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PubMed1995

Complete sequence of the RNA genome of human rhinovirus 16, a clinically useful common cold virus belonging to the ICAM-1 receptor group.

We report here the complete nucleotide sequence and predicted polyprotein sequence of HeLa cell-adapted human rhinovirus 16 (HRV16). This virus is more suitable than human rhinovirus 14 (HRV14) for clinical studies, and its growth and physical properties are favorable for biochemical and crystallographic analysis. The complete message-sense RNA genome of HRV16 is composed of 7124 bases, not including the poly(A) tail. An open reading frame, extending from base 626 to 7084 predicts a polyprotein containing 2152 amino acid residues. Comparison with other rhinovirus sequences shows HRV16 is much more representative of human rhinoviruses than HRV14. No apparent relationship was found between receptor group and amino acid sequence in VP1, the capsid protein bearing the binding site for the intercellular adhesion molecule-1 (ICAM-1) in both HRV14 and HRV16.

Base Sequence↗
PubMed2007

The cold case: are rhinoviruses perfectly adapted pathogens?

Rhinoviruses, which cause common cold, belong to the Picornaviridae family, small non-enveloped viruses (diameter 15-30 nm) containing a single-stranded RNA genome (about 7 kb). Over 100 different rhinoviral serotypes have been identified thus far, establishing rhinoviruses as the most diverse group of Picornaviridae. Based on receptor binding properties, rhinoviruses are divided into two classes: the major group binding to intracellular adhesion molecule-1 and the minor group binding to the very low density lipoprotein receptors. Interactions between virus and the receptor molecules cause a conformational change in the capsid, which is a prerequisite for viral uptake. Rhinoviruses trigger a chemokine response upon infection that may lead to exacerbation of the symptoms of common cold, i.e. asthma and inflammation. The following review aims to summarize the knowledge about rhinoviral infections and discusses therapeutical approaches against this almost perfectly adapted pathogen.

Antiviral Agents↗
PubMed1992

Model for the differential stabilities of rhinovirus and poliovirus to mild acidic pH, based on electrostatics calculations.

Previous calculations of electrostatic interactions in the rhinovirus capsid have identified a subset of histidine residues, paired with lysine or arginine, that may be involved in pH-induced conformational changes related to viral uncoating. Further calculations with the finite difference method, accounting for the dielectric environment of the ionizable groups, suggest that charge burial in the crystal conformation will prevent protonation of these histidine residues in the pentamer-pentamer interface. Calculations with a modelled pentamer-pentamer interface in which three beta-strands are removed recover mildly acidic pKa values for the histidines. These results are discussed in the context of the structural interactions of these three beta-strands, which form a beta-sheet extension from the rest of the capsid, and with regard to the conformation of the homologous beta-sheet extension in poliovirus, which also possesses homologous histidine-lysine/arginine pairs. A model is developed in which the structural stability of the beta-sheet extension is related to the difference in acid stability of rhinovirus and poliovirus. It is suggested that, for poliovirus prior to cell receptor binding, the beta-sheet extension is stable at pH 3, the pentamer-pentamer interface histidines remain buried, and the virus is acid-stable. Cell receptor binding of poliovirus destabilizes the beta-sheet extension and the acid lability that is proposed to result could be involved in viral uncoating. For rhinovirus it is suggested that the observed conformational change in the absence of cell receptor binding involves a further acidic pH-activated process or conformational fluctuations that rearrange the beta-sheet extension and expose the pentamer-pentamer interface histidine residues to the acidic medium. Sequence analysis and electrostatics calculations reveal an aspartic acid in the beta-sheet extension that may have different pKa values in rhinovirus and poliovirus.

Amino Acid Sequence↗
PubMed1991

A comparative test of fifteen compounds against all known human rhinovirus serotypes as a basis for a more rational screening program.

A systematic evaluation of 15 rhinovirus capsid-binding agents against all 100 serotyped human rhinoviruses revealed the existence of two virus groups, based upon differential susceptibility to antiviral compounds. Elongated and short-chained compounds preferentially inhibited groups A and B. The positions of the rhinoviruses within a map derived from a multivariate analysis allow for the selection of a panel of 17 rhinoviruses, for which the median antiviral inhibitory value against them will accurately predict the median value against 100 serotypes. This rationalizes the search for broad-spectrum capsid-binding antirhinovirus drugs, or combinations of drugs with complementary spectra that may be necessary to effectively inhibit both type A and type B viruses.

