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PubMed2000

The common cold as a trigger of asthma.

The common cold is a viral disease with predominant symptoms from the upper airways. Rhinovirus is the most important common cold virus, and rhinovirus infection is predominantly transmitted by direct contact (nasal secretion-hand (object)-hand-mucous membrane in eye and nose). The viral disease results in the release of IL-8 from nasal epithelial cells, causing a neutrophil-dominated inflammation in the nose. The biochemical mediators, causing nasal symptoms, have not yet been identified. A common cold is the most important cause of exacerbations of asthma in children and also in adults. The rhinovirus infection induces airway inflammation, bronchial hyperresponsiveness and asthma symptoms. However, the mode of action of the virus-induced inflammation on the asthma disease is poorly understood. As a routine, physicians give oral corticosteroid and increase the dosage of inhaled corticosteroid during a common cold-induced exacerbation of asthma, but there do not seem to be any placebo-controlled trials in support of this practice.

Asthma↗

PubMed2003

Rhinoviruses in the pathogenesis of asthma.

Using sensitive diagnostic methodologies, epidemiologic studies during the past decade have allowed the identification of human rhinoviruses (RVs), generally recognized as "common cold viruses," as major asthma precipitants. This association was further established by evaluating the impact of RV infection in airway obstruction and inflammation during naturally acquired or experimentally induced RV colds. There is now strong evidence that RVs can infect and propagate not only in the upper but also in the lower airways. Bronchial and pulmonary epithelia infected by RVs are rich sources of inflammatory mediators, which may initiate or augment airway inflammation and obstruction. Furthermore, in an atopic environment, responses to the virus are skewed by and toward an "atopic," Th2-like balance, which may further enhance inflammation and exacerbate asthma.

Asthma↗

PubMed1998

Activation of antiviral protein kinase leads to immunoglobulin E class switching in human B cells.

An epidemiologic association between viral infections and the onset of asthma and allergy has been documented. Also, evidence from animal and human studies has suggested an increase in antigen-specific immunoglobulin E (IgE) production during viral infections, and elevated levels of IgE are characteristic of human asthma and allergy. Here, we provide molecular evidence for the roles of viral infection and of activation of the antiviral protein kinase (PKR) (double-stranded-RNA [dsRNA]-activated protein kinase) in the induction of IgE class switching. The presence of dsRNA, a known component of viral infection and an activator of PKR, induced IgE class switching as detected by the expression of germ line epsilon in the human Ramos B-cell line. Furthermore, dsRNA treatment of Ramos cells resulted in the activation of PKR and in vivo activation of the NF-kappaB complex. Interestingly, infection of Ramos cells with rhinovirus (common cold virus) serotypes 14 and 16 resulted in the induction of germ line epsilon expression. To further evaluate the role of PKR in the viral induction of IgE class switching, we infected Ramos cells with two different vaccinia virus (cowpox virus) strains. Infection with wild-type vaccinia virus failed to induce germ line epsilon expression; however, a deletion mutant of vaccinia virus (VP1080) lacking the PKR-inhibitory polypeptide E3L induced the expression of germ line epsilon. Collectively, the results of our study define a common molecular mechanism underlying the role of viral infections in IgE class switching and subsequent induction of IgE-mediated disorders such as allergy and asthma.

B-Lymphocytes↗

PubMed1999

The impact of personality on the reporting of unfounded symptoms and illness.

This study examined the role of personality in the reporting of symptoms and illness not supported by underlying pathology. After assessment of the Big Five personality factors, 276 healthy volunteers were inoculated with a common cold virus. On each of the following 5 days, objective indicators of pathology, self-reported symptoms, and self-reported illness onset were assessed. Neuroticism was directly associated with reports of unfounded (without a physiological basis) symptoms in individuals at baseline and postinoculation in those with and without colds. Neuroticism was also indirectly associated with reports of unfounded illness through reports of more symptoms. Openness to Experience was associated with reporting unfounded symptoms in those with verifiable colds, whereas Conscientiousness was associated with reporting unfounded illness in those who were not ill.

Adolescent↗

PubMed1998

Types of stressors that increase susceptibility to the common cold in healthy adults.

