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PubMed2001

Upper respiratory tract infections.

Acute respiratory infections accounts for 20-40% of outpatient and 12-35% of inpatient attendance in a general hospital. Upper respiratory tract infections including nasopharyngitis, pharyngitis, tonsillitis and otitis media constitute 87.5% of the total episodes of respiratory infections. The vast majority of acute upper respiratory tract infections are caused by viruses. Common cold is caused by viruses in most circumstances and does not require antimicrobial agent unless it is complicated by acute otitis media with effusion, tonsillitis, sinusitis, and lower respiratory tract infection. Sinusitis is commonly associated with common cold. Most instances of rhinosinusitis are viral and therefore, resolve spontaneously without antimicrobial therapy. The most common bacterial agents causing sinusitis are S. pneumoniae, H. influenzae, M. catarrhalis, S. aureus and S. pyogenes. Amoxycillin is antibacterial of choice. The alternative drugs are cefaclor or cephalexin. The latter becomes first line if sinusitis is recurrent or chronic. Acute pharyngitis is commonly caused by viruses and does not need antibiotics. About 15% of the episodes may be due to Group A beta hemolytic streptococcus (GABS). Early initiation of antibiotics in pharyngitis due to GABS can prevent complications such as acute rheumatic fever. The drug of choice is penicillin for 10-14 days. The alternative medications include oral cephalosporins (cefaclor, cephalexin), amoxicillin or macrolides.

Anti-Bacterial Agents↗
PubMed2003

Mechanisms of virus-induced asthma.

In children and adults with asthma, infections with common cold viruses such as respiratory syncytial virus and rhinovirus frequently cause exacerbations of asthma. Recent studies suggest that these and other respiratory viruses infect the lower airways, and that the infected epithelial cells help to initiate immune responses to the virus. These immune responses have antiviral effects, but also enhance airway inflammation and may add to cold symptoms and airway obstruction. Moreover, there are data to suggest that there may be specific interactions between allergic and virus-induced inflammatory responses that contribute to lower airway dysfunction in asthma. Finally, impaired T-helper type 1-like lymphocyte responses during viral infections may be a risk factor for more severe viral illnesses in patients with allergies and asthma. It is hoped that these advances in our understanding of the relationship between viral infections and exacerbations of asthma will translate into new therapeutic targets for virus-induced exacerbations of asthma.

Asthma↗
PubMedDate not supplied

Preventing the common cold with a garlic supplement: a double-blind, placebo-controlled survey.

One hundred forty-six volunteers were randomized to receive a placebo or an allicin-containing garlic supplement, one capsule daily, over a 12-week period between November and February. They used a five-point scale to assess their health and recorded any common cold infections and symptoms in a daily diary. The active-treatment group had significantly fewer colds than the placebo group (24 vs 65, P < .001). The placebo group, in contrast, recorded significantly more days challenged virally (366 vs 111, P < .05) and a significantly longer duration of symptoms (5.01 vs 1.52 days, P < .001). Consequently, volunteers in the active group were less likely to get a cold and recovered faster if infected. Volunteers taking placebo were much more likely to get more than one cold over the treatment period. An allicin-containing supplement can prevent attack by the common cold virus.

Adult↗
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↗
PubMed1988

Viral proteases: an emerging therapeutic target.

Only a few viral diseases are presently treatable because of our limited knowledge of specific viral target molecules. An attractive class of viral molecules toward which chemotherapeutic agents could be aimed are proteases coded by some virus groups such as retro- or picornaviruses (poliomyelitis, common cold virus). The picornavirus enzymes were discovered first, and they have now been characterized by a combination of molecular-genetic and biochemical approaches. Several laboratories have expressed the picornaviral enzymes in heterologous systems and have reported proteolytic activity, as well as the high cleavage fidelity diagnostic of the viral proteases. After dealing with several technical difficulties often encountered in standard genetic engineering approaches, one viral protease is now available to us in quantity and is amendable to mutagenic procedures. The initial outcome of the mutagenesis studies has been the confirmation of our earlier work with inhibitors, which suggested a cysteine active-site class. There is a clustering of active-site residues which may be unique to these viruses. The requirement for an active-site cysteine-histidine pair in combination with detailed information on the viral cleavage sites has permitted design of selective inhibitors with attractive antiviral properties. Future goals include investigation of the structural basis for selective processing and application of the cleavage specificity to general problems in genetic engineering.

Humans↗
PubMed2005

Acute cooling of the feet and the onset of common cold symptoms.

BACKGROUND: There is a common folklore that chilling of the body surface causes the development of common cold symptoms, but previous clinical research has failed to demonstrate any effect of cold exposure on susceptibility to infection with common cold viruses. OBJECTIVE: This study will test the hypothesis that acute cooling of the feet causes the onset of common cold symptoms. METHODS: 180 healthy subjects were randomized to receive either a foot chill or control procedure. All subjects were asked to score common cold symptoms, before and immediately after the procedures, and twice a day for 4/5 days. RESULTS: 13/90 subjects who were chilled reported they were suffering from a cold in the 4/5 days after the procedure compared to 5/90 control subjects (P=0.047). There was no evidence that chilling caused any acute change in symptom scores (P=0.62). Mean total symptom score for days 1-4 following chilling was 5.16 (+/-5.63 s.d. n=87) compared to a score of 2.89 (+/-3.39 s.d. n=88) in the control group (P=0.013). The subjects who reported that they developed a cold (n=18) reported that they suffered from significantly more colds each year (P=0.007) compared to those subjects who did not develop a cold (n=162). CONCLUSION: Acute chilling of the feet causes the onset of common cold symptoms in around 10% of subjects who are chilled. Further studies are needed to determine the relationship of symptom generation to any respiratory infection.

