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In vitro assays using basophils obtained from patients infected with RSV, adenovirus, influenza A, parainfluenza and rhinoviruses have observed an increase in the release of histamine [37, 38, 39].Mast cells. A virus usually causes upper respiratory infection. A virus is a germ that attacks your body.
Antibiotics are not prescribed for treatment of upper respiratory infection. We do not prescribe a decongestant as we do not want to dry up the nasal secretions. Temporary immunity follows after any viral infection. If your child is known to have asthma, upper respiratory infection may trigger a wheezing attack. This leaflet gives some tips on what to do, and what symptoms to look out for which may indicate a more serious illness. Eugenia Manjarrez-Zavala1, Dora Patricia Rosete-Olvera1, Luis Horacio Gutierrez-Gonzalez1, Rodolfo Ocadiz-Delgado2 and Carlos Cabello-Gutierrez1[1] Departamento de Investigacion en Virologia y Micologia, Instituto Nacional de Enfermedades Respiratorias Ismael Cosio Villegas, D. These cells have a high affinity receptor for IgE and participate in hypersensitivity reactions, the release of histamine and leukotrienes, molecules that are increased in infants with respiratory wheezing [38, 39].Stimulation of chemical mediators. When a virus attacks the airway, the immune system of the nose and sinuses produce local antibodies to kill the viruses through mucus.
The viruses can infect the respiratory tract upper and occasionally, some of them can cause infections in the lower respiratory tracts. The viruses trigger the production of type – 1 interferons (IFNs) by plasmacytoid dendritic cells and other cytokines as interleukin – 12 (IL – 12).
It has been proposed that in the respiratory infections, viruses are able to originate the relase of inflammatory mediators, either directly or through viruses-activated cells. However, other infections can follow a viral respiratory infection, in which case the symptoms of respiratory difficulty may show up. Whatever leads to a vigorous inflammatory response, airway obstruction induces exacerbation of asthma.
Call the office or the emergency number provided to you if you are worried that your child’s condition is getting worse. Cough is a symptom due to the secretions of mucus and thus decongestants are better avoided.
IntroductionSpeaking of viral pathogenesis, it must describe the features and factors of viral pathogen, hosts and environment. Several mediators have been reported, which suggests that during infection can exist the interaction of more than one. IL – 15 trigger other pro – inflammatory cytokines, including either the secretion of IFN – ? by NK cells or the release of perforin and grazymes, which leads to citotoxicity. Over its lifetime, an individual is exposed to many infectious agents, however, in most situations does not develop a disease thanks to factors such as physical and chemical host barriers.
In other cases, pathogens circumvent these barriers and cause infection; however, a “biological war” will start between the determinants of pathogenicity and early host defenses.
Histamine is released from various cells as basophils, leukocytes, mast cells, among others. If the virus is able to overcome these first lines of defense, a type of highly specialized and specific protection will be activated.
The secretion of this mediator is inflammation and airway is inflammation and airway obstruction. This defense will achieve, in most situations, the infection control and subsequent eradication of the disease. In vitro and in vivo studies with respiratory virus have demonstrated high concentrations of histamine in nasopharyngeal secretions and in the plasma of infected individuals. Furthermore, this process will initiate the generation of the immunological memory, enabling the individual with a more quickly and effectively response at the next contact with the same agent.
However, therapeutic success with antihistamines in asthma has not been confirmed so several authors have questioned the effect of histamine [36, 38].Leukotrienes. See separate leaflets about other infections of the respiratory tract and related structures, called 'Bronchiolitis', 'Pneumonia', 'Tonsillitis', 'Sore Throat', 'Sinusitis - Acute', and 'Pleurisy'. In certain cases, the line of defense, when triggered, can also cooperate with the damage instead of healing, making the disease more severe. Leukotrienes are released by primary inflammatory cells involved in inflammation, as well as endothelial and epithelial cells of the airways. Thus, the immunopathology viral respiratory infection is a frequent consequence of the immune response against many of respiratory pathogens.
Furthermore, if the infection is established, the factors or viral virulence determinants and physiological conditions of the host cell will determine which direction the infection will take. It has also been shown to increase vascular permeability and production of mucus, in addition, some evidence suggests that leukotrienes play an important role in the origin of wheezings. A virus is pathogenic when it is able to infect and cause disease in a host, while it is virulent when it causes more severe disease than another virus of a different strain, although both remain pathogens.
Respiratory viruses such as RSV, parainfluenza 3 and influenza A, induce the release of leukotrienes which are detectable in nasopharyngeal secretions. Each virus can cause different cytopathic effects in the host cell, which may lead to several symptoms and disease.
