Relevant bibliographies by topics / Parainfluenza

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Parainfluenza'

Author: Grafiati
Published: 20 February 2023

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Journal articles on the topic "Parainfluenza"

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Henrickson, Kelly J. "Parainfluenza Viruses." Clinical Microbiology Reviews 16, no. 2 (April 2003): 242–64. http://dx.doi.org/10.1128/cmr.16.2.242-264.2003.

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SUMMARY Human parainfluenza viruses (HPIV) were first discovered in the late 1950s. Over the last decade, considerable knowledge about their molecular structure and function has been accumulated. This has led to significant changes in both the nomenclature and taxonomic relationships of these viruses. HPIV is genetically and antigenically divided into types 1 to 4. Further major subtypes of HPIV-4 (A and B) and subgroups/genotypes of HPIV-1 and HPIV-3 have been described. HPIV-1 to HPIV-3 are major causes of lower respiratory infections in infants, young children, the immunocompromised, the chronically ill, and the elderly. Each subtype can cause somewhat unique clinical diseases in different hosts. HPIV are enveloped and of medium size (150 to 250 nm), and their RNA genome is in the negative sense. These viruses belong to the Paramyxoviridae family, one of the largest and most rapidly growing groups of viruses causing significant human and veterinary disease. HPIV are closely related to recently discovered megamyxoviruses (Hendra and Nipah viruses) and metapneumovirus.
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Freymuth, François. "Virus parainfluenza." EMC - Biologie Médicale 1, no. 1 (January 2006): 1–4. http://dx.doi.org/10.1016/s2211-9698(06)76380-4.

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Weinberg, Geoffrey A. "Parainfluenza Viruses." Pediatric Infectious Disease Journal 25, no. 5 (May 2006): 447–48. http://dx.doi.org/10.1097/01.inf.0000218037.83110.c4.

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Kett, J. C., A. Loharikar, and H. M. Adam. "Influenza and Parainfluenza." Pediatrics in Review 30, no. 8 (July 31, 2009): 326–27. http://dx.doi.org/10.1542/pir.30-8-326.

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Kett, Jennifer Cobelli, and Anagha Loharikar. "Influenza and Parainfluenza." Pediatrics In Review 30, no. 8 (August 1, 2009): 326–27. http://dx.doi.org/10.1542/pir.30.8.326.

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Branche, Angela, and Ann Falsey. "Parainfluenza Virus Infection." Seminars in Respiratory and Critical Care Medicine 37, no. 04 (August 3, 2016): 538–54. http://dx.doi.org/10.1055/s-0036-1584798.

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Welliver, Robert C. "Parainfluenza Virus Bronchiolitis." American Journal of Diseases of Children 140, no. 1 (January 1, 1986): 34. http://dx.doi.org/10.1001/archpedi.1986.02140150036029.

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Zambon, Maria, Tim Bull, Carol J. Sadler, John M. Goldman, and Katherine N. Ward. "Molecular Epidemiology of Two Consecutive Outbreaks of Parainfluenza 3 in a Bone Marrow Transplant Unit." Journal of Clinical Microbiology 36, no. 8 (1998): 2289–93. http://dx.doi.org/10.1128/jcm.36.8.2289-2293.1998.

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Two consecutive nosocomial outbreaks of parainfluenza 3, in which 5 of 15 infected patients died, occurred in an adult bone marrow transplant unit. Parainfluenza 3 strain variation was assessed by reverse transcription-PCR sequencing of part of the parainfluenza 3 F gene, including the noncoding region, directly from clinical samples. Sequence data from the outbreaks were compared with those from 15 other parainfluenza 3 isolates circulating concurrently in the community; altogether, 13 strains which fell into three lineages were identified. Four immunosuppressed patients shed virus persistently for between 1 and 4 months without change in sequence. The first outbreak lasted 4 months and involved three parainfluenza 3 strains, and one persistently infected patient was implicated as the source of infection for three others. The second outbreak lasted for 1 month but involved only one strain. These data indicate that introduction of community parainfluenza 3 strains to the bone marrow transplant unit was followed by person-to-person transmission within the unit rather than reintroduction of virus from the community.
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Gülen, Figen, Candan Cicek, Zafer Kurugol, Esen Demir, Dost Zeyrek, Rahmi Özdemir, Remziye Tanac, and Tuba Karatas. "Parainfluenza type 3 outbreaks in Izmir children, Turkey." Tropical Doctor 37, no. 4 (October 1, 2007): 252–54. http://dx.doi.org/10.1258/004947507782333170.