Two-hundred seventy-six volunteers completed a life stressor interview and psychological questionnaires and provided blood and urine samples. They were then inoculated with common cold viruses and monitored for the onset of disease. Although severe acute stressful life events (less than 1 month long) were not associated with developing colds, severe chronic stressors (1 month or longer) were associated with a substantial increase in risk of disease. This relation was attributable primarily to under- or unemployment and to enduring interpersonal difficulties with family or friends. The association between chronic stressors and susceptibility to colds could not be fully explained by differences among stressed and nonstressed persons in social network characteristics, personality, health practices, or prechallenge endocrine or immune measures.

Adolescent↗

PubMed1993

Negative life events, perceived stress, negative affect, and susceptibility to the common cold.

After completing questionnaires assessing stressful life events, perceived stress, and negative affect, 394 healthy Ss were intentionally exposed to a common cold virus, quarantined, and monitored for the development of biologically verified++ clinical illness. Consistent with the hypothesis that psychological stress increases susceptibility to infectious agents, higher scores on each of the 3 stress scales were associated with greater risk of developing a cold. However, the relation between stressful life events and illness was mediated by a different biologic process than were relations between perceived stress and illness and negative affect and illness. That these scales have independently relations with illness and that these relations are mediated by different processes challenges the assumption that perceptions of stress and negative affect are necessary for stressful life events to influence disease risk.

Adaptation, Psychological↗

PubMed2000

Detection of rhinovirus in induced sputum at exacerbation of chronic obstructive pulmonary disease.

Common colds are associated with exacerbations of chronic obstructive pulmonary disease (COPD). However, the role of the common cold virus (human rhinovirus) in the production of symptoms and lower airway inflammation at COPD exacerbation is unknown. Thirty three patients with moderate-to-severe COPD were seen at baseline, when the number of chest infections in the previous year was noted, and acutely at COPD exacerbation. Within 48 h after the onset of the exacerbation and at baseline, nasal aspirates and induced sputum were taken for rhinovirus reverse transcriptase polymerase chain reaction (RT-PCR) analysis and determination of cytokine levels. Symptoms, recorded on diary cards, were noted and forced expiratory volume in one second (FEV1) and forced vital capacity (FVC) measured. At exacerbation, mean FEV1 and FVC fell significantly from baseline (p<0.001). Ten of 43 exacerbations were associated with rhinovirus infection, detected in induced sputum. In four of these, nasopharyngeal samples contained no detectable rhinovirus. All baseline samples were negative for rhinovirus. The simultaneous presence of increased nasal discharge/nasal congestion (in 26 of the 43 exacerbations) and increased sputum (29 exacerbations) was strongly associated with the presence of rhinovirus (odds ratio 6.15; p=0.036). Total symptom scores were greater for rhinovirus as compared to nonrhinovirus exacerbations (p=0.039). Median baseline sputum interleukin-6 levels rose from 90.2 to 140.3 pg x mL(-1) at exacerbation (p=0.005); the change was greater in the presence of rhinovirus infection (p=0.008). Rhinovirus infection can be detected at chronic obstructive pulmonary disease exacerbation. This is associated with elevation of lower airway interleukin-6 levels, which may mediate lower airway symptom expression during chronic obstructive pulmonary disease exacerbations.

Aged↗

PubMed2001

A model of viral wheeze in nonasthmatic adults: symptoms and physiology.