High concentrations of Leulotrienes have been found in infants with RSV infection [40-44].Products of cyclooxygenase, arachidonic acid, prostaglandins and thromboxane.
In addition, developing a disease reflects the existence of an abnormality of the host, either structural or functional, induced by the invading virus.2.
They are potent bronchoconstrictors and have shown an increase in the concentrations of the primary metabolite of prostaglandin type 2a in plasmatic cells from infants with RSV bronchiolitis and especially in those with recurrent wheezing. Viral pathogenesis The term “pathogenesis” refers to the processes or mechanisms to generate an injury or illness, in this case induced by a viral infection.
It is also reported that the prostaglandin E2 type has an inhibitory effect which may protect the airways of a bronchoconstrictor effect. The results of a viral infection depend on factors related to the nature of the virus, the host and the environment.
It is suggested that viral epithelial damage may result in the loss of these protective prostaglandins. They include: number of infectious particles, the way to reach the target tissue, the rate of multiplication, the effect of virus on cell functions and the host’s immune response. It was also found that complexes of RSV-antibody cause an increase in the release of thromboxane by neutrophils [36].Platelet activating factor (PAF).
Induces an inflammatory response and stimulates the production of mucus in the airways, alters mucociliary clearance and enhances pulmonary microvascular permeability. In vitro studies have shown that mononuclear phagocytes upon RSV replication, stimulates the synthesis of platelet activating factor.
Virulence is under polygenic control and is not assignable to any isolated property of the virus, but is often associated to characteristics that favor viral replication and cellular injury.
From these results it has been suggested that this factor may play an important role in the inflammatory response caused by RSV [45, 46].Kinins. For example, virulent viruses multiply themselves readily at high temperatures prevailing during the disease, block the synthesis of interferon and macromolecules related to immune system.
Kinins may be involved in the pathogenesis of diseases such as asthma by its inflammatory and bronchoconstrictor action. In general, a virulent virus causes significant disease, whereas an avirulent or attenuated virus causes no or reduced disease, respectively.Measuring Viral Virulence.
In unmyelinated sensory nerves in the airways is found the P substance, potent neuropeptide belonging to tachykinin group which when released by local axon reflex, potentiate the cholinergic neurotransmission [47].Nitric Oxide (NO). One approach is to determine the concentration of virus that causes death or disease in 50% of the infected organisms. This parameter is called the 50% lethal dose (LD50), the 50% paralytic dose (PD50), or the 50% infectious dose (ID50), depending on the parameter that is measured. They are small proteins that act generally in cellular processes such as differentiation, activation and immune defense. Other measurements of virulence include mean time to death or appearance of symptoms, as well as the measurement of fever or weight loss. All cytokines are secreted by cells due to the interaction with infectious agents and mechanical actions (e.g.
Virus-induced tissue damage can be measured directly by examining histological sections or blood samples.
For example, safety of live attenuated poliovirus vaccine is determined by assessing the extent of pathological lesions in the central nervous system in experimentally inoculated monkeys.
Indirect measures of virulence include assays for liver enzymes (alanine or aspartate amino-transferases) that are released into the blood as a result of virus-induced liver damage [1].The amount of inoculum. There are cytokines showing chemotactic properties, therefore, these cytokines are called chemokines.
It has been shown that, for rhinovirus, the size of the inoculum contributes to the kinetics of viral spread [2].
In viral infectious processes it has been described the participation of various chemokines as a pathological characteristic of the infection process, so that it has been established that chemokines are directly responsible for the inflammatory processes that occur in respiratory viral infections [49]. The amount of virus inoculated may influence or determine if it causes a mild or severe infection.Speed of replication. Among the viruses that induce the release of chemokines may be mentioned: RSV, rhinovirus, influenza and parainfluenza viruses 3 [50].
Some viruses replicate so rapidly that they often cause acute infections, others are slow virus replication, or some have to travel greater distances, which slows replication.Viral Spread.
It has been observed that, in cell lines, RSV increases the production of IL-6, IL-8, RANTES, macrophage inflammatory protein (MIP-1a), GM-CSF and IL-11.Interleukin 8 (IL-8). Following replication at the site of entry, virus particles can remain localized, or can spread to other tissues. IL-8 is a chemokine which promotes the recruitment of neutrophils and eosinophils that are responsible in part for the inflammatory process [49, 50].RANTES. Local spread of the infection in the epithelium occurs when newly released virus infects adjacent cells. These infections are usually contained by the physical constraints of the tissue and brought under control by the intrinsic and immune defenses.
