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PubMed2006

Nasal RANTES and eotaxin production pattern in response to rhinovirus infection.

Tissue eosinophilia is a hallmark of nasal polyposis and its pathogenesis is an area of high interest. RANTES and eotaxin are both known to recruit eosinophils, however, the mechanisms triggering their induction are still uncertain, and viral infections have been suggested to be involved in this process. Therefore, we investigated whether rhinovirus infection is a stimulus for RANTES and eotaxin expression and production. Fibroblasts were cultured from healthy nasal mucosa obtained during endonasal surgery. Cultured cells were infected with human rhinovirus-16 for one to 72 hours. Following total RNA isolation and reverse transcription, RANTES- and eotaxin-mRNA levels were analyzed. In addition, RANTES and eotaxin secretion was measured in culture supernatants by means of an ELISA. Rhinovirus infection induces RANTES-mRNA expression as early as one hour after infection, persisting for up to 72 hours. Eotaxin-mRNA profiles did not alter significantly from control. Protein production was confirmatory for both chemokines, indicating distinct translational latency. Our data suggest that RANTES functions as a host defence mechanism responding to rhinovirus infection, thus supporting a linkage between rhinovirus infections and the pathogenesis of nasal polyposis.

Cells, Cultured↗
PubMed1979

The spread of rhinoviruses in the Soviet Union (USSR) and in Czechoslovakia (CSSR) and the role of their pathology.

Virological, serological and immunofluorescence studies revealed circulation of rhinoviruses of the strains 1A, 1B, 2, 3, 7, 9, 10, 12, 13, 14, 16-23, 27, 29-33, 42, 48, 53, 56, 60 and 69 on the territory of Czechoslovakia and the Soviet Union. According to virological results, type 48 predominated and was followed in frequency of occurrence by types 27, 14 and 16 in the USSR and 30, 1A and 31 in the CSSR. RV infection in adults with ARD diseases was the aetiology in 28.5% of cases. Among the causative agents of acute rhinitis, rhinosinusitis and otitis, rhinovirus infection makes up a large proportion. Interrelation has been found between rhinovirus infection and chronic inflammation of the mucosa of the nose, the accessory sinuses and the ears. Prolonged course of rhinovirus infection and isolation of the virus in the late stages of disease (1-4 months after its onset) support the presumption that rhinoviruses promote chronicity of inflammation. RV was isolated from patients with chronic pneumonia from the lower respiratory passages (bronchial secretion). Rhinoviraemia was found in a child who died of ARD.

Adolescent↗
PubMed1998

Rhinovirus replication in HeLa cells cultured under conditions of simulated microgravity.

BACKGROUND: Rotating-wall vessels (RWVs) allow for the growth of cells under conditions of simulated microgravity. Information about the replication of viruses in simulated microgravity using RWVs has not been reported. Cells grown in RWVs are subjected to low shear motion, and the replication of certain viruses such as rhinoviruses has been reported to be enhanced by motion. HYPOTHESIS: Our research was based on the hypothesis that rhinovirus replication would be enhanced under conditions of simulated microgravity. METHODS: HeLa cells were cultured in three-dimensional cultures on microcarrier beads in simulated microgravity using RWVs and in sealed Teflon roller bottles. Two-dimensional cultures of HeLa cells were also grown in tissue culture flasks (T-150s). Viral infections for all cultures were carried out under standardized conditions at 1 x g. The amount of new virus released during the first viral replication cycle and the total viral yields obtained from multiple viral replication cycles were determined. RESULTS: Viral quantitation during the first viral replication cycle showed that after 10-13 h RWV and Teflon roller bottle supernatants contained significantly more virus than the supernatants from T-150 cultures. After multiple viral replication cycles (at 24, 48, 72, and 96 h following infection), total viral samples (both free and cell-associated virus) from RWV cultures contained significantly more virus than Teflon roller bottle cultures. CONCLUSIONS: The rhinovirus replication cycle was enhanced in cultures grown in the presence of motion (Teflon roller bottle cultures and RWV cultures). Additionally, multiple rounds of rhinovirus replication yielded more virus in simulated microgravity conditions. Viral transmission in cell cultures in RWVs was efficient and was similar to or better than what occurred in the Teflon roller bottles. The cultivation of cells in simulated microgravity possibly affected the rate of viral adsorption/uptake, the viral replication cycle, and/or the viral yield. RWVs provide an effective means for culturing human rhinoviruses.

