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Academic literature on the topic 'Parainfluenza viruses'

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Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Parainfluenza viruses"

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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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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Vainionpää, R., and T. Hyypiä. "Biology of parainfluenza viruses." Clinical Microbiology Reviews 7, no. 2 (April 1994): 265–75. http://dx.doi.org/10.1128/cmr.7.2.265.

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Parainfluenza virus types 1 to 4 (PIV1 to PIV4) are important human pathogens that cause upper and lower respiratory tract infections, especially in infants and children. PIV1, PIV2, and PIV3 are second only to respiratory syncytial virus as a cause of croup in young children. Although some clinical symptoms are typical of PIVs, etiologic diagnosis always requires detection of infectious virus, viral components, or an antibody response. PIVs are typical paramyxoviruses, causing a syncytial cytopathic effect in cell cultures; virus growth can be confirmed either by hemadsorption or by using immunological reagents. Currently, PIV is most often diagnosed by demonstrating viral antigens in clinical specimens by rapid and highly sensitive immunoassays. More recently, PCR has been used for the detection of PIVs. Serological diagnosis is made by detecting a rising titer of immunoglobulin G or by demonstrating immunoglobulin M antibodies. PIVs infect species other than humans, and animal models are used to study the pathogenesis of PIV infections and to test candidate vaccines. Accumulating knowledge on the molecular structure and mechanisms of replication of PIVs has accelerated research on prevention and treatment. Several strategies for vaccine development, such as the use of live attenuated, inactivated, recombinant, and subunit vaccines, have been investigated, and it may become possible to prevent PIV infections in the near future.

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Vainionpää, R., and T. Hyypiä. "Biology of parainfluenza viruses." Clinical Microbiology Reviews 7, no. 2 (1994): 265–75. http://dx.doi.org/10.1128/cmr.7.2.265-275.1994.

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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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Hilleman, Maurice R. "THE PARAINFLUENZA VIRUSES OF MAN." Annals of the New York Academy of Sciences 101, no. 2 (December 15, 2006): 564–75. http://dx.doi.org/10.1111/j.1749-6632.1962.tb18897.x.

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Ito, Y., M. Tsurudome, H. Komada, and H. Tomoto. "Antigenic structures of human parainfluenza viruses." Uirusu 39, no. 1 (1989): 29–45. http://dx.doi.org/10.2222/jsv.39.29.

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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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Maeda, Yasuko, Masato Hatta, Ayato Takada, Tokiko Watanabe, Hideo Goto, Gabriele Neumann, and Yoshihiro Kawaoka. "Live Bivalent Vaccine for Parainfluenza and Influenza Virus Infections." Journal of Virology 79, no. 11 (June 1, 2005): 6674–79. http://dx.doi.org/10.1128/jvi.79.11.6674-6679.2005.

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ABSTRACT Influenza and human parainfluenza virus infections are of both medical and economical importance. Currently, inactivated vaccines provide suboptimal protection against influenza, and vaccines for human parainfluenza virus infection are not available, underscoring the need for new vaccines against these respiratory diseases. Furthermore, to reduce the burden of vaccination, the development of multivalent vaccines is highly desirable. Thus, to devise a single vaccine that would elicit immune responses against both influenza and parainfluenza viruses, we used reverse genetics to generate an influenza A virus that possesses the coding region for the hemagglutinin/neuraminidase ectodomain of parainfluenza virus instead of the influenza virus neuraminidase. The recombinant virus grew efficiently in eggs but was attenuated in mice. When intranasally immunized with the recombinant vaccine, all mice developed antibodies against both influenza and parainfluenza viruses and survived an otherwise lethal challenge with either of these viruses. This live bivalent vaccine has obvious advantages over combination vaccines, and its method of generation could, in principle, be applied in the development of a “cocktail” vaccine with efficacy against several different infectious diseases.

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Ånestad, G. "Surveillance of respiratory viral infections by rapid immunofluorescence diagnosis, with emphasis on virus interference." Epidemiology and Infection 99, no. 2 (October 1987): 523–31. http://dx.doi.org/10.1017/s0950268800068023.