Episodic wheezing associated with viral infections of the upper respiratory tract (URT) is a common problem in young children but also occurs in adults. It is hypothesized that an experimental infection with human coronavirus (HCoV), the second most prevalent common cold virus, would cause lower respiratory tract (LRT) changes in adults with a history of viral wheeze. Twenty-four viral wheezers (15 atopic) and 19 controls (seven atopic) were inoculated with HCoV 229E and monitored for the development of symptoms, changes in airway physiology and provocative concentration of methacholine causing a 20% fall in forced expiratory volume in one second (FEV1) (PC20). At baseline, viral wheezers were similar to controls in PC20 (mean+/-SD log2PC20: 5.1+/-1.9 and 5.8+/-1.4 g x L(-1), respectively) but had a lower FEV1 than controls (mean+/-SD 85.8+/-11.4 and 95.6+/-13.2% predicted, respectively p < 0.05). Nineteen viral wheezers and 11 controls developed colds. Viral wheezers with colds reported significantly more URT symptoms than controls (median scores (interquartile range): 24 (10-37) and 6 (4-15), respectively p = 0.014). Sixteen viral wheezers and no controls reported LRT symptoms (wheeze, chest tightness and shortness of breath). The viral wheezers with colds had small (3-4%) reductions in FEV1 and peak expiratory flow on days with LRT symptoms (days 3-6), but a progressive reduction in PC20 from baseline on days 2, 4 and 17 after inoculation (by 0.82, 1.35 and 1.82 doubling concentrations, respectively). The fall in PC20 affected both atopic and nonatopic subjects equally. There were no changes in FEV1 or PC20 in controls. An adult model of viral wheeze that is independent of atopy and therefore, of classical atopic asthma was established.

Adult↗

PubMed1996

Reversal of malignancy by the adenovirus E1a gene.

Tumor suppressor genes such as Rb and p53 usually kill tumor cells when overexpressed ectopically. This is a consequence of their normal cell cycle regulatory functions. By contrast, the E1a gene of adenovirus, a common cold virus, converts tumor cells into viable normal cells. This has advantages for investigation and control of cancer. In particular, E1a is a master programmer of the epithelial phenotype. This provides a new tool for understanding the molecular basis of the epithelial-mesenchymal transition, and how it goes awry in cancer cells. Furthermore, epithelial cells are sensitive to a form of apoptosis - 'anoikis' - that is induced by detachment from extracellular matrix. This property confers strict anchorage-dependence. Transcriptional programming, by E1a or the formation of cell-cell junctional complexes, programs epithelial cells to be sensitive to anoikis.

Adenovirus E1A Proteins↗

PubMed2004

Respiratory infections and asthma: current treatment strategies.

Infections such as lower respiratory illness potentially contribute to the initiation of asthma and are major factors in recurring acute exacerbations of the condition. Although typical bacterial respiratory pathogens such as Streptococcus pyogenes, Streptococcus pneumoniae and Hemophilus influenzae do not initiate asthmatic exacerbations, data from a subgroup of adults suggest a potential role for Mycoplasma pneumoniae and Chlamydia pneumoniae in the onset of asthma. Common cold viruses, predominantly respiratory syncytial virus (RSV) in young children and rhinoviruses in older children and adults, are the major causes of acute exacerbations of asthma. These exacerbations are not prevented with maintenance therapies that are used for chronic asthma, but do respond to short courses of systemic corticosteroids. There are continued attempts to produce a successful vaccine and antiviral agents for the treatment of RSV that are more effective and more practical to use than ribavirin, which is currently the only available antiviral for RSV. The prevention and treatment of rhinovirus infections have focused on the major receptor for the virus, intercellular adhesion molecule-1 (ICAM-1), which is located on respiratory epithelial cells. A multivalent, recombinant, antibody fusion protein identified as CFY196 has high avidity for ICAM-1 and has the potential to protect against rhinovirus infection. Another approach for preventing and treating rhinovirus infection uses a recombinant, soluble, truncated form of ICAM-1 in which the transmembrane and intracellular domains of the protein have been deleted. An initial clinical study on this agent demonstrated clinical efficacy in ameliorating the symptoms of experimental rhinovirus infection in volunteers, but did not significantly prevent infection.

Acute Disease↗

PubMed2005

Milk consumption does not lead to mucus production or occurrence of asthma.

There is a belief among some members of the public that the consumption of milk and dairy products increases the production of mucus in the respiratory system. Therefore, some who believe in this effect renounce drinking milk. According to Australian studies, subjects perceived some parameters of mucus production to change after consumption of milk and soy-based beverages, but these effects were not specific to cows' milk because the soy-based milk drink with similar sensory characteristics produced the same changes. In individuals inoculated with the common cold virus, milk intake was not associated with increased nasal secretions, symptoms of cough, nose symptoms or congestion. Nevertheless, individuals who believe in the mucus and milk theory report more respiratory symptoms after drinking milk. In some types of alternative medicine, people with bronchial asthma, a chronic inflammatory disease of the lower respiratory tract, are advised not to eat so-called mucus-forming foods, especially all kinds of dairy products. According to different investigations the consumption of milk does not seem to exacerbate the symptoms of asthma and a relationship between milk consumption and the occurrence of asthma cannot be established. However, there are a few cases documented in which people with a cow's milk allergy presented with asthma-like symptoms.