Cell Culture Techniques↗
PubMed1990

Kinins are generated in nasal secretions during natural rhinovirus colds.

A prospective study compared the levels of inflammatory mediators in nasal lavages from noninfected, asymptomatic subjects with the mediator content of lavages from the same subjects during naturally occurring rhinovirus colds. Samples were obtained from 16 subjects who experienced natural colds that could be attributed to rhinovirus infections. Kinin levels during symptomatic colds were significantly elevated (P less than .01) compared with those measured when the subjects were noninfected and asymptomatic. Increases in kinins correlated with increased vascular permeability, as monitored by increased concentrations of albumin in lavages. In contrast, histamine levels in nasal lavages were not increased during symptomatic infections, suggesting that mast cell and basophil activation does not occur during rhinovirus colds. These data confirm and extend observations made during experimentally induced rhinovirus infections to the natural disease and are consistent with the hypothesis that kinins may play a role in the pathogenesis of symptomatic rhinovirus infections.

Adult↗
PubMed2024

Rhinovirus infection of airway epithelial cells uncovers the non-ciliated subset as a likely driver of genetic susceptibility to childhood-onset asthma.

Asthma is a complex disease caused by genetic and environmental factors. Epidemiological studies have shown that in children, wheezing during rhinovirus infection (a cause of the common cold) is associated with asthma development during childhood. This has led scientists to hypothesize there could be a causal relationship between rhinovirus infection and asthma or that RV-induced wheezing identifies individuals at increased risk for asthma development. However, not all children who wheeze when they have a cold develop asthma. Genome-wide association studies (GWAS) have identified hundreds of genetic variants contributing to asthma susceptibility, with the vast majority of likely causal variants being non-coding. Integrative analyses with transcriptomic and epigenomic datasets have indicated that T cells drive asthma risk, which has been supported by mouse studies. However, the datasets ascertained in these integrative analyses lack airway epithelial cells. Furthermore, large-scale transcriptomic T cell studies have not identified the regulatory effects of most non-coding risk variants in asthma GWAS, indicating there could be additional cell types harboring these "missing regulatory effects". Given that airway epithelial cells are the first line of defense against rhinovirus, we hypothesized they could be mediators of genetic susceptibility to asthma. Here we integrate GWAS data with transcriptomic datasets of airway epithelial cells subject to stimuli that could induce activation states relevant to asthma. We demonstrate that epithelial cultures infected with rhinovirus significantly upregulate childhood-onset asthma-associated genes. We show that this upregulation occurs specifically in non-ciliated epithelial cells. This enrichment for genes in asthma risk loci, or 'asthma heritability enrichment' is also significant for epithelial genes upregulated with influenza infection, but not with SARS-CoV-2 infection or cytokine activation. Additionally, cells from patients with asthma showed a stronger heritability enrichment compared to cells from healthy individuals. Overall, our results suggest that rhinovirus infection is an environmental factor that interacts with genetic risk factors through non-ciliated airway epithelial cells to drive childhood-onset asthma.

Preprint↗
PubMed2003

Respiratory consequences of rhinovirus infection.

