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PubMed1972

Coronative antibody tires in sera of healthy adults and experimentally infected volunteers.

Six coronaviruses isolated in the U.S.A. have been inoculated into volunteers and all produced colds. Between 10 and 20% of infected volunteers developed heterologous antibody responses after these and other experimental infections with coronaviruses. The haemagglutination-inhibition test with the OC43 virus strain was found to detect antibody rises after infection with a variety of strains.Studies on normal adult sera taken between 1965 and 1970 revealed a high frequency of neutralizing antibody to one strain (229 E) and a frequency of HI antibody to strain OC43 which fluctuated from year to year. Complement-fixing antibodies to these two viruses were also found, revealing an apparent increase in the activity of coronaviruses in the general population of the U.K., during the winter of 1968-9.

Antibodies↗
PubMed1999

The crystal structure of coxsackievirus A9: new insights into the uncoating mechanisms of enteroviruses.

BACKGROUND: Coxsackievirus A9 (CAV9), a human pathogen causing symptoms ranging from common colds to fatal infections of the central nervous system, is an icosahedral single-stranded RNA virus that belongs to the genus Enterovirus of the family Picornaviridae. One of the four capsid proteins, VP1, includes the arginine-glycine-aspartate (RGD) motif within its C-terminal extension. This region binds to integrin alpha v beta 3, the only receptor for CAV9 to be conclusively identified to date. RESULTS: The crystal structure of CAV9 in complex with the antiviral compound WIN 51711 has been solved to 2.9 A resolution. The structures of the four capsid proteins, VP1 to VP4, resemble those of other picornaviruses. The antiviral compound is bound in the VP1 hydrophobic pocket, and it is possible that the pocket entrance contains a second WIN 51711 molecule. Continuous electron density for the VP1 N terminus provides a complete picture of the structure close to the fivefold axis. The VP1 C-terminal portion is on the outer surface of the virus and becomes disordered five-residues N-terminal to the RGD motif. CONCLUSIONS: The RGD motif is exposed and flexible in common with other known integrin ligands. Although CAV9 resembles coxsackie B viruses (CBVs), several substitutions in the areas implicated in CBV receptor attachment suggest it may recognise a different receptor. The structure along the fivefold axis provides new information on the uncoating mechanism of enteroviruses. CAV9 might bind a larger natural pocket factor than other picornaviruses, an observation of particular relevance to the design of new antiviral compounds.

Amino Acid Sequence↗
PubMed1995

Rhinovirus infection of the normal human airway.

Selected events in rhinovirus infection of the normal human airway can be regarded as occurring sequentially. Initial steps in rhinovirus pathogenesis are believed to include viral entry into the nose, mucociliary transport of virus to the posterior pharynx, and initiation of infection in ciliated and non-ciliated epithelial cells of the upper airway. Viral replication peaks on average within 48 h of initiation of infection and persists for up to 3 wk. Infection is followed by activation of several inflammatory mechanisms, which may include release or generation of interleukins, bradykinins, prostaglandins, and possibly histamine and stimulation of parasympathetic reflexes. Pathophysiologic processes are initiated, which include vasodilatation of nasal blood vessels, transudation of plasma, glandular secretion, and stimulation of nerve fibers, causing pain and triggering sneeze and cough reflexes. The resultant clinical illness is a rhinosinusitis, pharyngitis, and bronchitis, which, on average, lasts 1 wk.

Common Cold↗
PubMed1985

Tolerance of one-month intranasal interferon.

Under double-blind conditions, groups of volunteers (68 in total) were allocated at random to take intranasal solutions of placebo or one of three doses of highly purified leucocyte interferon by intranasal spray twice a day for 28 days. The highest dose would have been expected to protect against experimental colds. Treatment was discontinued because of upper respiratory symptoms as often in each of the interferon groups as in the placebo group. However, it was possible to distinguish clinically between "colds" on placebo and low-dose interferon and "reactions to treatment" on high-dose interferon. The features of the reactions to treatment were a protracted build-up of local symptoms and minor epistaxis. None of the volunteers on the high-dose interferon were thought to have a definite cold, but viruses were isolated from four out of six volunteers on low-dose interferon who had definite colds. Previous experiments had also shown this dose to be insufficient to protect against experimental rhinovirus challenge. The dose of interferon that appeared to protect against virus infection caused significant unwanted effects. It is essential to find interferon preparations with less inflammatory activity before interferon can be considered for use as a long-term prophylactic against the common cold.

