Parainfluenza Virus Bronchiolitis

Welliver, Robert C.; Wong, David; Sun, Martha; McCarthy, Nancy

doi:10.1001/archpedi.1986.02140150036029

Cited by 101 publications

(39 citation statements)

References 22 publications

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“…After an incubation period of 2-8 days the virus replicates in the nasopharyngeal epithelium and may spread to the lower respiratory tract. Indeed, when parainfluenza virus type 3 produces severe disease, infection of the small air passages is likely with the development of bronchopneumonia, bronchiolitis or bronchitis (17)(18)(19).…”

Section: Introductionmentioning

confidence: 99%

Parainfluenza Virus Infection in Adult Lung Transplant Recipients: An Emergent Clinical Syndrome with Implications on Allograft Function

Vilchez

Dauber

McCurry

et al. 2003

American Journal of Transplantation

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Parainfluenza virus is a common cause of seasonal upper respiratory tract infections in children and adults. Studies indicate that parainfluenza virus may play an important role in the etiology of respiratory tract infections in lung transplant recipients with an estimated incidence of 5.3 per 100 patients. Parainfluenza virus type 3 is the most frequent serotype in lung transplant patients. The rate of lower respiratory tract infections with parainfluenza virus among lung transplant recipients is between 10 and 66% of cases. In addition, trans-bronchial biopsy at the time of parainfluenza infection shows signs of acute allograft rejection. Subsequently, 32% of patients have been found to have active bronchiolitis obliterans at a median time of 6 months (range 1-14) postviral infection. These findings indicate that parainfluenza virus infections may have long-term implications for lung transplant recipients. Further studies are required to identify the mechanisms of immunomodulation of parainfluenza virus among these patients. In addition, controlled studies are needed to evaluate the efficacy of aerosolized ribavarin in the treatment of parainfluenza virus infection and to determine whether vaccines may be effective in these high-risk patients.

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Section: Introductionmentioning

confidence: 99%

Parainfluenza Virus Infection in Adult Lung Transplant Recipients: An Emergent Clinical Syndrome with Implications on Allograft Function

Vilchez

Dauber

McCurry

et al. 2003

American Journal of Transplantation

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“…Two subgroups of RSV (A and B) circulate at any given time. The F proteins of the two RSV subgroups are highly conserved (98% amino acid identity), unlike the RSV attachment glycoproteins (G), which display only 53% identity at the amino acid level.hPIV3 is the causative agent of croup, an acute lower respiratory disease most often observed in young children (6,8,29). …”

mentioning

confidence: 99%

“…hPIV3 is the causative agent of croup, an acute lower respiratory disease most often observed in young children (6,8,29).…”

mentioning

confidence: 99%

Effects of Human Metapneumovirus and Respiratory Syncytial Virus Antigen Insertion in Two 3′ Proximal Genome Positions of Bovine/Human Parainfluenza Virus Type 3 on Virus Replication and Immunogenicity

Tang¹,

Schickli²,

MacPhail³

et al. 2003

J Virol

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A live attenuated bovine parainfluenza virus type 3 (PIV3), harboring the fusion (F) and hemagglutininneuraminidase (HN) genes of human PIV3, was used as a virus vector to express surface glycoproteins derived from two human pathogens, human metapneumovirus (hMPV) and respiratory syncytial virus (RSV). RSV and hMPV are both paramyxoviruses that cause respiratory disease in young children, the elderly, and immunocompromised individuals. RSV has been known for decades to cause acute lower respiratory tract infections in young children, which often result in hospitalization, while hMPV has only been recently identified as a novel human respiratory pathogen. In this study, the ability of bovine/human PIV3 to express three different foreign transmembrane surface glycoproteins and to induce a protective immune response was evaluated. The RNAdependent RNA polymerase of paramyxoviruses binds to a single site at the 3 end of the viral RNA genome to initiate transcription of viral genes. The genome position of the viral gene determines its level of gene expression. The promoter-proximal gene is transcribed with the highest frequency, and each downstream gene is transcribed less often due to attenuation of transcription at each gene junction. This feature of paramyxoviruses was exploited using the PIV3 vector by inserting the foreign viral genes at the 3 terminus, at position 1 or 2, of the viral RNA genome. These locations were expected to yield high levels of foreign viral protein expression stimulating a protective immune response. The immunogenicity and protection results obtained with a hamster model showed that bovine/human PIV3 can be employed to generate bivalent PIV3/RSV or PIV3/hMPV vaccine candidates that will be further evaluated for safety and efficacy in primates.Despite control of many infectious diseases in the industrialized world, acute viral respiratory tract infections remain a leading cause of illness and reason for hospitalization. Two paramyxoviruses, respiratory syncytial virus (RSV) and human parainfluenza virus type 3 (hPIV3), are the causative agents of acute respiratory diseases of infancy and early childhood, resulting in 20 to 25% of pneumonia and 45 to 50% of bronchiolitis in hospitalized children (8). In addition, a recently identified human metapneumovirus (hMPV) appears to be associated with lower respiratory tract infections in children (25). Preliminary epidemiological reports have estimated an hMPV disease incidence rate of 7 to 10% in young children (5,11,16,18,25). The symptoms of hMPV infections are similar to those caused by RSV and hPIV3, and hospitalizations of young children with acute lower respiratory tract infections are necessary in some cases (17). Recently, Greensill et al. reported the detection of hMPV in bronchoalveolar lavage fluids from 21 of 30 infants (70%) ventilated for RSV bronchiolitis (7).RSV remains one of the most common respiratory pathogens afflicting infants, the elderly, and immunocompromised individuals. Hospitalization and immunoglobulin treatment are of...