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The present study was aimed to investigate characteristics of lower respiratory tract infections caused by parainfluenza type 3 viruses. Nasopharyngeal smears were taken from 178 patients with lower respiratory infections for the diagnosis of respiratory syncytial virus, adenovirus, influenza and parainfluenza viruses between December 2004 and April 2005. Parainfluenza type 3 was isolated from the viral specimens of 96 (53.9%) patients and it was noticeable that the parainfluenza type 3 outbreak occurs during winter. Obviously, improving the aetiological diagnosis of viral infections might avoid unnecessary therapy, antibiotics in particular, and would allow for preventive isolation of infected patients.
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Mancini, Dalva Assunção Portari, Aparecida Santo Pietro Pereira, Rita Maria Zucatelli Mendonça, Adelia Hiroko Nagamori Kawamoto, Rosely Cabette Barbosa Alves, José Ricardo Pinto, Enio Mori, Leonardo José Richtzenhain, and Jorge Mancini-Filho. "PRESENCE OF RESPIRATORY VIRUSES IN EQUINES IN BRAZIL." Revista do Instituto de Medicina Tropical de São Paulo 56, no. 3 (June 2014): 191–95. http://dx.doi.org/10.1590/s0036-46652014000300002.

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Equines are susceptible to respiratory viruses such as influenza and parainfluenza. Respiratory diseases have adversely impacted economies all over the world. This study was intended to determine the presence of influenza and parainfluenza viruses in unvaccinated horses from some regions of the state of São Paulo, Brazil. Blood serum collected from 72 equines of different towns in this state was tested by hemagglutination inhibition test to detect antibodies for both viruses using the corresponding antigens. About 98.6% (71) and 97.2% (70) of the equines responded with antibody protective titers (≥ 80 HIU/25µL) H7N7 and H3N8 subtypes of influenza A viruses, respectively. All horses (72) also responded with protective titers (≥ 80) HIU/25µL against the parainfluenza virus. The difference between mean antibody titers to H7N7 and H3N8 subtypes of influenza A viruses was not statistically significant (p > 0.05). The mean titers for influenza and parainfluenza viruses, on the other hand, showed a statistically significant difference (p < 0.001). These results indicate a better antibody response from equines to parainfluenza 3 virus than to the equine influenza viruses. No statistically significant differences in the responses against H7N7 and H3N8 subtypes of influenza A and parainfluenza 3 viruses were observed according to the gender (female, male) or the age (≤ 2 to 20 years-old) groups. This study provides evidence of the concomitant presence of two subtypes of the equine influenza A (H7N7 and H3N8) viruses and the parainfluenza 3 virus in equines in Brazil. Thus, it is advisable to vaccinate equines against these respiratory viruses.
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Dissertations / Theses on the topic "Parainfluenza"

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Bacon, Matthew Neil. "An antiviral peptide targeting influenza and parainfluenza." Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/17861.