Less potent than RANTES as eosinophil chemotactic, but it is important mediator in the inflammatory response during virus infection because it stimulates the release of histamine by basophils and mast cells.
An infection that spreads beyond the primary site of infection is called disseminated (for example: measles virus). Its properties suggest that may be important mediators of asthma exacerbations induced by viral infections. In children, have been found in high concentrations in nasal secretions during asthma exacerbations associated with infection caused by RSV and rhinovirus [50,51].Eotaxin. For an infection to spread beyond the primary site, physical and immune barriers must be breached. Eotaxin has additional functions such as endothelial migration, release of reactive oxygen, Ca+ ions mobilization, actin polymerization and is also chemotactic for basophils and Th2 lymphocytes. The integrity of that structure may be compromised by epithelial cell destruction and inflammation. It is soluble in serum and has been found in high concentrations in patients with asthma and is associated with the severity of the disease [52, 53].Intercellular adhesion molecule 1 (ICAM-1).
Below the basement membrane are sub-epithelial tissues, where the virus encounters tissue fluids, the lymphatic system and phagocytes. This a receptor is located in the vascular endothelium, epithelium of the airways and in antigen presenting cells. All three biological environments play significant roles in clearing viruses, but also may disseminate infectious virus from the primary site of infection.
One important mechanism for avoiding local host defenses and facilitating spread within the body is the directional release of virus particles from polarized cells at the mucosal surface.
Several studies have shown that, in vitro, epithelial cells of human airways produce increased levels of ICAM-1. Virions can be released from the apical surface, from the basolateral surface, or from both.
This ICAM-1 expression is observed also during the adhesion of eosinophils and neutrophils in response to inflammatory cytokines and in infection processes of various respiratory viruses such as RSV, rhinovirus and parainfluenza [53, 56, 57]. Rhinoviruses attach to the surface of cells via ICAM-1 receptor, suggesting that infection with rhinovirus leads to an increase in the expression of ICAM-1 in the upper airways.

In this way, ICAM-I and induces the recruitment of eosinophils and neutrophils, thereby increasing and causing inflammatory activity and wheezing [58, 59, 60].11.
In contrast, virus particles released from the basolateral surfaces of polarized epithelial cells have been moved away from the defenses of the lumenal surface.
In general, viruses released at apical membranes establish a localized or limited infection.
Release of viruses at the basal membrane provides access to the underlying tissues and may facilitate systemic spread [1].Virulence genes.
Part of the problem is that many of the effects of viral pathogenesis are the result of the action of the immune response mechanisms, including both innate and adaptive, and can not reproduce these effects in tissue culture assays.
Another problem limiting the studies is that no one knows precisely what is being observed and what for. So, to address this field, most studies begin with the premise that if a virus has a defective virulence gene, it may not cause disease or, if at all, can only cause a weak disease, such that this reasoning can cause confusion. Molecular directed mutations has been a tool that, although difficult to control, has greatly contributed to the characterization of virulence genes. Thus, the reversion of mutations (mutations repair), the mixture of mutant and wild viruses, among others, have identified genetic defects in virulence. Some mutations lead to eliminated, reduced or increased protein function, whereas other proteins affect the level of transcription, translation or replication of the genetic information [1]. The viral genes that affect virulence status can be classified into four groups or classes: 1. These factors and the presence of specific cellular receptors for a given virus can determine resistance or susceptibility to viral infection.
Subsequently, adaptive immune defense will enter into action and influence the success or the elimination of the infection.Cellular virulence genes. Numerous studies have shown that certain cellular genes can be considered as virulence determinants [1]. Among the candidate genes are genes encoding components of the host immune response such as proteins required for T- and B-cell function, as well as cytokines. When these genes are altered, proteins do not perform correctly their function, which can have adverse effects during viral infection; thus, the disease may be more or less severe. Other candidate genes are cellular genes that encode proteins required for replication, translation, transcription and mRNA synthesis and are considered cellular virulence determinants; however, there are few studies that demonstrate this condition [1]. This field is still poor studied, but with the current tools and knowledge on the pathogenesis mechanisms, results are being achieved that in a near future will help us to learn more about the subject.Enviromental factors. Environmental conditions such as temperature, moisture, pH, aeration, etc., can influence the viability of the virus before reaching their target organ and affect or facilitate its infectivity. A well-known example is the winter predominance of respiratory viral viruses and the summer propagation of enteric viruses.3. Many viruses are passed on by touch, especially from hands that are contaminated with a virus.