Rhinoviruses, a genus of the family Picornaviridae, are the cause of more than 50% of respiratory tract infections. Complications of rhinovirus infections, which include otitis media, sinusitis, exacerbations of asthma, and other pulmonary diseases, can be significant in certain populations. Reverse transcriptase-polymerase chain reaction has allowed the identification of rhinoviruses and led to a greater appreciation of the role of this pathogen in upper and lower respiratory tract disease. Furthermore, antiviral agents with broad activity against rhinoviruses have recently been developed, have undergone clinical trials, but have not been approved for clinical use. By altering the clinical course of picornavirus infections, it may be possible to minimize their potential adverse consequences.

Acute Disease↗
PubMed1999

Efficacy of tremacamra, a soluble intercellular adhesion molecule 1, for experimental rhinovirus infection: a randomized clinical trial.

CONTEXT: Attachment of most rhinovirus subtypes to cells depends on a cellular receptor, the intercellular adhesion molecule 1 (ICAM-1). A recombinant soluble ICAM-1 (tremacamra, formerly BIRR 4) has shown possible efficacy in early studies. OBJECTIVE: To determine the efficacy and safety of intranasal administration of tremacamra in experimental rhinovirus colds in humans. DESIGN: Four randomized, double-blind, placebo-controlled trials conducted in January to March 1996. SETTING AND SUBJECTS: Volunteers between the ages of 18 and 60 years who had an antibody titer of 1:4 or less to the challenge virus. Subjects were isolated in a hotel room during study days 0 to 8; symptoms were recorded through day 14. A total of 198 subjects were randomized, of whom 196 received drug or placebo and were included in the safety analysis. A total of 177 subjects were included in the efficacy analysis. INTERVENTIONS: Tremacamra or placebo was given beginning 7 hours before inoculation with rhinovirus type 39 (preinoculation studies) or 12 hours after (postinoculation studies). Tremacamra as an inhaled solution or as a powder (each given preinoculation and postinoculation for a total of 4 studies) and placebo were given in 6 doses at 3-hour intervals daily during days 1 through 7. Recipients of active treatment received 367 microg of tremacamra per nostril per dose for a total of 4.4 mg/d. MAIN OUTCOME MEASURES: Effect of tremacamra on infection, as determined by virus isolation and seroconversion, and on illness, as determined by symptom scores, clinical colds, and nasal mucus weights. Treatment-by-study interaction was not significant, so results were pooled for the main analysis. RESULTS: A total of 88 (92%) of the 96 subjects in the placebo groups and 69 (85%) of the 81 subjects in the active treatment groups were infected (P=.19). For placebo vs tremacamra, respectively, the total symptom score (+/- 95% confidence interval [CI]) was 17.6 (+/- 2.7) vs 9.6 (+/- 2.9), the proportion of clinical colds was 64/96 (67% +/- 9%) vs 36/81 (44% +/- 11%), and the nasal mucus weight was 32.9 (+/- 8.8) g vs 14.5 (+/- 9.4) g (P<.001 for all comparisons). Tremacamra was not associated with adverse effects or evidence of absorption through the nasal mucosa and did not interfere with development of neutralizing antibody. CONCLUSION: Tremacamra reduced the severity of experimental rhinovirus colds. Whether tremacamra will be useful clinically will require further study.

Administration, Intranasal↗
PubMed1999

Enatioseparation and anti-rhinovirus activity of 3-benzylchroman-4-ones.

In a series of homo-isoflavonoids, chloro-substituted rac-3-benzylchroman-4-ones (3 d-f) showed an antiviral in vitro activity against selected picornaviruses. In order to study the anti-rhinovirus activity of each stereoisomer, racemic mixtures of 3 d and 3 e were successfully resolved by high-performance liquid chromatography, using a Whelk-O 1 column as chiral stationary phase. The CD spectra confirm that the two eluates of each compound are enantiomers but do not allow the assignment of their absolute configurations. The antiviral activity of the isomers and their racemates was tested in vitro against human rhinovirus serotype 1B and 14 infection, by means of the plaque reduction assay. All homoisoflavonoids tested exhibited an inhibitory effect on rhinovirus replication with an activity depending on virus serotype and compound. The two enantiomers of each compound and the corresponding racemate were equipotent, clearly showing that the configuration of the chiral center in position 3 does not influence the activity against both rhinovirus serotypes.