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Respiratory virus infections, such as those caused by influenza, parainfluenza and respiratory syncytial virus (hRSV), continue to be a major cause of morbidity and mortality in both the developed and developing world. Currently, the main means of control of influenza virus infection is vaccination, which requires advanced knowledge of the strain that will be prevalent each year. Alternative strategies involve the use of anti-viral drugs, which function primarily as a prophylactic. Currently, there are five main drugs available against influenza, the adamantanes (amantadine and rimantidine) and the neuraminidase inhibitors (oseltamivir, zanamivir and peramivir). However, major problems exist with antivirals, notably the development of drug resistance. This means that new drugs are urgently required that also satisfy the need to intervene at specific phases of the infection. This thesis describes the development of a peptide with anti-influenza virus activity (Flupep), from which a library of closely related peptides were synthesised, with the aim of optimising antiviral efficacy. Peptides were tested in vitro using a plaque reduction assay on cultured cell lines, Vero and MDCK for parainfluenza and influenza respectively. Two strains of influenza and two of parainfluenza were used, covering the main subtypes that infect humans: Influenza A, Influenza B, PIV2 and PIV3. The plaque assay involved mixing a fixed dose of virus with dilutions of peptide and infecting the cultured cells, followed by incubation for between 3 and 14 days. The cells were then fixed, stained and plaques counted as a measure of viral infectivity. Previous work had shown that Flupep both interacts with haemagglutinin and is an antagonist of inflammatory cytokines. As a possible explanation for antiviral activity, binding affinity of the peptide to haemagglutinin was measured utilising enzyme linked immunosorbent assays. However, significant binding was not detected, suggesting non-specific binding and anti-inflammatory potential are more important routes for antiviral activity. Peptides which demonstrated greater than 90% plaque knockdown in vitro were evaluated in vivo. Anaesthetised mice were infected with influenza A and administered with the peptide concurrently. Following infection, body weights were measured daily and clinical signs, such as shortness of breath, quality of coat and posture, were monitored as indicators of overall health. Most mice were culled on the seventh day post-infection and lung viral titres were determined using a plaque assay. Two peptides were identified with high efficacy against influenza. These peptides, when used in vivo, improved clinical signs of and dramatically reduced levels of infectious virus in the lungs by 7 days post infection. The peptide with highest efficacy was PEGylated and subsequently shown to possess therapeutic potential. Intranasal administration of the PEG-peptide to anaesthetised mice, on the two days subsequent to infection with influenza A, revealed a 17-fold fall in lung viral titres by the fourth day post-infection. Overall, Flupep demonstrates great potential as a future therapeutic agent for treatment of Influenza and potentially Parainfluenza.
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Wu, Ying, and 武盈. "Discovery and characterization of a novel porcine paramyxovirus." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hdl.handle.net/10722/196086.