Antiviral Agents↗
PubMed1993

The structure of human rhinovirus 16.

BACKGROUND: Rhinoviruses and the homologous polioviruses have hydrophobic pockets below their receptor-binding sites, which often contain unidentified electron density ('pocket factors'). Certain antiviral compounds also bind in the pocket, displacing the pocket factor and inhibiting uncoating. However, human rhinovirus (HRV)14, which belongs to the major group of rhinoviruses that use intercellular adhesion molecule-1 (ICAM-1) as a receptor, has an empty pocket. When antiviral compounds bind into the empty pocket of HRV14, the roof of the pocket, which is also the floor of the receptor binding site (the canyon), is deformed, preventing receptor attachment. The role of the pocket in viral infectivity is not known. RESULTS: We have determined the structure of HRV16, another major receptor group rhinovirus serotype, to atomic resolution. Unlike HRV14, the pockets contain electron density resembling a fatty acid, eight or more carbon atoms long. Binding of the antiviral compound WIN 56291 does not cause deformation of the pocket, although it does prevent receptor attachment. CONCLUSIONS: We conjecture that the binding of the receptor to HRV16 can occur only when the pocket is temporarily empty, when it is possible for the canyon floor to be deformed downwards into the pocket. We further propose that the role of the pocket factor is to stabilize virus in transit from one host cell to the next, and that binding of ICAM-1 traps the pocket in the empty state, destabilizing the virus as required for uncoating.

Amino Acid Sequence↗
PubMed2006

Human rhinovirus in bronchial epithelium of infants with recurrent respiratory symptoms.

BACKGROUND: Human rhinoviruses (HRVs) are a common cause of upper respiratory tract infections. There is growing evidence that HRVs are also important in lower respiratory tract infections and often induce asthma exacerbations. OBJECTIVE: We evaluated the presence of HRV in the lower respiratory tract by obtaining bronchial biopsies from infants with recurrent asthmalike respiratory symptoms. METHODS: A total of 201 steroid-naive infants age 3 to 26 months with recurrent respiratory symptoms for at least 4 weeks within the preceding 2 months were studied for lung function using body plethysmography. Bronchoscopy was performed in 68 children, and bronchial biopsies were available from 59 infants for HRV detection with in situ hybridization. RESULTS: Human rhinovirus was detected in 21 of 47 (45%) specimens. Abnormal lung function (decreased airways conductance) was found in 18 of 21 (86%) HRV(+) infants and in 15 of 26 (58%) HRV(-) infants (P = .037). Occurrence of a respiratory infection in the 6 weeks preceding bronchoscopy correlated with HRV positivity (P = .036). CONCLUSION: Human rhinovirus is frequently found in the lower airways in infants with recurrent respiratory symptoms, and the majority of these HRV(+) infants also showed increased airway resistance. CLINICAL IMPLICATIONS: Human rhinovirus is a common pathogen causing upper and lower respiratory symptoms. Follow-up of these infants will reveal whether the presence of HRV in the bronchial biopsy and abnormal lung function with recurrent respiratory symptoms predicts subsequent asthma.

Asthma↗
PubMed1982

Concurrent outbreaks of rhinovirus and respiratory syncytial virus in an intensive care nursery: epidemiology and associated risk factors.

An outbreak of viral respiratory disease occurred in eight infants in a neonatal intensive care unit during the 1980 winter respiratory season. Four infections with respiratory syncytial virus and four infections with rhinovirus were identified. Epidemiologic investigation revealed that viral respiratory infection was significantly associated with intubation with orotracheal tubes (P = 0.001), with the presence of both a nasal feeding tube plus an orotracheal tube together (P = 0.007), and with assisted ventilation (P = 0.009) when compared to uninfected controls. Twenty-seven of 85 (30.6%) personnel working in the unit at the time of the outbreak reported a history of upper respiratory illness during the week prior to the outbreak, and 46 (54.1%) of them had had contact with patients in areas of the hospital where patients infected with RSV and rhinovirus were housed. The data suggest that both viruses were transmitted to the babies by hospital personnel. Rhinoviruses can be nosocomial pathogen in neonates with compromised pulmonary function, and the clinical presentation of rhinovirus infection in neonates may be difficult to distinguish from that produced by RSV.