Cellular level pathogenesisMolecular interactions between the virus and the cell result in a phenomenon called pathogenesis.
It can be analyzed at different levels ranging from the early interactions (cellular receptors) to the expression and suppression of cellular and viral genes, resulting in the production of inflammatory, pro-apoptotic or anti-apoptotic proteins, whose presence or absence induce the activation of complex networks of proteins that interact in cellular signaling pathways [3]. The sensitivity or resistance of a cell to viral infection is determined by early interactions with the virus, such as the adhesion and release of nucleic acids in the cell, and is strongly related to the characteristics of the cell, such as physiological maturation, genetic characteristics and specific receptors for a given virus [4].Molecular gateway and viral spread. Also, the gateway sets the path of its spread and consequently the disease process, which in some viral infections are not always predictable.Usually, viruses that cause respiratory infections penetrate through the epithelium replicating at the site and causing localized infections. It is the ability of a virus to infect or damage specific cells, tissues, organs or specific cells. In some virus is strictly limited, other are pantropic and are able to infect and replicate in different types of cells and tissues. The tropism contributes significantly to the virulence and pathogenesis of viral infections, and is determined by several factors that intervere in the virus-host relationship such as the gateway and route of viral spread, the permissibility of the cell (receptors, cell differentiation), the nature of the innate and adaptive immune response of the host and specific tisular features.Cell membrane receptors. A cell may be susceptible to viral infection if viral receptors are present and functional. In epithelial cells from human respiratory tract, some receptors habe been identified such as N-acetyl neuraminic acid, glycosaminoglycans and glycolipids, ICAM integrin and molecules of the Major Histocompatibility Complex. This receptor is found in several tissues of the body, although the infection in humans is restricted to the respiratory tract. While viruses that infect humans bind to sialic acid type ?-2,6, in birds they bind to ?-2,3 type that is localized in the gastrointestinal epithelium where the virus replicates. In pigs, the virus can recognize both types, which facilitates the generation of gene arrangements between strains of different origin [1, 5, 6].Virus-cell interaction.
The interaction of a virus with its cellular receptor is mediated by one or more surface proteins.
Enveloped viruses have the ability to fuse directly to the cell membrane allowing the entry of the nucleocapside into the cytoplasm.
Naked viruses and some enveloped viruses have the capacity to fuse to che cell membrane by means of endocytosis. Some viruses require co-receptor molecules to penetrate the cell as happens with Adenovirus [7].Some viruses require cellular proteases that cut viral proteins to form an infectious viral particle. During an influenza virus infection, a cellular protease cuts an HA precursor generating two subunits in order to activate and allow the fusion between the viral envelope and the cell membrane. It has been described that alterations in the cleavage site of the HA of influenza virus causes changes in the pathogenicity of the virus, in fact, highly pathogenic strains of birds contain multiple basic amino acids at the cleavage site of the HA that is recognized by different proteases. As a result these strains are capable of infecting various organs such as spleen, liver, lung, kidney and brain. This same cutting activation procedure is performed with the F protein of the virus of the Paramyxoviridae family.Sensitive cells. These cells have specific receptors on the cell membrane, capable of interacting with the virus antigenic proteins and to allow the infectious process. According to whether the cell allows or not the virus replication, it can differentiate them into permissive and non-permissive [8].Permissive cells.
Are those that allow the virus enter and allowing the complete viral life cycle, dividing, and producing offspring. In what is called early phase, several viral components are synthesized such as viral proteins. In the subsequent phase, these components are assembled and, in the final or lytic phase, cell death occurs, then freeing new generation virus. In some cases, if the virus is lysogenic, or it is an oncogenic virus, it can be observed the phenomenon of integration of the viral genome into the host ?genome.
In all types of infection, the initial event is the interaction between the virus and the corresponding receptor present on the cell surface.
If a cell lacks the appropriate receptor for a particular virus, is then automatically resistant to infection by that virus [8 ].4. Viruses cause morphological alterations known as cytopathic effect (CPE) and occur in both the cells of living organisms and in vitro culture cells. The ECP is a manifestation of the infectious process, and is defined as "morphological and functional changes of cells caused by a virus and is visible under the microscope, resulting in cell death". In cultures infected with influenza virus, cells were rounded and clustered like a bunch of grapes (Figure 1a) Adenovirus also rounded the cells but retract into a sphere. Respiratory syncytial virus (Figure 1b) and herpes simplex type I and II induce fusion of cell membranes forming syncytia or multinucleated giant cells (figure 1c).Alteration of membranes. The plasmatic membrane is the first part of the cell with a virus contacts, this interaction occurs at the junction between the individual components of the cell surface proteins and the virus surface.