Animals↗

PubMed2003

RNA cleaving '10-23' DNAzymes with enhanced stability and activity.

'10-23' DNAzymes can be used to cleave any target RNA in a sequence-specific manner. For applications in vivo, they have to be stabilised against nucleolytic attack by the introduction of modified nucleotides without obstructing cleavage activity. In this study, we optimise the design of a DNAzyme targeting the 5'-non-translated region of the human rhinovirus 14, a common cold virus, with regard to its kinetic properties and its stability against nucleases. We compare a large number of DNAzymes against the same target site that are stabilised by the use of a 3'-3'-inverted thymidine, phosphorothioate linkages, 2'-O-methyl RNA and locked nucleic acids, respectively. Both cleavage activity and nuclease stability were significantly enhanced by optimisation of arm length and content of modified nucleotides. Furthermore, we introduced modified nucleotides into the catalytic core to enhance stability against endonucleolytic degradation without abolishing catalytic activity. Our findings enabled us to establish a design for DNAzymes containing nucleotide modifications both in the binding arms and in the catalytic core, yielding a species with up to 10-fold enhanced activity and significantly elevated stability against nucleolytic cleavage. When transferring the design to a DNAzyme against a different target, only a slight modification was necessary to retain activity.

Binding Sites↗

PubMed1995

Effect of rhinovirus 39 (RV-39) infection on immune and inflammatory parameters in allergic and non-allergic subjects.

The economic impact and medical complication rate of the common cold are well documented, but many of the physiological, inflammatory, and immune responses to common cold viruses have only recently been investigated. The purpose of this study was to compare selected systemic immune and inflammatory responses to experimental rhinovirus (RV)-39 challenge in seronegative allergic rhinitis and non-allergic rhinitis subjects. Peripheral blood was obtained before (baseline), during (acute), and 23 days after (convalescent) RV-39 intranasal challenge and assayed for leucocyte histamine release, serum immunoglobulins, allergen-specific IgE antibodies, plasma histamine, and platelet aggregation. All subjects were infected, as manifested by viral shedding in nasal secretions or seroconversion. RV-39 infection induced significant acute increases in serum IgE, leucocyte histamine release, and platelet aggregation, but caused no changes in serum IgG, serum IgA, serum IgM, and plasma histamine. The first change was confined to the allergic rhinitis subjects. There was no evidence that the acute rise in total serum IgE was due to an elevation of a pre-existing, pollen-specific serum IgE antibody. The results show that intranasal challenge with RV-39 induced changes in systemic immune and inflammatory parameters with a unique response pattern in allergic rhinitis subjects.

Adolescent↗

PubMed2004

Vaccination for asthma exacerbations.

Most asthma exacerbations are caused by common cold virus infections, predominantly rhinovirus infections. Full protection against repeat infections with the same rhinovirus serotype is given by serum neutralizing antibody, but cross-reactive antibody developed against other serotypes could yield partial protection and result in attenuated cold and airway symptoms. It is proposed that vaccine-mediated induction of cross-reactive antibody might not prevent rhinovirus infections but might reduce severe asthma symptoms and exacerbations.

Asthma↗

PubMed2006

Transforming growth factor-beta expression induced by rhinovirus infection in respiratory epithelial cells.