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Most emerging infectious diseases in humans are zoonotic agents. Since the emergence of severe acute respiratory syndrome (SARS), swine-origin influenza and avian influenza epidemics, the study of novel and emerging viruses with zoonotic potential has been considered more and more important. Paramyxoviruses have been known for their potential to cross species barrier and infect new hosts. In the last decade, a number of novel and emerging paramyxoviruses have been reported in various animals. Our research group recently identified three novel bat paramyxoviruses, Tuhoko viruses 1, 2 and 3 (ThkPV-1, 2, and 3) from fruit bats in mainland China, an unclassified paramyxovirus, named Tailam virus (TlmPV) from Sikkim rats and a novel feline paramyxovirus, called Feline morbillivirus(FmoPV) from domestic cats in Hong Kong, suggesting that there is still a diversity of undescribed paramyxoviruses in animals. In this study, a novel porcine paramyxovirus, Swine parainfluenza virus 1 (SpiPV-1), was discovered and characterized from deceased pigs in Hong Kong. A total of 951 samples from 386 deceased pigs were collected, including 386 nasopharyngeal swab, 303 rectal swab, 153 blood, 56 lung and 53 liver samples. And SpiPV-1 was detected in 12 (3.1%) of 386 nasopharyngeal swab and 2 (0.7%) of 303 rectal swab samples by RT-PCR. All the blood, lung and liver samples showed negative results. The complete genome sequences of three strains (SpiPV-1 S033N, SpiPV-1 S119N and SpiPV-1 S206N) from three pigs were amplified and determined. The genome organization of SpiPV-1 is similar to that of viruses under genus Respirovirus, subfamily Paramyxovirinae. The genome contains six genes (3’-N-P/V/C-M-F-HN-L-5’) and putatively codes for the nucleocapsid (N), phosphoprotein (P/V/C), matrix (M), fusion (F), attachment (HN) and large (L) proteins.Like other respiroviruses, the P gene of SpiPV-1 can produce more than one protein, including P, V and W proteins by mRNA editing and C protein by alternative translation initiation. And phylogenetic analysis showed that in all six phylogenetic trees constructed byusing the N, P, M, F, HN and L genes, the three strains SpiPV-1 S033N, S119N and S206N formed a distinct cluster among the known respiroviruses and were most closely related to Sendai virus (SenPV) and Human parainfluenza virus 1 (HpiPV-1). The genome organization, P gene analysis and phylogenetic analysis all suggested that SpiPV-1 is a novel paramyxovirus under genus Respirovirus, subfamily Paramyxovirinae. Seven porcine samples positive for SpiPV-1 were cultured in five different cell lines for viral isolation. However, no cytopathic effect was observed and no viral replication was detected in any of the cell lines. The pathogenicity and emergent potential of SpiPV-1 remain to be determined. Further studies on serology and development of cell cultures for viral isolation may provide better insight into this novel paramyxovirus.
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Saffran, Holly Anne. "Regulation of human parainfluenza virus type 3 transcription." Thesis, University of Ottawa (Canada), 1995. http://hdl.handle.net/10393/9503.

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To elucidate the roles of the junctional elements in HPIV3 transcription, cDNAs were constructed containing CAT and luciferase reporter genes flanked by sequences representing the HPIV3 termini necessary for transcription, replication and packaging. Mutations to the gene end sequence abolished expression of the upstream and downstream genes. Deleting the gene start sequence at the junction resulted increased expression of the upstream gene, but abrogated downstream gene activity. Alterations in the length of the intergenic trinucleotide resulted in decreased expression of both upstream and downstream genes. Mutations in the sequence of this nontranscribed trinucleotide resulted in decreased activity of the upstream gene but no change in expression of the downstream gene. The gene end sequence does not appear to contain the only signals for termination of transcription. The purine trinucleotide intergenic region is important for termination, but only the presence of three nucleotides appears to be necessary and sufficient for expression of the following gene. Results obtained from assaying reporter activity could often be interpreted in several ways. For example, the data could not distinguish between polymerase readthrough and premature termination. Two RNA detection methods were investigated and show promise as means for detecting and analyzing specific RNA species in transfected cells. (Abstract shortened by UMI.)
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Chapman, Amanda Ruth. "Regulation of the human parainfluenza virus (hPIV3) fusion protein." View the abstract Download the full-text PDF version, 2008. http://etd.utmem.edu/ABSTRACTS/2008-048-Chapman-index.htm.

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Thesis (M.S.)--University of Tennessee Health Science Center, 2008.
Title from title page screen (viewed on January 6, 2009). Research advisor: Charles J. Russell, Ph.D. Document formatted into pages (ix, 41p. : ill.). Vita. Abstract. Includes bibliographical references (p. 38-41).
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Norsted, Hanna. "The effect of interferon on the transcription pattern of parainfluenza virus 5." Thesis, University of St Andrews, 2013. http://hdl.handle.net/10023/3403.