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SUMMARYDuring the 7-year period from September 1978 to August 1985, smear specimens of nasopharyngeal secretions from 3132 patients mainly hospitalized children, taken in different regions in Norway, were examined for respiratory viruses by the rapid immunofluorescence (IF) technique. A positive diagnosis for respiratory syncytial virus (RSV), parainfluenza virus type 1, 2 and 3 or influenza A and B virus was made for 896 patients (29%). The greatest prevalence for all these viruses was observed during the colder months with only sporadic cases during the summer months. A relative increase in parainfluenza virus activity, involving several parainfluenza virus types, was observed in every second autumn and during these periods only sporadic cases of RSV infection were diagnosed. Also both RSV and parainfluenza viruses were less frequently found during influenza virus epidemics and regional differences in RSV activity were observed. During the four autumn periods 1982–85 the monthly number of positive virus identifications by IF followed an epidemic curve, while the corresponding number of negative samples was relatively constant. The results of this study suggest interference between RSV, parainfluenza viruses and influenza virus in reaching their epidemiological peaks. It is suggested that interferon might be a mediator of this effect.

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Dissertations / Theses on the topic "Parainfluenza viruses"

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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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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Chan, Yuk-on. "Impact of respiratory viruses on mortality." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/b39724025.

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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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Chan, Yuk-on, and 陳旭安. "Impact of respiratory viruses on mortality." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B39724025.

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Alias, Nadiawati. "Multivalent sialic acid binding proteins as novel therapeutics for influenza and parainfluenza infection." Thesis, University of St Andrews, 2014. http://hdl.handle.net/10023/4479.

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In nature, proteins with weak binding affinity often use a multivalency approach to enhance protein affinity via an avidity effect. Interested in this multivalency approach, we have isolated a carbohydrate binding module (CBM) that recognises sialic acid (known as a CBM40 domain) from both Vibrio cholerae (Vc) and Streptococcus pneumoniae (Sp) NanA sialidases, and generated multivalent polypeptides from them using molecular biology. Multivalent CBM40 constructs were designed either using a tandem repeat approach to produce trimeric or tetrameric forms that we call Vc3CBM and Vc4CBM, respectively, or through the addition of a trimerization domain derived from Pseudomonas aeruginosa pseudaminidase to produce three trimeric forms of proteins known as Vc-CBMTD (WT), Vc-CBMTD (Mutant) and Sp-CBMTD). Due to the position and flexibility of the linker between the trimerization domain and the CBM40 domain, site directed mutagenesis was employed to introduce a disulphide bond between the monomers at positions S164C and T83C of the CBM40 domain in order to promote a stable orientation of the binding site for easier access of sialic acids. Data from isothermal titration calorimetry (ITC) reveals that interaction of multivalent CBM40 proteins with α(2,3)-sialyllactose was mainly enthalpy driven with entropy contributing unfavorably to the interaction suggesting that these proteins establish a strong binding affinity to their ligand minimizing dissociation to produce stable multivalent molecules. However, using surface plasmon resonance (SPR), a mixed balance of entropy and enthalpy contributions was found with all constructs as determined by Van't Hoff plots. This proved that binding does not occur through a simple protein-ligand interaction but through disruption of hydrophobic and/or ionic hydration that provide the driving force to the process. Interestingly, the valency of multiple-linked polypeptides also plays an important part in the protein stabilization. However, little is known about their detailed structure when in multivalent form, as attempts to crystallize the whole protein molecule of Vc-CBMTD (WT) failed due to linker and domain flexibility. Only the trimerization domain (TD) part from Pseudomonas aeruginosa pseudaminidase was successfully crystallized and structure was determined to 3.0 Å without its CBM40 domain attached. In this thesis, we have also reported on the potential anti-influenza and anti- parainfluenza properties of these proteins, which were found to block attachment and inhibit infection of several influenza A and parainfluenza virus strains in vitro. As widely mentioned in literature, terminal sialic acids on the cell surface of mammalian host tissue provide a target for various pathogenic organisms to bind. Levels of viral inhibition were greatest against A/Udorn/72 H3N2 virus for Vc4CBM and Vc3CBM constructs with the lowest EC50 of 0.59 µM and 0.94 µM respectively, however most of the multivalent proteins tested were also effective against A/WSN/33 H1N1 and A/PR8/34 H1N1 subtypes. For parainfluenza virus, all constructs containing V. cholerae sialidase CBM40 domain showed great effect in inhibiting virus infection during cell protection assay. The best EC50 values were 0.2 µM from Vc-CBMTD (WT) followed by 1.17 µM from Vc4CBM and 1.78 µM from Vc-CBMTD (Mutant) which was against hPIV2, hPIV3 and hPIV5 infections respectively. Only a construct from S. pneumoniae sialidase known as Sp-CBMTD showed negligible effect on cell protection. All constructs were further tested for cytotoxicity in mammalian cell culture as well as undergoing an inhibition study on viral replication proteins. For the in vivo study, we also demonstrated the effectiveness of Vc4CBM to protect cotton rats and mice from hPIV3 and Streptococcus pneumoniae infections, when given intranasally in advance or on the day of infection. Therefore, these novel multivalent proteins could be promising candidates as broad-spectrum inhibitors or as a prophylactic treatment for both influenza and parainfluenza associated diseases.