Administration, Intranasal↗
PubMed2000

AG-7088 Pfizer.

Pfizer (formerly Agouron) is developing AG-7088, a peptide aldehyde that targets the human rhinovirus (HRV) 3C proteinase enzyme and has potential for the treatment of the common cold. A phase II efficacy study has been completed in healthy patients infected with the virus [318668] and in November 1999, Agouron initiated a large, double-blind, placebo-controlled trial in the US, in individuals within 36 h of experiencing cold symptoms [346362]. AG-7088 is derived from AG-6084, the development of which has been discontinued. In order to develop human rhinovirus 3C protease inhibitors with improved pharmacological properties, Agouron replaced the backbone amide moiety of the series which yielded AG-6084, with a ketomethylene isostere. Such compounds displayed slightly reduced anti-3CP inhibitory activity, but improved antiviral properties, due to increased cell membrane permeability [324627]. Compounds in which P1 lactam moieties were incorporated in lieu of an L-glutamine residue displayed significantly increased 3CP inhibition activity and improved antirhinoviral properties relative to the corresponding molecules. Of this series, AG-7088 was the most potent inhibitor [324635]. In May 2000, Merrill Lynch predicted that phase III trials would begin in the first half of 2000 and that US filing would take place in the second half of 2001 [375962].

Antiviral Agents↗
PubMedDate not supplied

[Efficacy and distribution pattern of the medical device Prima Difesa on rhinosinusal area].

AIM: Common cold is the commonest form of acute rhinitis and the first pathology of the upper airways. Viruses, the main responsible of this pathology, carry out their cytopathic effect on the ciliated cells of the airways mucosa. Mucociliary transport shows their dangerous effect. The aim of our study is to evaluate the effect of the medical device Prima Difesa on the functioning of the mechanism thanks to its composition and its distribution modality in the nasal cavities. MATERIALS AND METHODS: The present study has been performed on three groups of subjects with their informed consent: Group A (30 healthy subjects: 19 M, 11 F; 18-36 yrs, mean age: 29.1 yrs), Gruppo B (30 patients affected by rhinosinusal pathology: 7 M, 13 F; 19-38 yrs, mean age 30.7 yrs) and Group C (20 healthy subjects: 12 M, 8 F; 20-40 yrs, mean age: 32.2 yrs). The protocol of administration for the Group A and B, in order to evaluate the efficacy of Prima Difesa, consisted of 2 puff per nostril of Prima Difesa 4 times a day over 15 days. The follow-up of patients belonging to Grup A and Group B was articulated in three consecutive visits, each consisting of: anterior rhinoscopy, active anterior rhinomanometry, measurement of mucociliary transport (TMCt). The C patients underwent only one administration of the device to the extent of evaluating through endoscopy its distribution modality in the nasal cavities. RESULTS: The results show that clinical effects, evaluated in term of improvement of MCTt and in term of decreasing of nasal resistance, are particularly clear in patients with alterations of these parameters caused by rhinosinusal pathologies. The device can reach the "key" areas of rhinosinusal pathologies that are: middle turbinate and osteomeatal complex. Beside, the percentage of diffusion, about 30% of the middle turbinate head, justifies its clinical effect. CONCLUSIONS: The medical device Prima Difesa has resulted to be able in interfering with the correct maintenance and performance of the Mucociliary Transport mechanism, that represents an important aspecific machinery for the local defence of nasal mucosa by microbial injuries.

Acute Disease↗
PubMed1983

Changes of mucociliary function during colds.

We have investigated, using chicken and Newcastle disease virus, the relationship between the mucociliary function and acute upper respiratory infection. Average nasal transit time of the dye was 53 sec at the age of two to four weeks in controls. The average transit times were significantly longer than those of controls at day 6 and 12 postinoculation. A histopathological study has revealed that repair of the mucosal injury is usually completed within 13 days after virus challenge. This was confirmed with 3H-thymidine autoradiography. However, there were patches where cilia almost disappear as seen in the scanning electron microscope. The mucous blanket was tethered to the mucosal surface by strands of mucus from the acini of the nose after 7 days of infection. More extensive tethers were observed on the 14th day. This phenomenon is one of the factors which may affect mucociliary transport in vivo only. Nasal secretion from patients with a common cold was transported more slowly than that of controls on a frog palate from which mucus had been removed. The reduction in mucociliary transport rate in the nose during a common cold could be due to a combination of damage to the ciliated system, a change in the biorheological property of nasal secretion and in vivo factors, or other causes.