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Interferon (IFN) is activated in response to virus infections and upregulates interferon-stimulated genes (ISGs) resulting in the expression of hundreds of proteins, many of which have direct or indirect antiviral activity. Parainfluenza virus 5 (PIV5) of the Paramyxoviridae family is a non-segmented negative sense single-stranded RNA virus with seven genes encoding eight proteins. Here we present that IFN induces alterations in the pattern of both virus transcription and translation and that ISG56 is primarily responsible for these effects. We report that when cells were treated with IFN post-infection, virus protein synthesis was inhibited while virus transcription levels were increased. These results suggest that ISG56 selectively inhibits the translation of viral mRNAs. In addition, the relationship of various PIV5 isolates was analysed by next generation sequencing. Four areas with a high degree of single nucleotide polymorphisms (SNPs) were identified and mapped to the intergenic regions of NP-V/P, M-F and HN-L, as well as the entire SH gene. Three of the isolates, the porcine strain SER and the canine strains CPI+ and CPI-, did not express an SH protein due to the lack of a start codon. A low degree of variation was found in the amino acid sequence of the HN glycoprotein suggesting that PIV5 may be less pressured to evolve in order to evade immune responses, such as neutralising antibodies.
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Murphy, Lise. "Regulation of human parainfluenza virus type 3 fusion protein expression." Thesis, University of Ottawa (Canada), 2004. http://hdl.handle.net/10393/26723.

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Human parainfluenza virus type 3 (HPIV3) is an enveloped, negative-strand, non-segmented RNA virus. HPIV3 is a human respiratory pathogen that primarily causes diseases such as croup, bronchiolitis and pneumonia in children. The virus has two glycoproteins that allow it to interact with host cells, the receptor binding protein hemagglutinin-neuraminidase (HN) and the fusion protein (F), which enables the virus to enter the cell by fusion of the viral envelope to the target cell plasma membrane. This research was initiated with the goal of determining mechanisms by which HPIV3 regulates the expression of the fusion protein. Evidence indicated that the transcription of the F gene differed from that of the other genes because there was a very high level of read-through transcription at the junction of the matrix (M) gene and the F gene. This read-through transcription caused >80% of the potential F gene transcripts to be present in biscistronic M/F mRNA, in which the F open reading frame cannot be translated. (Abstract shortened by UMI.)
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Smielewska, Anna Alexandra. "Human parainfluenza virus 3 : genetic diversity, virulence and antiviral susceptibility." Thesis, University of Cambridge, 2019. https://www.repository.cam.ac.uk/handle/1810/287954.

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Human parainfluenza 3 (HPIV3) is a member of the Paramyxoviridae, a single strain negative-sense non-segmented RNA virus in the order Mononegavirales. It is a respiratory pathogen with a broad spectrum of presentations for which there is currently neither a vaccine nor licensed treatment for HPIV3. To date most research on HPIV3 has been conducted using significantly culture adapted reference strains. Therefore, minimally adapted clinical strains were grown in two cell culture systems: immortalised and primary. Plaque phenotype, growth kinetics and inflammatory response triggered were evaluated and it was found that there is a range of phenotypes exhibited by clinical strains with potential implications in vivo. To examine the genetic diversity of circulating strains of HPIV3 in the UK, a new amplicon based sequencing pipeline for whole genome sequencing of HPIV3 was developed and validated. A short hypervariable region in the HPIV3 genome was identified and evaluated as a potential candidate for subsequent phylogenetic analysis compared to whole genome data. This method was then applied to tracking an HPIV3 outbreak that took place on a paediatric oncology ward. It was found to be a point-source outbreak and the clinical impact in this setting, as well as the infection control procedures involved were evaluated. Finally a robust in vitro model for the evaluation of potential therapeutic candidates for HPIV3, based on a panel of minimally passaged clinical strains as well as a culture-adapted reference strain, was set up. This model was applied to three potential inhibitors of HPIV3: ribavirin, favipiravir and zanamivir. The results showed that clinical strains were at least as susceptible to ribavirin and favipiravir as the laboratory reference strain and significantly more susceptible to zanamivir. This indicates that further work on minimally adapted clinical strains is essential to further the understanding of this important virus.
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Jogalekar, Prachi. "Analysis of gene junction sequences of human parainfluenza virus type 3." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0019/MQ58465.pdf.