Cross Infection↗
PubMed2000

Anti-rhinovirus activity of 3-methylthio-5-aryl-4-isothiazolecarbonitrile derivatives.

A series of 3-methylthio-5-aryl-4-isothiazolecarbonitriles has been evaluated as anti rhinovirus agents against a panel of 17 representative human rhinovirus (HRV) serotypes, belonging to both A and B groups. No anti rhinovirus activity was detected for 3-methylthio-5-phenyl-4-isothiazolecarbonitrile (IS-2). Isothiazole derivatives with bulky substituents (O-Bn or O-But groups) on the para position of the phenyl ring were the most effective compounds of this series. In fact, a reduction in virus-induced cytopathogenicity was demonstrated for the O-Bn substituted IS-50 compound against the majority (88%) of the rhinoviruses tested, whereas the compound with an O-Ts group (IS-44) was found to be a specific inhibitor of group B serotypes, exhibiting the lowest IC(50) against HRVs type 2, 85 and 89. Our studies on the mechanism of action of IS-44 demonstrated that it prevents the thermal inactivation of HRV 2 infectivity, probably due to a conformational shift in the viral capsid and a decrease in affinity for the cellular receptor, resulting in an inhibition of attachment of the virions.

Antiviral Agents↗
PubMed1999

The role of oxidative stress in rhinovirus induced elaboration of IL-8 by respiratory epithelial cells.

A direct correlation has been reported between the severity of symptoms associated with rhinovirus infection and the concentration of interleukin-8 in nasal secretions. The purpose of these studies was to examine the mechanism of rhinovirus-induced IL-8 elaboration. Rhinovirus infection induced oxidative stress in Beas-2b cells and the concentration of H2O2 in supernatant media from rhinovirus challenged cells was 12.5 +/- 6.1 microM 1 h after challenge compared to 0.7 +/- 0.3 microM in supernatant from control cells. N-acetyl cysteine inhibited RV-induced NF-kappaB activation and IL-8 elaboration. IL-8 concentrations were 36 +/- 2 pg/ml and 10 +/- 1 pg/ml 6 h after virus challenge in untreated and NAC-treated (30 mM NAC) cells, respectively. Despite the effects of NAC on IL-8 elaboration and NF-kappaB activation, RV stimulated increases in supernatant H2O2 were not altered by NAC. These data suggest that RV stimulation of IL-8 in respiratory epithelium is mediated through production of oxidative species and the subsequent activation of NF-kappaB.

Acetylcysteine↗
PubMed2003

Rhinovirus increases human beta-defensin-2 and -3 mRNA expression in cultured bronchial epithelial cells.

Human beta-defensins (hBDs) are antimicrobial peptides that play important roles in host defense against infection, inflammation and immunity. Previous studies showed that micro-organisms and proinflammatory mediators regulate the expression of these peptides in airway epithelial cells. The aim of the present study was to investigate the modulation of expression of hBDs in cultured primary bronchial epithelial cells (PBEC) by rhinovirus-16 (RV16), a respiratory virus responsible for the common cold and associated with asthma exacerbations. RV16 was found to induce expression of hBD-2 and -3 mRNA in PBEC, but did not affect hBD-1 mRNA. Viral replication appeared essential for rhinovirus-induced beta-defensin mRNA expression, since UV-inactivated rhinovirus did not increase expression of hBD-2 and hBD-3 mRNA. Exposure to synthetic double-stranded RNA (dsRNA) molecule polyinosinic:polycytidylic acid had a similar effect as RV16 on mRNA expression of these peptides in PBEC. In line with this, PBEC were found to express TLR3, a Toll-like receptor involved in recognition of dsRNA. This study shows that rhinovirus infection of PBEC leads to increased hBD-2 and hBD-3 mRNA expression, which may play a role in both the uncomplicated common cold and in virus-associated exacerbations of asthma.