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Baumgärtner, Wolfgang K. "Mechanisms of in vitro persistence of two canine paramyxoviruses and in vivo neuropathogenecity of canine parainfluenza virus /." The Ohio State University, 1986. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487265555440015.

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Roth, Jason Peter. "The Use of Reverse Genetics to Clone and Rescue Infectious, Recombinant Human Parainfluenza Type 3 Viruses." DigitalCommons@USU, 2009. https://digitalcommons.usu.edu/etd/467.

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Reverse genetics is a discipline that involves the use of genetic manipulation and modification to study an organism's altered phenotype. In this study, infectious recombinant viruses were rescued from altered cDNA clones encoding the antigenome of human parainfluenza virus type 3 and the resulting phenotypes were examined. In one clone, the gene for the enhanced green fluorescent protein was inserted into the virus antigenome to be expressed during viral replication, resulting in infected cells emitting green fluorescence. Viral titers, mRNA replication, and genomic replication for the virus expressing the enhanced green fluorescent protein were reduced when compared to the human parainfluenza virus type 3 wild-type strain. In addition, the sensitivity of the virus expressing the enhanced green fluorescent protein to antiviral compounds is increased when compared to the wild-type strain, which may lead to the identification of false positive antiviral compounds. An assay that measures the enhanced green fluorescent protein as a direct indicator of virus replication can be shortened to 3 days in duration and is a more robust assay compared to assays that measure cellular viability. In other clones, mutations were introduced into the phosphoprotein gene to eliminate the expression of the D domain of the PD protein in order to understand its function. The titers of two recombinant knockout viruses that are deficient in the expression of the D domain are reduced when compared to the wild-type strain in both MA-104 and A549 cells. In MA 104 cells, viral mRNA transcription and genomic replication of the two knockout viruses are reduced when compared to the wild-type strain. In A549 cells, cellular expression and secretion of antiviral cytokines infected with the two knockout viruses are either reduced or remain unchanged when compared to the wild-type strain. These results suggest that the D domain may play a role in viral RNA synthesis and not in counteracting the host cell's antiviral response. The results of these studies shed light on the influence an additional gene has on viral replication and possible functions of the D domain.

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Lam, Siu-yan. "Multiplex reverse transcription-PCR for detection and identification of human parainfluenza viruses 1,2,3 and 4 infection in hospitalized children with respiratory disease in Hong Kong /." View the Table of Contents & Abstract, 2007. http://sunzi.lib.hku.hk/hkuto/record/B3848058X.

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Xiao, Han. "Virus and interferon : a fight for supremacy : comparison of the mechanisms of influenza A viruses and parainfluenza virus 5 in combatting a pre-existing IFN-induced antiviral state." Thesis, University of St Andrews, 2011. http://hdl.handle.net/10023/2070.

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The Interferon (IFN) family of cytokines are produced in direct response to virus infection and they constitute the first line of defence against virus infection by inducing hundreds of interferon stimulated genes (ISGs) which act in concert to establish the so-called “antiviral state”. Influenza A viruses and parainfluenza virus type 5 (PIV5) are both small negative strand RNA viruses that must circumvent their hosts’ interferon (IFN) response for replication. However, the ways in which these viruses interact with the IFN system are very different. Although PIV5 replication is initially severely impaired in cells in a pre-existing IFN-induced antiviral state, it manages to overcome the antiviral state by targeting an essential component of type I IFN signalling, STAT1, for degradation. Thus the cells cannot maintain the antiviral state indefinitely without continuous signalling. Consequently, the virus resumes its normal replication pattern after 24-48 hours post-infection. In clear contrast, influenza virus fails to establish its replication in the majority of infected cells (90-95%) with a pre-existing IFN-induced antiviral state, although a few cells are still able to produce viral antigens. To further investigate how influenza virus interacts with cells in a pre-existing IFN-induced antiviral state, I have used in situ hybridization to follow the fate of input and progeny genomes in cells that have, or have not, been treated with IFN prior to infection. Here I show for the first time that IFN pre-treatment blocks the nuclear import of influenza A virus genome, which prevents the establishment of virus replication, but this can be overcome by increasing multiplicities of infection. Of those IFN-induced antiviral molecules, human MxA is an essential component of the IFN-induced antiviral state in blocking influenza virus genome import, as this block can be abolished by lentivirus-mediated knockdown of MxA. I also show that in cells constitutively expressing MxA the viral genome still manages to be transported into the nucleus, indicating that MxA might require an unidentified IFN-induced factor to block nuclear import of the influenza virus genome. These results reveal that IFN exerts its action at an early stage of virus infection by inducing MxA to interfere with the transport of viral genome into the nucleus, which is the factory for viral RNA production.