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Bradford, Hannah Elizabeth Linda. "Cell-mediated immunity to parainfluenza type 3 virus in young calves." Thesis, Queen's University Belfast, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.334497.

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Bamford, Anona Isabelle. "Interactions between cytotoxic effector cells and bovine parainfluenza type 3 virus." Thesis, Queen's University Belfast, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.241326.

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Books on the topic "Parainfluenza"

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Collins, Kay R. Variation in the haemagglutinin-neuraminidase gene of human parainfluenza 3 virus. [s.l.]: typescript, 1994.

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Berger, Stephen, and Inc Gideon Informatics. Parainfluenza Virus: Global Status. Gideon Informatics, Incorporated, 2021.

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Berger, Stephen, and Inc Gideon Informatics. Parainfluenza Virus: Global Status. Gideon Informatics, Incorporated, 2019.

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Berger, Stephen, and Inc Gideon Informatics. Parainfluenza Virus: Global Status. Gideon Informatics, Incorporated, 2022.

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Basaraba, Randall Joseph. Mechanisms of in vitro immunosuppression by bovine parainfluenza virus type 3. 1991.

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Silflow, Ronald Mark. Effects of omega-3 polyunsaturated fatty acids on bovine alveolar macrophages infected with parainfluenza virus, type 3. 1992.

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Wilson, John W., and Lynn L. Estes. Respiratory Tract Infections. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199797783.003.0067.

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Diagnostic criteria include productive cough, symptoms of upper respiratory infection, and negative findings on chest radiographs. Viral agents are the most common cause; antibiotics are therefore not beneficial.•Viral causes: Influenza, parainfluenza, and other respiratory viruses affect >70% of patients•Less common but potentially antibiotic-responsive infectious agents...
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Harrison, Mark. Respiratory viruses. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198765875.003.0027.

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This chapter describes the microbiology of respiratory viruses as it applies to Emergency Medicine, and in particular the Primary FRCEM examination. The chapter outlines the key details of the epidemiology, clinical features, basis of immunity, and management and treatment of rhinovirus, influenza, parainfluenza and respiratory syncytial virus. This chapter is laid out exactly following the RCEM syllabus, to allow easy reference and consolidation of learning.
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Publications, ICON Health. The Official Parent's Sourcebook on Human Parainfluenza Viruses: A Revised and Updated Directory for the Internet Age. Icon Health Publications, 2002.

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Newton, Pippa. Upper respiratory tract infections, including influenza. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0128.

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Infections of the nasal cavity, sinuses, pharynx, epiglottis, and larynx are termed upper respiratory tracts infections. These include acute coryza, pertussis, sinusitis, pharyngitis, tonsillitis, epiglottitis, laryngitis, laryngotracheobronchitis, and influenza. Rhinoviruses and coronaviruses account for the majority of acute coryzal illnesses. Acute sinusitis (<4 weeks duration) is also usually viral in origin. About 70% of pharyngitis and tonsillitis cases are viral in etiology. Haemophilus influenzae (Type B) is responsible for most cases of epiglottitis. Acute laryngitis and laryngotracheobronchitis are usually caused by human parainfluenza viruses. This chapter focuses on upper respiratory tract infections, including their etiology, symptoms, demographics, natural history, complications, diagnosis, prognosis, and treatment.
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Book chapters on the topic "Parainfluenza"

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Gooch, Jan W. "Parainfluenza." In Encyclopedic Dictionary of Polymers, 913. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_14420.

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Glezen, W. Paul, Frank A. Loda, and Floyd W. Denny. "Parainfluenza Viruses." In Viral Infections of Humans, 493–507. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0705-1_18.

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Stöcker, W., and C. Krüger. "Parainfluenza-Viren." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-49054-9_2344-1.

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Stöcker, W., and C. Krüger. "Parainfluenza-Viren." In Springer Reference Medizin, 1821. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_2344.

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Khayyata, Said H., and Carol Farver. "Parainfluenza Virus." In Viruses and the Lung, 87–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-40605-8_10.