After entry of the intact viral particle, and if penetration was by endocytosis, the genome is released into the cytoplasm after disruption of the membrane endocytic. In the case of paramyxovirus, a family of enveloped viruses and RNA genome, viruses contain two glycoproteins on its surface, one is the F protein that is able to initiate membrane fusion at acidic pH, the viral genome is introduced directly into the cell as a result of the fusion between the viral envelope and the cell plasma membrane. During the acute infection by cytolytic virus, especially the non-enveloped in the infected cell which finally releases large amounts of virus, the plasma membrane is damaged until to rupture. At this time, cytoplasmic proteins that are filtered, and ions such as Na + and ?+ allow the entry of water and the development of cellular inflammation (cell swelling), which leads to cell lysis.Cell lysis. Besides membrane damage by the entry of viral particles there are differene cell membrane alterations, including the nucleous and organelles that lead to cell lysis. Cell lysis is mainly due to the inhibition of cellular macromolecular synthesis by some viral proteins.
DNA viruses inhibit early the cellular DNA synthesis and during late periods cellular RNA and proteins (e.g.
The accumulation of viral products causes cell lysis and release of virions.Effect on the cytoskeleton.
Some viral and cellular proteins synthesized during infection act on the cell cytoskeleton. This alteration induces that cell is made round; this occurs mainly in cells infected with adenovirus. Other changes in the cytoskeleton are caused by oncogenic viruses that cause a cell morphology change (e.g. Cells that possess cilia, such as respiratory tract, lack their ciliary functionality during influenza virus infection [9].Cellular fusion. In infected cells, same viral protein allows the fusion between neighboring cells, giving rise to multinucleated cells that are called polykaryocytes or syncytia.
Among the viruses that show syncytia formation are RSV, measles, parainfluenza, herpes simplex, as they have fusion proteins and are able to move from one cell to another without having to leave cell.Inclusion bodies. Its location is variable, can be intracytoplasmic as those induced by rabies virus, nuclear such as adenovirus or those caused by the virus of measles which are both nuclear and intracytoplasmic.
Inclusion bodies break or change the cellular structure and function inducting cell death [1].Induction of chromosomal aberrations. Viruses can cause changes at nuclear level that lead to the disintegration of the chromatin of infected cells as occurs in the herpes simplex virus infections. However, nuclear or chromosomal abnormalities can be as subtle to be detected by molecular methodologies, as example, as in the integration of viral genomes into the cellular genome during transformation mediated by certain viruses, in which the cell is alive, but altered in its properties.
Other viruses that cause aberrations are mumps virus, measles, rubella, parainfluenza and adenovirus [10].Cellular Transformation and cell proliferation. DNA and RNA viruses may integrate its genome into the cell, generating transformed cells that behave similarly in vitro to cancer cells. Cellular transformation corresponds to a phenomenon that occurs both in vivo and in vitro and has yielded valuable information regarding the etiology of certain cancers. Some viral proteins inactivate cell proteins which control the cell cycle and hyperplastic processes occur, inducing proliferation or cell growth, for instance, papilloma virus causing laryngeal papillomatosis that can lead to cancer [11] 5.
Description and characteristics of virusViruses are microscopic infectious agents that are composed of genetic material (DNA or RNA), surrounded by a protein coat called capsid (naked virus), other viruses have a lipid membrane (enveloped viruses) showing glycoprotein spikes. The proteins of the capsid of both, naked and enveloped viruses and the glycoproteins of enveloped viruses are the major antigens for inducing immune response of the host.
Viruses must evade host innate immunity and defense mechanisms, such as mucociliary barriers, phagocytic cells and NK cells, and to adhere to achieve target.Incubation period. As a result of the alteration of immunity mentioned above, usually the immune response shows short duration or it is incomplete.Evasion of the immune response.
The strategies used by viruses to evade the immune response are varied, from antigenic variation to the blocking of on inflammation process, and decrease of apoptosis levels [10-12].Association with other microorganisms. Not much is known about this, but there have been some events that suggest it, for example, the bacterium Staphylococcus aureus produces a protease that can activate the influenza virus hemagglutinin, thus increasing the virulence level of the virus.6. Types of infectionThe interactions that occur between the virus and the host can take many forms, there are four basic patterns of infection:Subclinical infections. They are very common in airways and are epidemiologically important because they represent an important source of transmission.Clinical infections.
