at lower airway temperatures.

Rhinoviruses are epidemiologically connected to the majority of acute asthma exacerbations; however, their ability to infect and replicate in the lower airways is disputed. A frequent argument against this possibility involves the temperature preference for rhinovirus replication, generally accepted to be 33 degrees C, the temperature of the nasal passages. However, this argument is based on studies with a single rhinovirus serotype. In this study, differences in temperature preferences were evaluated between several serotypes and relative titers were determined than can be achieved at upper and lower airway temperatures. Rhinovirus serotypes 1b, 2, 7, 9, 14, 16, 41, and 70 were titrated in Ohio-HeLa cell cultures at either 33 degrees C or 37 degrees C. Possible selection by culture temperature was examined by continuous culture at 33 degrees C and 37 degrees C for 2-4 passages and subsequent titration at both temperatures. Finally, nasal aspirate samples derived from patients with wild-type rhinoviral common colds were cultured at 33 degrees C and 37 degrees C and RT-PCR was used to assess rhinovirus replication at each temperature. The majority of the serotypes and wild-type viruses replicated slightly better at 33 degrees C than at 37 degrees C. However, titers achieved after one or more replicative cycles at 37 degrees C were still high enough to initiate infection. Furthermore, in some instances equal or even better replication was observed at 37 degrees C. It is concluded that temperature preferences may vary between rhinoviruses and are not likely to be a prohibitive factor for infection of the lower airways.

HeLa Cells↗
PubMed1994

Polymerase chain reaction and sequencing for typing rhinovirus RNA.

Primers were designed and tested for their ability to distinguish rhinoviruses from enteroviruses. A primer set derived from the 5'-UTR/VP coding region junction was able to amplify all the rhinovirus serotypes tested. Enteroviruses were either not amplified by these primer pairs or produced a band of larger size that could easily be discriminated from the rhinovirus-specific product. In contrast, primers embedded in the 5'-UTR region alone were able to amplify both rhinovirus and enterovirus RNA. It is shown that rhinoviruses could be specifically typed by sequencing the amplicon derived from the 5'-UTR set. The sequences of the 5'-UTR region of ten previously unsequenced rhinoviruses were derived. The sequences obtained cluster into two groups: 1B, 41, 15, 30, 63, 31, 56, and 44; and 17, 69, and 70. Amplicons from serotypes 17,69, and 70 also group by sequence with the equivalent region of HRV14 from the genetic database, while the others group with 2 and 89.

Animals↗
PubMed1999

Review: rhinoviruses and their ICAM receptors.

The normal function of human intercellular adhesion molecule-1 (ICAM-1) is to provide adhesion between endothelial cells and leukocytes after injury or stress. ICAM-1 binds to leukocyte function-associated antigen or macrophage-1 antigen. However, ICAM-1 is also used as a receptor by the major group of human rhinoviruses and is a catalyst for the subsequent viral uncoating during cell entry. The three-dimensional atomic structure of the two amino-terminal domains (D1 and D2) of ICAM-1 has been determined to 2.2 A resolution and fitted into a cryoelectron microscopy reconstruction of a rhinovirus-ICAM-1 complex. Rhinovirus attachment is confined to the BC, CD, DE, and FG loops of the amino-terminal Ig-like domain (D1) at the end distal to the cellular membrane. The loops are considerably different in structure to those of human ICAM-2 or murine ICAM-1, which do not bind rhinoviruses. There are extensive charge interactions between ICAM-1 and human rhinoviruses, which are mostly conserved in both major and minor receptor groups of rhinoviruses.

Animals↗