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Books on the topic "Parainfluenza viruses"

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

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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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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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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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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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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 viruses"

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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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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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, 1989. http://dx.doi.org/10.1007/978-1-4613-0705-1_18.

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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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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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Grandien, Monica. "Paramyxoviridae: The Parainfluenza Viruses." In Laboratory Diagnosis of Infectious Diseases Principles and Practice, 484–506. New York, NY: Springer New York, 1988. http://dx.doi.org/10.1007/978-1-4612-3900-0_25.

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Leland, Diane S. "Parainfluenza and Mumps Viruses." In Manual of Clinical Microbiology, 1487–97. Washington, DC, USA: ASM Press, 2015. http://dx.doi.org/10.1128/9781555817381.ch85.

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Williams, John V., Pedro A. Piedra, and Janet A. Englund. "Respiratory Syncytial Virus, Human Metapneumovirus, and Parainfluenza Viruses." In Clinical Virology, 873–902. Washington, DC, USA: ASM Press, 2016. http://dx.doi.org/10.1128/9781555819439.ch37.

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van Wyke Coelingh, Kathleen. "Antigenic Variation among Human Parainfluenza Type 3 Viruses." In Virus Variability, Epidemiology and Control, 143–57. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4757-9271-3_10.

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Conference papers on the topic "Parainfluenza viruses"

Smatti, Maria K., Hamad E. Al-Romaihi, Hebah A. Al-Khatib, Peter V. Coyle, Asmaa A. Al Thani, Muna A. Al Maslamani, and Hadi M. Yassine. "Influenza, RSV, and Other Respiratory Infections among Children in Qatar." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0133.

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Background: Acute respiratory infections (ARIs) lead to high rates of mortality and morbidity among children. However, studies on the etiology of respiratory infections among children in Qatar and surrounding countries are still limited. Objectives: To describe the prevalence and seasonality of RSV, influenza, and other respiratory pathogens among children in Qatar. Methods: We retrospectively collected data of 33,404 patients <15 years old presented with Influenza-like illness (ILI) from 2012 to 2017. All samples were tested for influenza viruses, while 30,946 were tested for a complete panel of 21 respiratory pathogens. Results: At least one respiratory pathogen was detected in 26,138 (78%) of patients. Together, human rhinoviruses (HRV), respiratory syncytial virus (RSV), and influenza viruses comprised nearly two-thirds of all ILI cases, detected in 24%, 19.7%, and 18.5%, respectively. A detection rate of 5-10% was recorded for adenovirus, human parainfluenza viruses (HPIVs), bocavirus (HboV), and human coronaviruses (HCoVs). Other pathogens such as human metapneumovirus (HMPV), enteroviruses, mycoplasma pneumonia, and parechovirus had prevalence rates below 5%. ILI positive cases were detected throughout the year. RSV, influenza, HMPV exhibited strong seasonal activity in the winter, while HRV was primarily active during low RSV and influenza activity. The burden of RSV exceeds that of influenza among young age groups (<5 years), affecting 17-30% of ILI cases. Prevalence of influenza, on the other hand, correlated positively with age, ranging from 23% to 32% in age groups above five years. Further, male patients had higher rates of HRV (26%) and adenovirus (9%), whereas females showed a higher prevalence of influenza (22%), and RSV (20%) infections. Conclusion: This comprehensive report provides insights into the etiology of ILI among children in Qatar, which represents the Gulf region. Our results reinforce the significance of active surveillance of respiratory pathogens to improve infection prevention and control strategies, particularly among children.

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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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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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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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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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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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Drake, Matthew G., Michael J. Tuvim, Scott E. Evans, Burton Dickey, Allison D. Fryer, and David B. Jacoby. "TLR2/6 And TLR9 Agonists Promote Resistance To Parainfluenza Infection, But Not Virus-Induced M2 Receptor Dysfunction In Guinea Pigs." 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.a5551.

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Reports on the topic "Parainfluenza viruses"

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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