These infections show symptoms and signs, the most common are acute respiratory infections which are characterized by quickly presentation with short incubation period as well as the duration of the disease.
Usually, the virus is eliminated by the immune system and the physiological condition of the organism. A clear example is the infection with poliomyelitis virus, which causes frequent abortive infections in early stages.Persistent infections. After an acute infection, the virus is not eliminated and it can still replicate for long periods. The virus remains most of the time hidden without replication, however, it can reactivate resulting in clinical manifestations. After clinical or subclinical infection, the virus continues to multiply very slowly but continuously.

A typical example, although not a respiratory infection, is the Hepatitis B virus.Slow Infections.
This kind of infections have a long incubation period that lasts for months or years, symptoms usually do not occur during the incubation period.
A well known example is the persistent infection showed by measles in the nervous system causing SSPE, usually conducting to death.Transforming infections. Few respiratory viruses induce transforming infections, usually, the viral genome integrates into cellular DNA or remain as an episome. Some of the expressed proteins interact with genes and other cellular proteins, causing changes in cell growth rates. The respiratory system consists of a set of organs that are grouped into upper respiratory tract (nasal cavity, pharynx, larynx, trachea) and lower airways (bronchi, bronchioles and lungs). The inner part of these organs is covered by epithelial cells which constitute an active physical barrier against pathogens being an important part of the innate immunity. Another structure of the respiratory amembrane is a mucociliary structure found from the nasal cavity to the distal areas of the lungs, consisting of a layer of mucus produced by goblet cells that maintain a continuous flow through the ciliary movement in the luminal surface respiratory epithelium.
The lungs have not these structures, alveolar macrophages are the cells that are responsible for eliminating pathogens. However, despite these protection mechanisms, respiratory system of a host may be infected by a virus by binding to specific receptors present in epithelial cells of the mucosa, thereby avoiding its removal by the mucociliary system or by phagocytic cells. Most viruses that infect humans enter into the body through the respiratory tract as in aerosols produced by coughing or sneezing of other infected hosts.
Large particles are usually trapped in the turbinates and sinuses and could cause upper respiratory infections. Smaller particles can reach the alveolar spaces and cause infections in the lower respiratory tract [1, 13]. The viruses that cause respiratory infections in both upper and lower airways are distributed in different families: Orthomyxoviridae, Paramyxoviridae, Picornaviridae, Reoviridae, Adenoviridae, Herpeviridae and Coronaviridae.
After penetration of the virus, they can cause local respiratory infections as with most respiratory viruses such as influenza, rhinovirus, respiratory syncytial virus, parainfluenza virus, coronavirus, bocavirus and metapneumovirus occasionally causing lower respiratory infections. Other viruses such as herpes, measles, rubella, mumps and varicella among others enter through airways but move to other organs.Viral infection in upper respiratory tract.
Infections of the upper respiratory tract usually present acutely and are the most common infections in humans, arise throughout the year but the incidence is higher in winter, are generally of low severity, however, are the main cause of medical consultation and, in consequence, school and work absenteeism is frequent.
A virus can cause several syndromes, also too a syndrome may be caused by different viruses such that the clinical manifestations are variable. All individuals can be infected by these viruses, however, it has been observed that children are the most affected. Viral infections in lower respiratory airways occupy a smaller percentage, but with high mortality rates.
Bronchiolitis occurs primarily in young infants and preschool children, the most related virus to this syndrome is the RSV (50-75% of the cases). Pneumonia occurs most often in children younger than 3 years of age, as in bronchiolitis, the RSV virus are involved (50%), as well as the parainfluenza 1 and 3 virus (25%), other viruses participate with lower percentages. Immune response in the respiratory system (innate and adaptive), cells and mechanismsThe human immune system is divided in two defense mechanisms or responses: a) Innate or nonspecific response that lacks specificity and memory, is the first line of defense of the organism, its components are always present to act immediately and b) Specific or adaptive response. This response is more complex, has a memory and identifies the viral specific peptides processed by antigen presenting cells, which activate the humoral immune response mediated by B cells or a T cell mediated cellular response. An efficient immune response depends on a correct interaction between the innate and adaptive immune system.Nonspecific or innate response. Cells of the innate immune system use a pattern recognition receptors (PRR) that are expressed on their surface and bind to pathogen-associated molecular patterns (PAMs), which are present in microorganisms. Viral PAMs can be: double stranded RNA or RNA produced during replication, surface proteins or glycoproteins. Toll-like receptors (TLR) represent a PRR family expressed in most cells of the organism, it have been identified 10 human types. The TLRs are formed by a binding domain ligand consisting of leucine repeats that interacts directly with viral antigens; a transmembrane domain and a cytoplasmatic domain responsible for initiating the extracellular signaling. Viral infections activate different TLR receptors (TLRs 3, 7, 8 and 9) that generally induce a protective immune response, however, also can be a part of pathogenic mechanisms.