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Clover, Richard D. "Parainfluenza Viruses." In Pulmonary Infections and Immunity, 309–18. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4899-1063-9_17.

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Glezen, W. Paul, Frank A. Loda, and Floyd W. Denny. "Parainfluenza Viruses." In Viral Infections of Humans, 493–507. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-8138-3_18.

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Glezen, W. Paul, and Floyd W. Denny. "Parainfluenza Viruses." In Viral Infections of Humans, 551–67. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-0036-4_19.

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Gooch, Jan W. "Parainfluenza Virus." In Encyclopedic Dictionary of Polymers, 913. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_14421.

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Englund, Janet A., and Anne Moscona. "Paramyxoviruses: Parainfluenza Viruses." In Viral Infections of Humans, 579–600. Boston, MA: Springer US, 2014. http://dx.doi.org/10.1007/978-1-4899-7448-8_25.

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Conference papers on the topic "Parainfluenza"

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Ibe, U., D. Spinelle, N. Jiwa, A. Latifi, M. Alvi, and V. Yap. "Inflammatory Cardiomyopathy from Parainfluenza 3 Virus." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6607.

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Drake, Matthew, Elizabeth Bivins-Smith, Becky Proskocil, Zhenying Nie, Jamie Lee, Nancy Lee, Allison Fryer, and David Jacoby. "Eosinophils attenuate parainfluenza virus infection through nitric oxide." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.oa4470.

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Sun, Y. "Clinical Manifestations of Parainfluenza Virus Type 4 in Hospitalized Children in South Korea: A Large-Scale and Comparative Study to Parainfluenza Types 1-3." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1187.

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Chang, C. H., J. R. Wagner, B. J. Proskocil, D. B. Jacoby, A. D. Fryer, C. M. Evans, and M. G. Drake. "Antiviral Role for Airway Mucins Muc5ac and Muc5b Against Parainfluenza Virus." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a5653.

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Drake, Matthew, Becky Proskocil, Zhenying Nie, Fryer Allison, and Jacoby David. "Human eosinophil toll-like receptor 7-induced nitric oxide is antiviral against parainfluenza." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa3970.

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Rynko, Abby E., Allison D. Fryer, and David B. Jacoby. "Etanercept Blocks Parainfluenza Downregulation Of M2 Muscarinic Receptor MRNA In Parasympathetic Nerves In Vivo." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2150.

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Rynko, Abby E., Allison D. Fryer, and David B. Jacoby. "Parainfluenza And Influenza A Virus Can Not Be Detected In Airway Sensory Neurons Of Infected Mice." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5546.

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Padappayil, R. P., R. Tiperneni, and B. Li. "Non-COVID Viral Pneumonia in the COVID-19 Era: A Severe Case of Human Parainfluenza Virus Infection." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a3109.

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Olson, M. T., R. Walia, M. F. Hahn, and A. Arjuna. "Parainfluenza-Mediated High Grade Airway Rejection in a Patient with Respiratory Symptoms Post-Lung Transplantation: A Case Report." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a3979.

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Kummerfeldt, Carlos E., John Huggins, Richard Monk, and Charlie Strange. "Legionella Londiniensis And Parainfluenza Virus Type 3 Co-Infection In A Patient With Chronic Graft-Versus Host Disease." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a6118.

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Reports on the topic "Parainfluenza"

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Welch, Michael, Jie Park, Phillip Gauger, Karen Harmon, Kevin Lin, Pablo Pineyro, and Jianqiang Zhang. Porcine Parainfluenza Virus Type 1 (PPIV-1) in U.S. Swine: Summary of Veterinary Diagnostic Laboratory Data. Ames (Iowa): Iowa State University, January 2017. http://dx.doi.org/10.31274/ans_air-180814-389.

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You might also be interested in the extended bibliographies on the topic 'Parainfluenza' for particular source types:
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