Adolescent↗
PubMed2000

Viral and bacterial infections in the development and progression of asthma.

Viral respiratory infections produce wheezing illnesses in patients of all ages. In infancy, infections with respiratory syncytial virus and parainfluenza virus are the major cause of bronchiolitis and croup, whereas infections with common cold viruses such as rhinoviruses are the principal triggers for wheezing in older children and adults with asthma. In addition to causing increased wheezing in asthma, there is mounting evidence that infections early in childhood can affect the development of the immune system and thereby modify the risk for the subsequent development of allergies and asthma. Both of these effects appear to be mediated by virus-induced immune responses. Early during the course of viral infection, resident cells in the airway are activated in an antigen-independent fashion, triggering antiviral responses but also activating and recruiting cells to the airway that could contribute to airway obstruction and respiratory symptoms. Virus-specific T- and B-cell responses may also have dual effects in the presence of preexisting airway inflammation. Finally, there is evidence of synergistic interactions between allergen- and virus-induced airway inflammation. It is likely that greater definition of mechanisms of virus-induced inflammation will provide therapeutic targets for the treatment and possibly the prevention of allergies and asthma.

Animals↗
PubMed2004

Systemic therapy of malignant human melanoma tumors by a common cold-producing enterovirus, coxsackievirus a21.

PURPOSE: The incidence of malignant melanoma continues to increase worldwide; however, treatment of metastatic melanoma remains unsatisfactory, and there is an urgent need for development of effective targeted therapeutics. A potential biological target on the surface of malignant melanoma cells is the up-regulated expression of intercellular adhesion molecule (ICAM)-1 and decay-accelerating factor (DAF), relative to surrounding benign tissue. Coxsackievirus A21 (a common cold virus) targets and destroys susceptible cells via specific viral capsid interactions with surface-expressed virus receptors comprising ICAM-1 and DAF. EXPERIMENTAL DESIGN: The oncolytic capacity of a genetically unmodified wild-type common cold-producing human enterovirus (Coxsackievirus A21, CAV21) was assessed against in vitro cultures and in vivo xenografts of malignant human melanoma cells. RESULTS: In vitro studies established that human melanoma cells endogenously express elevated levels of ICAM-1/DAF and were highly susceptible to rapid viral oncolysis by CAV21 infection, whereas ICAM-1/DAF-expressing peripheral blood lymphocytes were refractile to infection. In vivo studies revealed that the tumor burden of nonobese diabetic severe combined immunodeficient mice bearing multiple s.c. melanoma xenografts was rapidly reduced by oncolysis mediated by a single administration of CAV21. The antitumor activity of CAV21 was characterized by highly efficient systemic spread of progeny CAV21, with oncolysis of tumors also occurring at sites distant to the primary site of viral administration. CONCLUSIONS: Overall, the findings presented herein demonstrate an important proof of principle using administration of replication-competent CAV21 as a potential biological oncolytic agent in the control of human metastatic melanoma.

Animals↗
PubMed1992

Viruses as precipitants of asthma symptoms. II. Physiology and mechanisms.

The upper and lower airways have complimentary roles in the ultimate object of supplying the body with oxygen whilst removing waste products of metabolism. Pathology in one area may trigger a response in another, the physiology of which, in the case of virus-induced asthma exacerbations remains poorly characterized. Viral infection of the upper airways by common cold viruses frequently triggers a response in the lower airways leading to prolonged morbidity, especially in subjects with significant pre-existing airway disease. The induction or amplification of BHR may be an important mechanism whereby asthmatic symptoms are produced although the cellular and tissue events or reflex mechanisms activated by viral illnesses and underlying BHR changes are poorly defined and may be dependent on the type and the severity of infection. Children and asthmatics tend to develop frequent colds setting in motion a sequence of events culminating in airway obstruction and symptoms of wheezing, coughing and chest tightness. This may reflect independent inflammatory changes caused by a simply additive effect of viral damage to the mucosa superimposed upon pre-existing allergic inflammation (Fig. 1). Few if any symptoms will develop in normal subjects with a mild cold whereas significant symptoms may ensue if the cold is severe and induces marked lower airway swelling, secretions and smooth muscle contraction; pathology to which children who have small calibre airways may be particularly susceptible. In asthmatics even a mild cold frequently induces exacerbation of symptoms, while serious life-threatening asthma attacks may occur associated with a severe cold. Some studies have suggested that this effect is not only additive but also synergistic and brought about by release of the mediators already present in increased quantities, the induction of IgE synthesis, or by the potentiation of neural and epithelial damage. The combined effect of both asthma and viruses may thus be amplified and result in a sustained and refractory period of airway obstruction, severe symptoms and unstable asthma. As most hospital admissions for asthma occur over the winter months and soon after the start of the school terms [115], spread of viruses through the community to susceptible individuals may be the single most important cause of sustained exacerbations of asthma. Definition of the pathological and physiological mechanisms involved will lead to better understanding and may thus provide a basis for prevention and the development of effective forms of treatment for virus-induced asthma.

Airway Obstruction↗
PubMed1988

Limbic encephalitis after inhalation of a murine coronavirus.

The spread of a neurotropic coronavirus, mouse hepatitis virus strain A59, in the mouse central nervous system was studied after intranasal inoculation. Mouse hepatitis virus strain A59 spread during the 3- to 5-day postinoculation period, through the olfactory pathway into the limbic system. Coronavirus particles were detected in the limbic system by electron microscopy. The combination of temporal propagation through an anatomical-physiological central nervous system pathway and anatomical restriction of viral infection suggests that specific interneuronal transport is important in spread of the virus. This experimental system may represent a model for diseases associated with human coronaviruses (common cold viruses) and/or the human limbic system.

Administration, Intranasal↗