These cells are actively involved in the production of proteins (lactoferrin), enzymes (lysozyme) and antimicrobial peptides (defensins) which together eliminate or neutralize the virus. An antibody binds to the surface of a cell infected by a virus, interacts with the Fc receptors and NK cells release proteins (perforins and granzymes) causing cell death.
NK cells can be activated by the stimulation of IFN-? and ? and other cytokines such as IL-12, IL15 and IL18 produced by infected cells, dendritic cells (DC) or macrophage (fig.3), [16, 17, 18, 19]. DC express MHC molecules on their surface localize the virus and migrate to the closest lymph node traveling through the lymphatic vessels eliminating the microorganism [17, 18].Soluble molecules. Complement is a system consisting of over 30 proteins that are activated by proteolysis in sequence. Complement is more efficient during the attack to enveloped viruses, because complement activation finished with the formation of a attack complex which is inserted in to viral membrane, causing the lysis of the virus [16, 19]. Complement anaphylatoxins (C3a and C5a) induce histamine, prostaglandins and leukotrienes release, promoting bronchoconstriction.
C3a and C5a have been found in high concentrations in the upper airways during infection by influenza virus. Are efficiently induced by the presence of double-stranded viral RNA (viral replication intermediary), the process involves three antiviral proteins: protein kinase (PKR), Oas1 and RnasaL, which block the translation and degradation of viral and cellular RNAs.
Interesntingly, influenza virus induces high levels of interferon with protective properties [20, 21, 22, 23] figure 5.Defensins. They are syntethized in leukocytes, macrophages and epithelial cells constitutively, in response to infection or during inflammation. Viral infections induce the production of defensins, which regulate the innate and adaptive immune response (positive and negative). The mechanisms of action and induction of defensins are multiple, generally depend on the type of infecting virus (enveloped and non-enveloped), defensin type and the target cell infected [18, 24].The respiratory epithelium induces production of ?-defensins, mainly of ?-defensin-2.
The mechanisms of action include: a) direct, when the peptide binds to the viral membrane by electrostatic attraction, form pores and cause lysis of the viral membrane. This mechanism occurs in the majority of enveloped viruses (influenzavirus, herpes, HIV); and b) indirect, when the defensin inactivate any signaling pathway in any step of the virus replication cycle (herpes, adenovirus). There are few studies on the mechanisms of induction of ?-defensins in the respiratory epithelium. When rhinovirus infects the respiratory epithelium, the ?-defensin-2 is induced by virus replication, mRNA activates the transcription factor NF-kB, and therefore, the gene that codifies for defensins; however, defensin has no direct effect on the virus.
Influenza virus induces the expression of ?-defensin-3, which inhibits the binding of the viral hemagglutinin with epithelium membrane. This same defensin inhibits viral fusion with the cell membrane during a RSV infection [25, 26].Acute phase proteins (APP). APP are serum proteins whose its concentration increases or decreases when there is an infection. APP are induced by pro-inflammatory cytokines like TNF-?, IL-6 and IL-1 that are synthesized in the liver. Examples of APP are the lectin that binds to mannose, C reactive protein and surfactant proteins A and D.
Specific or acquired immunityWhen the adaptive immune system contacts with a antigen it is developed a primary response that generates immunological memory, which at a second contact (secondary response) the response is more rapid and intense. The humoral response has as a major component the B lymphocytes that differentiate into antibody-producing plasmatic cells. When antibodies interact with phagocytic cells and complement, the viruses are neutralized.
In viral respiratory infections, IgA is of great importance as it is secreted by mucous epithelia, preventing the establishment of virus. IgM is the first antibody that is synthesized and prevailing in a primary response, also fix complement. The IgG is found in greater concentration in serum and is the only one that can cross the placenta in humans. Most respiratory viruses induce such antibodies that persist, and when a second exposure to the same antigen, the disease is less severe; unfortunately, virus may have mutations that are not recognized by the antibodies, therfore, reinfections are common. IgE is the antibody with the lowest concentration in the serum, but is the most important in allergic disorders. It has been reported that some viruses such as RSV, influenza, bocavirus, parainfluenza and metapneumovirus produce bronchial hyperreactivity or asthma increasing concentrations of this immunoglobulin in blood and secretions. Basophils and mast cells have receptors for these antibodies, when the antigen-antibody binding occurs and consequently activate, these cells release inflammatory mediators that cause many manifestations of these respiratory diseases [27].Cellular response.