Antiviral Agents↗
PubMed2003

Detection of rhinovirus RNA in middle turbinate of patients with common colds by in situ hybridization.

Human rhinovirus 14 RNA was determined by in situ hybridization from middle turbinate biopsies in 32 patients with diagnosed common colds and in five control individuals. Twenty-two (69%) biopsies from common colds patients but none of the five control biopsies showed reactivity for human rhinovirus 14 antisense probe. The signal was detected both in the respiratory epithelium and in mucosal inflammatory cells. In situ hybridization of the middle turbinate tissue yielded more positive results than RT-PCR (47%) or virus culture (34%) assayed from nasopharyngeal aspirates, but no statistical significant differences were observed (P = 0.265, P = 0.425, respectively). The results indicated that in situ hybridization procedure was slightly more sensitive than PCR assays and classical culture for the detection of human rhinovirus infection of upper respiratory tract. However, in situ hybridization procedure appeared to be an interesting methodology to investigate the physiopathology of respiratory tract infection by rhinoviruses.

Adult↗
PubMed1986

Detection of human rhinoviruses and their molecular relationship using cDNA probes.

We describe here a cDNA:RNA hybridization system for the study of human rhinoviruses. We have constructed an M13 probe from the 5' end of the genome of rhinovirus 14 (HRV-14) and used this to detect directly viral RNA. Of the 56 human rhinoviruses so far investigated 54 or 96.4% gave clearly positive hybridization signals. However, the strength of this signal depended very much on the molecular relationship of these viruses. Thus, HRV-3, 4, 17, 72, and, to a slightly lesser extent, HRV-2, 6, 9, 13, 19, 31, 42, 49, 64, and 69 appear to be closely related to HRV-14 whereas HRV-5, 7, 8, 16, 32, 40, 45, 55, 56, 63, 80, 82, and 85 appear to be relatively divergent. Further, evidence is provided in this study that indicates that it would be feasible to use cDNA probes to detect human rhinoviruses in nasal washings. However, the sensitivity of detection was clearly affected by both the inclusion of inhibitors of endogenous RNase activity in the RNA extraction mixture and also in the method of extracting the viral RNA. From reconstruction experiments in nasal washings and under optimal conditions, we can detect virus at 10(2.8) TCID50/ml.

Common Cold↗
PubMed1987

Direct detection of rhinoviruses by an enzyme-linked immunosorbent assay.

This paper describes the first enzyme-linked immunosorbent assay for the detection of rhinovirus antigens in clinical specimens (nasal washings), either directly or following overnight cell culture amplification. The assay takes approximately 48 hours to perform and utilizes the same rabbit antirhinovirus hyperimmune serum as both the capture and detecting antibody. The latter has been biotin-labelled and is detected via a streptavidin beta-galactosidase preformed complex. This new assay has been found to be very sensitive, detecting human rhinovirus (HRV)-EL and HRV-2 at titres as low as 10(1.8) TCID50 100 microliter-1 and less than 10(1)TCID50 100 microliter -1, respectively. Furthermore, when 57 different human rhinovirus serotypes were tested in both the HRV-EL and HRV-2 ELISA systems a total of 49 (86%) were found to be cross-reactive. Of 36 clinical specimens tested by virus isolation, cell-culture-amplified (CCA) ELISA, and direct ELISA, 15 were positive by isolation, 11 by CCA-ELISA, and 11 by direct ELISA. The overall correlation of the CCA and direct ELISA techniques with virus isolation was found to be 88.9% and 66.7%, respectively. The present study demonstrates that the ELISA system developed is a sensitive technique for the diagnosis of rhinovirus infections.

Antigens, Viral↗
PubMed1988

Evaluation of an enzyme-linked immunosorbent assay that measures rhinovirus-specific antibodies in human sera and nasal secretions.