Bronchi↗
PubMed2003

Human rhinoviruses.

Human rhinoviruses are the most important causative agents of upper respiratory infections and are also implicated in more severe clinical entities. Although often present, very little is known about human rhinoviruses. Molecular methods have been used in the classification of this large group of viruses into two separate clades. In addition, one known serotype was found to be a member of enterovirus group D. Laboratory diagnosis of human rhinovirus infection is based on reverse transcription polymerase chain reaction methods or the more tedious virus culture but a rapid "bedside" method is unavailable. Anti-rhinoviral therapy has been under extensive study over the past few decades but symptomatic treatment of the common cold is still the only useful approach in clinical use. More data on circulating human rhinovirus strains would facilitate both detection and treatment of these common pathogens.

Acute Disease↗
PubMedDate not supplied

Different rhinovirus serotypes neutralized by antipeptide antibodies.

Recently, Rossman et al. have described the three-dimensional structure of a human rhinovirus. A possible host cell surface receptor binding site was identified with a cleft on each icosahedral face. Two highly conserved amino-acid sequences found in rhino-, polio-, and foot-and-mouth disease (FMD) viruses are located near the base of this site and could be important in maintaining its topology. We have prepared site-specific antibodies to two synthetic peptides which include these sequences. The antibodies bind to the predicted capsid proteins of rhinovirus and neutralize approximately 60% of 48 rhinovirus serotypes tested. These results could provide a route to a rhinovirus vaccine effective against most of the numerous serotypes of this virus.

Antibodies, Viral↗
PubMed1999

Rhinovirus infections: induction and modulation of airways inflammation in asthma.

There is renewed interest in the role of respiratory virus infections in the pathogenesis of asthma and in the development of exacerbations in pre-existing disease. This is due to the availability of new molecular and experimental tools. Circumstantial evidence points towards a potentially causative role as well as to possibly protective effects of certain respiratory viruses in the cause of allergic asthma during early childhood. In addition, it now has become clear that exacerbations of asthma, in children as well as adults, are mostly associated with respiratory virus infections, with a predominant role of the common cold virus: rhinovirus. Careful human in vitro and in vivo experiments have shown that rhinovirus can potentially stimulate bronchial epithelial cells to produce pro-inflammatory chemokines and cytokines, may activate cholinergic- or noncholinergic nerves, increase epithelial-derived nitric oxide synthesis, upregulate local ICAM-1 expression, and can lead to nonspecific T-cell responses and/or virus-specific T-cell proliferation. Experimental rhinovirus infections in patients with asthma demonstrate features of exacerbation, such as lower airway symptoms, variable airways obstruction, and bronchial hyperresponsiveness, the latter being associated with eosinophil counts and eosinophilic cationic protein levels in induced sputum. This suggests that multiple cellular pathways can be involved in rhinovirus-induced asthma exacerbations. It is still unknown whether these mechanisms are a distinguishing characteristic of asthma. Because of the limited effects of inhaled steroids during asthma exacerbations, new therapeutic interventions need to be developed based on the increasing pathophysiological knowledge about the role of viruses in asthma.

Adult↗
PubMed1985

Molecular cloning and complete sequence determination of RNA genome of human rhinovirus type 14.

The genomic RNA of human rhinovirus type 14 was cloned in Escherichia coli and the complete nucleotide sequence was determined. The RNA genome is 7212 nucleotides long. A single large open reading frame of 6536 nucleotides was identified, which starts at nucleotide 678 and ends 47 nucleotides from the 3' end of the RNA genome. Comparisons of the specified proteins with those of other picornaviruses showed a striking homology (44-65%) between rhinovirus and poliovirus. The rhinovirus genomic RNA is rich in adenosine (32.1%) and strongly favors an adenosine or uridine in the third position of codons. The predicted map locations of all the rhinovirus structural and non-structural proteins and their proposed proteolytic cleavage sites are described.

Amino Acid Sequence↗
PubMed1987

Evolutionary relationships within the human rhinovirus genus: comparison of serotypes 89, 2, and 14.