Rhinovirus infection of the lower airways is now a recognized disease, associated with bronchiolitis and asthma. The bronchial epithelial cells are the host cells when rhinovirus infection occurs in the airway. It was hypothesized that a pro-fibrotic growth factor response may occur in these infected cells, leading to production of a key transforming growth factor, TGF-beta-1. Bronchial epithelial cells were inoculated with human rhinovirus and compared at day 1, 3 and 5 to control non-infected cells. Cell culture supernatant fluid and cellular RNA were isolated. The amount of released TGF-beta protein was measured by enzyme-linked immunosorbent assay (ELISA). Expression of TGF-beta at the level of transcription was measured by polymerase chain reaction (PCR) and gel electrophoresis. The results show that at all time points studied, TGF-beta production is greater in the infected cells, as demonstrated by ELISA (P<0.05) and by semi-quantitative PCR analysis. It was concluded that bronchial epithelial cells infected with common cold virus and rhinovirus, showed higher levels of TGF-beta. The production of TGF-beta may be indicative of a normal repair mechanism to counter inflammation, or in the setting of persistent asthma, could potentially lead to increased fibrosis and collagen deposition.

Cells, Cultured↗

PubMed1986

The site of attachment in human rhinovirus 14 for antiviral agents that inhibit uncoating.

WIN 51711 and WIN 52084 are structurally related, antiviral compounds that inhibit the replication of rhino (common cold) viruses and related picornaviruses. They prevent the pH-mediated uncoating of the viral RNA. The compounds consist of a 3-methylisoxazole group that inserts itself into the hydrophobic interior of the VP1 beta-barrel, a connecting seven-membered aliphatic chain, and a 4-oxazolinylphenoxy group (OP) that covers the entrance to an ion channel in the floor of the "canyon." Viral disassembly may be inhibited by preventing the collapse of the VP1 hydrophobic pocket or by blocking the flow of ions into the virus interior.

Antiviral Agents↗

PubMed1990

Two groups of rhinoviruses revealed by a panel of antiviral compounds present sequence divergence and differential pathogenicity.

A variety of chemically different compounds inhibit the replication of several serotypes of rhinoviruses (common-cold viruses). We noticed that one of these antiviral compounds, WIN 51711, had an antiviral spectrum clearly distinctive from a consensus spectrum or other capsid-binding compounds, although all of them were shown to share the same binding site. A systematic evaluation of all known rhinovirus capsid-binding compounds against all serotyped rhinoviruses was therefore initiated. Multivariate analysis of the results revealed the existence of two groups of rhinoviruses, which we will call antiviral groups A and B. The differential sensitivity of members of these groups to antiviral compounds suggests the existence of a dimorphic binding site. The antiviral groups turned out to be a reflection of a divergence of rhinovirus serotypes on a much broader level. Similarities in antiviral spectra were highly correlated with sequence similarities, not only of amino acids lining the antiviral compound-binding-site, but also of amino acids of the whole VP1 protein. Furthermore, analysis of epidemiological data indicated that group B rhinoviruses produced more than twice as many clinical infections per serotype than group A rhinoviruses did. Rhinoviruses belonging to the minor receptor group were without exception all computed to lie in the same region of antiviral group B.

Amino Acid Sequence↗

PubMed2001

Viral evolution toward change in receptor usage: adaptation of a major group human rhinovirus to grow in ICAM-1-negative cells.

Major receptor group common cold virus HRV89 was adapted to grow in HEp-2 cells, which are permissive for minor group human rhinoviruses (HRVs) but which only marginally support growth of major-group viruses. After 32 blind passages in these cells, each alternating with boosts of the recovered virus in HeLa cells, HRV89 acquired the capacity to effectively replicate in HEp-2 cells, attaining virus titers comparable to those in HeLa cells although no cytopathic effect was observed. Several clones were isolated and shown to replicate in HeLa cells whose ICAM-1 was blocked with monoclonal antibody R6.5 and in COS-7 cells, which are devoid of ICAM-1. Blocking experiments with recombinant very-low-density lipoprotein receptor fragments and enzyme-linked immunosorbent assays indicated that the mutants bound a receptor different from that used by minor-group viruses. Determination of the genomic RNA sequence encoding the capsid protein region revealed no changes in amino acid residues at positions equivalent to those involved in the interaction of HRV14 or HRV16 with ICAM-1. One mutation was within the footprint of a very-low-density lipoprotein receptor fragment bound to minor-group virus HRV2. Since ICAM-1 not only functions as a vehicle for cell entry but has also a "catalytic" function in uncoating, the use of other receptors must have important consequences for the entry pathway and demonstrates the plasticity of these viruses.

Evolution, Molecular↗