Rhinovirus-specific antibodies have traditionally been detected by their ability to neutralise the homologous rhinovirus serotype in tissue culture. Recently, however, we have described an enzyme-linked immunosorbent assay that detects rhinovirus-specific antibodies in sera and nasal secretions [Barclay and Al-Nakib, 1987]. Here we describe an evaluation of the ELISA in a study involving 71 adult volunteers inoculated intranasally with human rhinovirus type 2 (HRV-2). Pre- and post-inoculation serum samples and pre-inoculation nasal washings were tested for the presence of HRV-2-specific antibodies by ELISA. Such antibodies were associated with protection against infection when present locally in nasal secretions, but when also present in the serum they were associated with protection against both infection and the development of illness. The antibody concentrations showed strong correlation with each other and with that of antibodies detected by the neutralisation test. Following HRV-2 infection, rises in HRV-2-specific IgA in sera detected by ELISA occurred more frequently than rises in neutralising antibody. These results suggest that the ELISA is a sensitive and reliable indicator of recent infection, as well as a predictor of homologous immune status.

Adult↗
PubMed1989

Amplification of rhinovirus specific nucleic acids from clinical samples using the polymerase chain reaction.

We describe a novel method for the detection of human rhinoviruses in clinical samples, using the polymerase chain reaction. Two synthetic oligonucleotide primers were produced that bind in the 5' noncoding region of all rhinovirus serotypes tested, about 350 nucleotides apart, and were used to prime polymerase chain reaction amplification of the intervening stretch of DNA. The product of this reaction, which can be clearly visualized by gel electrophoresis, is a discrete 380 bp band, the occurrence of which is diagnostic of the presence of a rhinovirus in the clinical sample analysed. The technique, which is rapid, sensitive, and reliable, has been used successfully for all the different rhinovirus serotypes tested to date in our laboratory. However, the sensitivity of detection is greatly dependent on the inclusion of both tRNA and vanadyl complexes during the viral RNA extraction process. Using this technique, under optimal conditions, we were able to detect virus in clinical samples with titres as low as TCID50 10(2.5).

Base Sequence↗
PubMed1994

Rapid culture-amplified immunofluorescent test for the detection of human rhinoviruses in clinical samples: evidence of a common epitope in culture.

Ohio HeLa cells in multichamber slides were inoculated with nasal samples from patients presenting with common cold symptoms and incubated at 33 degrees C with gentle shaking for 48 hours. The cultures were fixed with cold acetone, and viral antigens were detected by immunofluorescence using an antirhinovirus type 2 (HRV-2) polyclonal serum. Of 158 samples, 58 (36.7%) and 57 (36%) were positive for HRV by virus isolation (confirmed by acid lability test) and by culture-amplified immunofluorescent (CAIF) test, respectively. The correlation between the two tests was highly significant (P = 0.0001). Nasal washings or nasal/throat swabs were equally suitable for detecting virus by isolation but not by CAIF. On the other hand, nasal washings were better than nasal/throat swabs for detecting HRV by CAIF. In an ELISA system, the polyclonal anti-HRV-2 serum recognized a rhinovirus antigen expressed in situ within 48 hr postinfection by all the 11 HRV serotypes investigated. However, 60 hr postinfection, the anti-HRV-2 serum recognized only homologous and closely related HRV antigens. These results suggest that a rhinovirus "common" antigen may be expressed some 48 hr after infection of Ohio HeLa cells with rhinoviruses. The CAIF test provides a sensitive, rapid and reliable procedure to detect wild-type rhinovirus infection as well as a clear alternative to detection by isolation.

Antigens, Viral↗
PubMed2004

Persistence of rhinovirus and enterovirus RNA after acute respiratory illness in children.