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“…In addition, RSV and parainfluenza virus have the capacity to induce an IgE-specific antibody response in the airway, the presence and quantity of virus-specific IgE possibly being specifically related to the severity of symptoms [37].…”

Section: Infectionsmentioning

confidence: 99%

In 2532 Children we Report the Developmental Factors Influencing the Development of Atopic Diseases

Cantani¹

2017

Austin J Allergy

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Allergic asthma and rhinitis, Atopic Dermatitis (AD), urticaria and gastrointestinal allergy, are common diseases of infants and children. It was recently estimated that 14% of children suffer from AD, 8% from food allergy, and 12% from asthma [1,2]. The cumulated incidence of these diseases in adolescents has been estimated between 25-35%, while the prevalence is about 20% [3]. The phenotypic expression of these illnesses varies extensively, being very mild in some cases, severe in many, and even life threatening in others. Specific IgE antibodies to foods and positive challenge tests to a number of food allergens are frequently present in children with these disorders. Cow's Milk (CM) appears to be the most common offending food both in gastrointestinal (vomiting, diarrhea, etc) and in cutaneous manifestations (urticaria and AD). About 0.5-7% of infants suffer from more or less adverse reactions to CM [4]. Babies particularly of atopic parents are at high risk of developing atopic diseases; therefore they are defined as at-risk babies [5][6][7].conditions. It has been known for centuries that heredity plays an important role in the development of atopy. A child with a negative family history still has about a 5-15% risk of developing atopy. However, children with a parental history of atopic disease are at higher risk for the development of atopic symptoms. It has been found that if one parent is affected, the chances of an offspring being affected vary between 20 and 40%. If both parents are affected the figure increases up to 40-60%, and 50-80% if both show the same allergic manifestations. The risk of atopy in children who have an allergic sibling ranges between 25 and 35% [3,10].The importance of genetic factors is also demonstrated by other data:(I) children with positive family history for atopy develop allergic symptoms earlier than those with a negative family history [11], (II) The higher the incidence the higher the number of affected subjects in the same family [3].Notable differences exist in the so-called predisposition to atopic diseases, and further study appears to be necessary to better delineate the role played by genetic factors in the development of such disorders.In many allergic patients total serum IgE levels are found to be elevated, and it has been shown that a high total serum IgE level in infants is often associated with the subsequent development of atopic symptoms. Therefore, it was proposed that the measurement of IgE by PRIST testing in infants or at birth would have a predictive value in the atopy development. Several investigators have demonstrated that the risk of developing atopic diseases was very high when the cord IgE level was above 0.5 IU/ml [5,8,9,12].Our data shows that a newborn can be considered at risk for atopy when the cord IgE level is above 0.8 IU/ml [5]. We have also shown that neonates of non atopic parents (0.032 + 0

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Parainfluenza Virus Bronchiolitis

Cited by 101 publications

References 22 publications

Parainfluenza Virus Infection in Adult Lung Transplant Recipients: An Emergent Clinical Syndrome with Implications on Allograft Function

Parainfluenza Virus Infection in Adult Lung Transplant Recipients: An Emergent Clinical Syndrome with Implications on Allograft Function

Effects of Human Metapneumovirus and Respiratory Syncytial Virus Antigen Insertion in Two 3′ Proximal Genome Positions of Bovine/Human Parainfluenza Virus Type 3 on Virus Replication and Immunogenicity

In 2532 Children we Report the Developmental Factors Influencing the Development of Atopic Diseases

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