Animals↗
PubMed2001

The role of viruses in the induction and progression of asthma.

Viral respiratory infections have been related to asthma in several ways. It is well established that viral common colds precipitate exacerbations of asthma. Severe bronchiolitis in early life is related to subsequent wheezing and therefore may represent a marker of susceptibility to asthma; alternatively, it could be involved in the initiation of the disease. Finally, it is possible that some infections may protect from the development of asthma and allergies by promoting a type-1 host response. However, whether respiratory or other viruses could mediate such a protective effect is debated. The design and implementation of novel anti- or proviral strategies targeting asthma depends on the resolution of these questions. This review presents current evidence on the epidemiologic correlations and proposed mechanisms for the involvement of viral infections in the development and progression of asthma.

Animals↗
PubMed2005

Comparative host gene transcription by microarray analysis early after infection of the Huh7 cell line by severe acute respiratory syndrome coronavirus and human coronavirus 229E.

The pathogenesis of severe acute respiratory syndrome-associated coronavirus (SARS-CoV) at the cellular level is unclear. No human cell line was previously known to be susceptible to both SARS-CoV and other human coronaviruses. Huh7 cells were found to be susceptible to both SARS-CoV, associated with SARS, and human coronavirus 229E (HCoV-229E), usually associated with the common cold. Highly lytic and productive rates of infections within 48 h of inoculation were reproducible with both viruses. The early transcriptional profiles of host cell response to both types of infection at 2 and 4 h postinoculation were determined by using the Affymetrix HG-U133A microarray (about 22,000 genes). Much more perturbation of cellular gene transcription was observed after infection by SARS-CoV than after infection by HCoV-229E. Besides the upregulation of genes associated with apoptosis, which was exactly opposite to the previously reported effect of SARS-CoV in a colonic carcinoma cell line, genes related to inflammation, stress response, and procoagulation were also upregulated. These findings were confirmed by semiquantitative reverse transcription-PCR, reverse transcription-quantitative PCR for mRNA of genes, and immunoassays for some encoded proteins. These transcriptomal changes are compatible with the histological changes of pulmonary vasculitis and microvascular thrombosis in addition to the diffuse alveolar damage involving the pneumocytes.

Apoptosis↗
PubMed2000

Transmission of viral respiratory infections in the home.

Respiratory viruses in the home exploit multiple modes of transmission. RSV is transmitted primarily by contact with ill children and contaminated objects in the environment. Influenza appears to be spread mainly by airborne droplet nuclei. Despite many years of study, from the plains of Salisbury, to the hills of Virginia, to the collegiate environment of Madison, WI, the precise routes rhinovirus takes to inflict the misery of the common cold on a susceptible population remain controversial.

Aerosols↗
PubMed2000

IL-12-activated NK cells reduce lung eosinophilia to the attachment protein of respiratory syncytial virus but do not enhance the severity of illness in CD8 T cell-immunodeficient conditions.

Bronchiolitis caused by respiratory syncytial virus (RSV) infection is a major cause of hospitalization in children under 1 year of age. RSV causes common colds in older children and adults, but can cause serious disease in immunodeficient patients and the elderly. Development of effective vaccines and treatments for RSV infection is therefore a priority. Because bronchiolitis and vaccine-augmented disease are thought to be caused by exuberant T cell activation, attention has focused on the use of immunomodulators that affect T cell responses. In mice, IL-12 treatment down-regulates type 2 cytokine responses to the attachment protein G of RSV, reducing lung eosinophilia but further enhancing illness. We now show that CD8(+) T cells are responsible for enhanced weight loss, whereas IL-12-activated NK cells express high levels of IFN-gamma and inhibit lung eosinophilia without causing illness. Moreover, unlike immunocompetent mice, virus is detected in the mediastinal lymph nodes after elimination of both CD8(+) T cells and NK cells. These studies show that innate immune responses to viral infections direct the pattern of subsequent specific immunity and are critical to the development of nonpathogenic antiviral effects. We speculate that IL-12 treatment might be beneficial and safe in T cell-deficient patients with RSV pneumonitis.