The persistence of rhinovirus and enterovirus RNAs was studied in the nasal secretions of children with acute expiratory wheezing (median age: 1.7 years). On admission, 84 samples from 161 (52%) children admitted to hospital were positive by reverse transcriptase-polymerase chain reaction (RT-PCR), which detects rhino- and enteroviruses simultaneously. Of the samples, 26 (16%) were positive for rhinovirus, 29 (18%) enterovirus and 29 (18%) nontypable rhino-enterovirus. After 2 weeks, 16 of these 84 (19%) samples were still positive. Rhinovirus RNA remained positive in 13 of 26 (50%) cases, whereas enterovirus RNA remained positive only in 1 of 29 (3%) cases (P=0.0001). Respiratory symptoms at 2 weeks or systemic glucocorticoid treatment during hospital stay were not related to the persistence of viral RNA. After 5 weeks, only one sample remained PCR-positive. Thirteen of the 79 (16%) asymptomatic control children were PCR-positive for respiratory picornavirus. Five of the 13 (38%) PCR-positive children developed respiratory symptoms in the following week. The study shows that after the onset of symptomatic respiratory infection enterovirus RNA may take 2-3 weeks and rhinovirus RNA 5-6 weeks to disappear from nasal mucus.

Adolescent↗
PubMed2000

Structure of human rhinovirus serotype 2 (HRV2).

Human rhinoviruses are classified into a major and a minor group based on their binding to ICAM-1 or to members of the LDL-receptor family, respectively. They can also be divided into groups A and B, according to their sensitivity towards a panel of antiviral compounds. The structure of human rhinovirus 2 (HRV2), which uses the LDL receptor for cell attachment and is included in antiviral group B, has been solved and refined at 2.6 A resolution by X-ray crystallography to gain information on the peculiarities of rhinoviruses, in particular from the minor receptor group. The main structural differences between HRV2 and other rhinoviruses, including the minor receptor group serotype HRV1A, are located at the internal protein shell surface and at the external antigenic sites. In the interior, the N termini of VP1 and VP4 form a three-stranded beta-sheet in an arrangement similar to that present in poliovirus, although myristate was not visible at the amino terminus of VP4 in the HRV2 structure. The betaE-betaF loop of VP2, a linear epitope within antigenic site B recognized by monoclonal antibody 8F5, adopts a conformation considerably different from that found in the complex of 8F5 with a synthetic peptide of the same sequence. This either points to considerable structural changes impinged on this loop upon antibody binding, or to the existence of more than one single conformation of the loop when the virus is in solution. The hydrophobic pocket of VP1 was found to be occupied by a pocket factor apparently identical with that present in the major receptor group virus HRV16. Electron density, consistent with the presence of a viral RNA fragment, is seen stacked against a conserved tryptophan residue.

Antibodies, Viral↗
PubMed1979

Rhinoviruses: kinetics of ultraviolet inactivation and effects of UV and heat on immunogenicity.

The kinetics of ultraviolet inactivation for two human rhinoviruses and poliovirus were compared. No major differences in the rates of ultraviolet inactivation were detectable. All viral preparations inactivated by ultraviolet irradiation induced neutralizing antibody in guinea pigs. In contrast, when guinea pigs were immunized with a heat inactivated rhinovirus preparation, little or no neutralizing antibody was elicited. Immune electron microscopy of the heated rhinovirus preparations revealed the presence of particles resembling empty capsids. These results suggest that rhinoviruses and enteroviruses are affected in a similar manner when subjected to ultraviolet or heat inactivation.

Antibodies, Viral↗
PubMed1990

A novel method of typing rhinoviruses using the product of a polymerase chain reaction.

At present rhinoviruses are detected and serotyped in tissue cultures, a slow and laborious process. Previously we have described how the polymerase chain reaction can be used as a rapid method for detecting the presence of a rhinovirus, or enterovirus, in clinical samples without the need to culture. Here we describe a new method which uses the product of the polymerase chain reaction to determine the type of the rhinovirus. The technique is rapid and simple and should eventually greatly facilitate studies on rhinovirus infections.

Gene Amplification↗