The complete nucleotide sequence of the genome of human rhinovirus type 89 was determined from the cDNA that had been cloned into Escherichia coli. The genome is 7152 nucleotides long and contains a single large open reading frame of 2164 codons. Translation commences at position 619 and ends 42 nucleotides before the poly(A) tract. The positions of three proteolytic cleavage sites in the polyprotein were determined by N-terminal amino acid sequencing of the capsid proteins; the remainder were predicted from comparisons with other picornaviruses. Extensive similarity between the derived amino acid sequences of human rhinovirus types 89 and 2 was found, whereas the similarity between human rhinovirus types 89 and 14 was considerably less. It is apparent that human rhinoviruses may be more closely related than has been previously thought.

Amino Acid Sequence↗
PubMed1992

Development of common cold symptoms following experimental rhinovirus infection is related to prior stressful life events.

Previous studies of rhinovirus infection indicate that about one third of the persons with confirmed viral infection do not show evidence of cold symptoms. Factors that determine which infected individuals will develop colds are not known. Using a rhinovirus inoculation protocol, the authors explored the possible role of recent life events, current mood, and perceived stress in the development of symptoms in individuals known to be infected. As part of a larger study, 17 subjects were exposed to a rhinovirus and were individually isolated for 5 consecutive days; cold symptoms, mucus weights, and tissue use were monitored on a daily basis during this period. Although all 17 subjects had confirmed rhinovirus infection, only 12 subjects developed clinical colds, as indicated by self-reported symptoms and by objective symptom indices. The average number of reported major life events for the previous year was significantly higher for those who developed colds than for those who did not (p < .05). Measures of affect and perceived stress before the inoculation were not different for those who did and did not develop colds. Complementing recent research demonstrating psychosocial influences on experimental infection rates, these results provide evidence that the development of cold symptomatology in experimentally infected individuals is related to prior life events.

Adolescent↗
PubMed2002

Effect of rhinovirus challenge on antioxidant enzymes in respiratory epithelial cells.

The host inflammatory response appears to be an important contributor to the pathogenesis of human viral respiratory illness. Virus-induced oxidative stress appears to mediate an early phase of elaboration of the proinflammatory cytokine interleukin-8 by respiratory epithelial cells. The purpose of these studies was to determine if virus-induced alterations in either the expression or function of antioxidant enzymes contributes to the cellular oxidative stress following rhinovirus challenge. The activities of Mn superoxide dismutase (MnSOD), catalase and glutathione peroxidase (GPX) were not significantly changed by rhinovirus challenge. CuZn superoxide dismutase (CuZnSOD) activity six hours after challenge was 2.55 +/- 0.56 U/mg protein in rhinovirus-challenged cells compared to 1.16 +/- 0.54 U/mg protein in control cells (p = 0.029). This increased activity was associated with a concomitant increase in CuZnSOD mRNA and protein concentration. These data suggest that rhinovirus-induced changes in the host cell redox state that result in the early elaboration of interleukin-8 are not mediated by inhibition of either the expression or function of these antioxidant enzymes.

Antioxidants↗
PubMed1998

Association between interleukin-8 concentration in nasal secretions and severity of symptoms of experimental rhinovirus colds.

The purpose of this study was to examine the association between experimental rhinovirus infection and the elaboration of interleukin-8 (IL-8) into nasal secretions of volunteers and to determine the effect of pentoxifylline on IL-8 elaboration and rhinovirus-associated common cold symptoms. Fifty-four subjects with experimental rhinovirus infections and 20 sham-inoculated subjects were studied. Pentoxifylline had no effect on rhinovirus-induced symptoms or nasal-secretion IL-8 concentrations. IL-8 concentrations were significantly greater in nasal secretions from infected symptomatic subjects than in those from infected asymptomatic or sham-challenged subjects on days 2-4 after virus challenge. In infected subjects, there was significant rank correlation between nasal obstruction severity, rhinorrhea severity, and nasal-wash albumin concentrations and the change in IL-8 concentration from baseline on days 2-4 after virus challenge.

Adolescent↗