The cellular response has as its principal components the T lymphocytes, which are divided into two populations according to their surface markers and the pattern of cytokines produced: CD4+, also called helper T cells (Th) and CD8 +, the cytotoxic lymphocytes (CTL). These specialized cells can proliferate and differentiate into effector and memory cells.In viral infections, CD8+ T cell response is essential for viral clearance. Lymphocytes are able to recognize through its receptor (TCR) by antigen processing performed by antigen presenting cells (dendritic cells or macrophages) associated with MHC molecules. For the differentiation and activation of T lymphocyte are required two signals are requare: the first is the specific recognition of the antigen on the target MHC class I-associated cel, and the second produced the cytokines produced by CD4+ T cells which recognize MHC-associated viral antigens class II. Cytotoxic T lymphocytes exert their antiviral effects by three mechanisms: producing lysis of infected cells, stimulate the production of enzymes that degrade viral genomes, and secrete cytokines. Evasion of the immune responseDespite effective defenses, some virus can to evade it by using different mechanisms, for example, in respiratory tract infections influenza virus inhibits the production of interferon by the protein NS1, a non-structural protein that is abundantly expressed in the nucleus of infected cells.
NS1 binds to double-stranded RNA by preventing activation of the dsRNA-dependent protein kinase (PKR) [28], commonly synthesized during induction of interferon (Figure 5).
PI and RSV respiratory viruses have a surface protein (F), which mediates the fusion of the viral membrane with the cell membrane. This mechanism enables the virus to spread from one cell to another without exposure and avoiding the effect of circulating antibodies. Viruses such as adenovirus and herpes employ transcription and replication strategies to maintain the viral genome in any cell type where the immune response is not efficient and viral particles are not produced for long periods. Other mechanisms used by respiratory viruses in the pathogenesisIn most infections, the viruses cause upper respiratory infections, while others reach the lower airways, may even cause necrosis and cell death, also induce inflammatory processes such as wheezing and hyperreactivity, both important in the development of chronic diseases such as asthma and chronic bronchitis for which some mechanisms have been proposed. In viral respiratory infections has been observed recruitment of inflammatory cells such as eosinophils, neutrophils, basophils, monocytes, macrophages, mast cells and T lymphocytes. Thus, when activated, these cells release mediators, cytokines or other compounds that increase inflammatory response [29, 30]. Alveolar macrophages are one of the first lines of cellular defense against virus infections. During viral replication in macrophages antiviral mechanisms are activated by stimulating, by stimulating the release of interferons or other cytokines, for example, studies have shown that alveolar macrophage infection by RSV, causes increased secretion of tumor necrosis factor alpha (TNF-?), as well as interleukins IL-8 and IL-6. It has also been observed that the macrophages express high levels of intercellular adhesion molecule-1 (ICAM-1), receptor molecule specific for some virus [17, 31, 32].Monocytes.
When human monocytes are infected by viruses, monocytes are activated, producing and releasing IFN-?, IFN-?, IL-1?, IL-6 and TNF-?. The production of these cytokines (with the exception of IFN-?) potentiates the production of granulocyte macrophage-colony stimulating factor (GM-CSF) [33].T Lymphocytes. According to the pattern synthesis of cytokines, helper T cells (Th) are classified into two types: Th1 cells secreting IL-2, IF-? and lymphotoxin, while Th2 cells secrete IL-4, IL-5, IL -6 and IL-10.
The RSV G protein stimulates Th2 type response and this would explain the symptoms of lower respiratory tract caused by this virus [34].Neutrophils. In viral respiratory infections, neutrophils are activated and recruited into the airways and probably generate oxygen metabolites or other metabolites or inflammatory cytokines that cause damage and late hyperreactivity 36. They are found in high concentrations in bronchial secretions of children infected with RSV, with parainfluenza virus and in nasal biopsies of subjects with rhinovirus infection [34].Eosinophils. Eosinophils release mediators such as leukotrienes (LTC4), platelet activating factor (PAF), major basic protein and cationic eosinophilic protein. When eosinophils are activated by virus are recruited into the airways causing damage and causing a late hyperreactivity reaction [35].

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