Animals↗
PubMed2000

Heated, humidified air for the common cold.

OBJECTIVES: To assess the effects of inhaling heated water vapour with the help of a rhinotherm (an equipment designed to deliver heated water vapour to a person's nasal cavity), in the treatment of the common cold by comparing a. symptoms b. viral shedding c. nasal resistance after a natural or experimentally induced common cold. SEARCH STRATEGY: We searched MEDLINE with MeSH headings: common cold, rhinopharyngitis, inhalation, steam, heated vapour, rhinothermy, till July 1999. EMBASE, Current Contents, review articles, cross references were also searched. Attempts were also made to contact the manufacturers for any unpublished data. SELECTION CRITERIA: Randomized trials using heated water vapour in a standardized way in patients with the common cold or volunteers with experimental induction of rhinovirus infection were included in the review. DATA COLLECTION AND ANALYSIS: All the articles retrieved were initially subjected to a review for inclusion / exclusion criteria. Review articles, editorials, abstracts with inadequate outcome description were excluded. Studies selected for inclusion were subjected to a methodological assessment. MAIN RESULTS: The results of a systematic review of six trials with 319 participants, support the use of warm vapour inhalations in the common cold in terms of relief of symptoms (Odds Ratio with 95 % CI 0.31, 0.16-0.60, Relative risk 0.56, 0.4-0. 79). Results on symptom score indices were equivocal. None of the studies demonstrated a worsening of clinical symptom scores. One study demonstrated increased nasal resistance one week after steam inhalation in contrast to an earlier study which showed improvement in the nasal resistance. There was no evidence of decreased viral shedding measured by virus isolation in the nasal secretions (Tyrrell 1989) or measurement of viral titres in nasal washings among treatment group. The rhinovirus titres in the nasal washings from the treatment group were the same as those of the placebo group on day one prior to the treatment and on all four days after the treatment. The area under curve (Hendley 1994) was also similar in the placebo and treatment groups for titres of virus in the nasal washings as were the average viral titres across five days of follow up, the maximum values after treatment, and viral shedding velocity i.e. amount of virus shed per day (Hendley 1994). Minor side effects due to thermal stress were reported in all the studies. REVIEWER'S CONCLUSIONS: Three trials demonstrated beneficial effects on the symptoms of the common cold. One study from Israel showed a decrease in nasal resistance measured by peak nasal expiratory and inspiratory flow rate. Studies done in North America failed to show any objective improvement in outcome measures with the study intervention. A multi-centre double blind randomised controlled trial testing this therapy with uniform outcome measures is recommended.

Air↗
PubMed1999

The role of the common cold in asthma.

It has long been known that patients with viral respiratory infections develop temporary asthma-like symptoms or see a worsening of their existing asthmatic symptoms or develop full-blown asthma during the infection. It should not be surprising, in view of this observation, that these same viruses have been found to initiate the same inflammatory processes as seen and characterized in the asthmatic patient. This has clear implications for therapy of asthmatic patients.

Asthma↗
PubMed1999

Clinical virology of rhinoviruses.

Rhinoviruses cause more infections in humans than any other micro-organism. These acid-sensitive picornaviruses infect epithelial cells following inoculation onto the nasal mucosa and are detected reliably in nasopharyngeal secretions. Rhinovirus colds occur year round, with a peak of illness in the fall. Type-specific serum antibody correlates with protection against infection. The fact that there are at least 100 different immunotypes makes development of an effective vaccine unlikely. Nasopharyngeal secretions must be sampled for detection of rhinovirus by culture or RT-PCR. Efficient isolation of virus requires inoculation into two different types of sensitive cell cultures (i.e., fibroblasts and HeLa cells). RT of conserved sequences in the 5' noncoding region of the viral RNA to produce cDNA for PCR amplification has been coupled with detection of amplimers either by gel electrophoresis after nested PCR or by hybridization with labeled oligonucleotide probes to detect one viral genome in samples. In two studies in which both RT-PCR and cell cultures were used, virtually all of the positives were identified with RT-PCR; culture in two cell lines identified 75-80% of the positives. In year-round surveillance, 50% of colds in adults and children were rhinovirus positive. The symptoms occurring during rhinovirus colds are caused by the host's response to the virus, not by the virus itself. Elaboration of cytokines by infected epithelial cells is central to symptom pathogenesis.

Common Cold↗