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Epithelial Function and Airway Responsiveness
Published in Alastair G. Stewart, AIRWAY WALL REMODELLING in ASTHMA, 2020
Roy G. Goldie, Janet M. H. Preuss
Neutrophil adherence to bovine bronchial epithelium was increased by exposure to cigarette smoke, lipopolysaccharide, or phorbol ester and was associated with epithelial cell cytotoxicity.66 Furthermore, human parainfluenza virus type 2 markedly increased adherence of neutrophils to human tracheal epithelial cells. This response apparently involved adhesion molecule-1 (ICAM-1) and ICAM-1-independent mechanisms.273 Mast cells also selectively adhered to canine epithelial cells, to surface epithelial or submucosal glands, but not to basal membrane or connective tissue.274 Interestingly, ICAM-1 expression was increased in airway epithelium in vitro and in vivo in a monkey model of airway hyperreactivity following antigen inhalation accompanied by increased epithelial eosinophils.275
Severe Non-influenza Viral Pneumonia in the Critical Care Unit
Published in Cheston B. Cunha, Burke A. Cunha, Infectious Diseases and Antimicrobial Stewardship in Critical Care Medicine, 2020
David Waldner, Thomas J. Marrie, Wendy Sligl
Four serotypes of human parainfluenza virus (PIV) have been identified (PIV-1, PIV-2, PIV-3, PIV-4) [23]. Similar to other respiratory viruses belonging to the Paramyxoviridae family, their significance as childhood respiratory pathogens has long been recognized; however, their role in causing severe disease in adults has been poorly appreciated. Notable to PIV are the seasonal variations unique to each serotype. PIV-1 accounts for approximately 17%–30% of illnesses and typically circulates biennially, with most cases occurring in the Northern Hemisphere during September and December on odd-numbered years [23,24]. PIV-2 is less frequently encountered, causing only 8%–15% of infections, and like PIV-1, infections tend to peak in September and December; however, seasonal outbreaks occur annually [23,24]. Most clinically significant infections, however, are caused by PIV-3 (52%–71%) [23,24]. PIV-3 causes annual epidemics in the spring and early summer (April to June), with increased activity and longer seasons noted in even years due to the absence of circulating PIV-1 [23,24]. PIV-4 is infrequently encountered, and thus data on seasonality are sparse [23].
Viruses
Published in Loretta A. Cormier, Pauline E. Jolly, The Primate Zoonoses, 2017
Loretta A. Cormier, Pauline E. Jolly
Human parainfluenza viruses belong to two genera. HPIV-1 and −3 are members of the genus Respirovirus, and HPIV-2 and −4 belong to the genus Rubulavirus, which also includes the mumps virus. Both Respirovirus and Rubulavirus are transmitted through direct contact, respiratory droplets, or fomites (Ison 2015; Litman and Baum 2015). The parainfluenza viruses occur worldwide and are responsible for upper and lower respiratory tract infections, particularly in children (Ison 2015). Most infections are mild and self-limiting, but HPIV-3 can be more severe and is the most likely of the four types to be associated with bronchiolitis and pneumonia (Ison 2015). Mumps infection also occurs worldwide and typically occurs in children and adolescents but is less common since the development of a vaccine in the late 1960s (Litman and Baum 2015). Mumps is typically mild and self-limiting with characteristic swelling of the parotid or salivary glands; rarely it progresses to meningitis, encephalitis, epididymo-orchitis, and oophoritis (Litman and Baum 2015). A few cases of HPIV and mumps have been documented in wild primates, with HPIV-2 and HPIV-3 in Kenyan baboons and HPIV-3 and mumps in Bornean orangutans.
Potential use of endemic human coronaviruses to stimulate immunity against pathogenic SARS-CoV-2 and its variants
Published in Libyan Journal of Medicine, 2023
Narges S. Shamabadi, Anisah B. Bagasra, Shrikant Pawar, Omar Bagasra
In addition to the three known pathogenic viruses, there are four species of COVID namely, OC43, HKU1, NL63, and 229E, referred to as endemic human Coronaviruses or eCOVIDs, causing the common cold in immunocompromised patients [2–5]. The symptoms of infection with eCOVIDs are similar to that of other ‘common colds’ caused by other seasonal human respiratory viruses like human rhinoviruses (HRVs), adenoviruses (AV), respiratory syncytial virus (HRSV), and human parainfluenza viruses. All eCOVIDs have originated by zoonotic transmission from animals to humans, and their possible ancestors share similar natural animal reservoirs and intermediate hosts (Table 1) [2–8]. For example, it appears that human coronavirus (HCoV) −229E, HCoV-NL63 SARS- CoV-1 and 2 as well as MERS-CoV primarily originated from bats, while intermediate hosts for H229E and MERS appear to be Arabian camels/Alpaca. The primary reserve for HKU1 and OC43 appears to be rodents. The intermediate host for HCoV-OC43 is most likely domestic animals such as cattle or swine [2–5,7,8].
Protective antibodies against human parainfluenza virus type 3 infection
Published in mAbs, 2021
Jim Boonyaratanakornkit, Suruchi Singh, Connor Weidle, Justas Rodarte, Ramasamy Bakthavatsalam, Jonathan Perkins, Guillaume B.E. Stewart-Jones, Peter D. Kwong, Andrew T. McGuire, Marie Pancera, Justin J. Taylor
Human parainfluenza virus type III (HPIV3) is a common cause of respiratory illness in infants and children. Over 11,000 hospitalizations per year in the US occur for fever or acute respiratory illness due to HPIV3.1 HPIV3, like respiratory syncytial virus (RSV), infects early in life and frequently causes severe bronchiolitis and pneumonia in infants under 6 months of age who are unable to mount a robust antibody response.2,3 HPIV3 is also an important cause of mortality, morbidity, and health-care costs in other vulnerable populations, such as immunocompromised hematopoietic stem cell transplant (HCT) recipients.4 Up to a third of HCT recipients acquire a respiratory viral infection within 6 months of transplant.5–11 In up to a third of those patients, the virus progresses from the upper to the lower respiratory tract.6,9 Once the virus gains a foothold in the lower tract, little can be done for most patients beyond supportive care, and up to 40% of patients with lower tract disease die within 3 months. HPIV3 is an important cause of serious respiratory viral infections after HCT, with a cumulative incidence of 18% post–transplant at the Fred Hutchinson Cancer Research Center.5,12–14 In the absence of any vaccine or therapy, there is a substantial need for preventive and therapeutic interventions against HPIV3.
The Ebola virus glycoprotein and its immune responses across multiple vaccine platforms
Published in Expert Review of Vaccines, 2020
Human parainfluenza virus type 3 (HPIV3), a member of the family Paramyxoviridae, has a negative-sense RNA genome and is a common pediatric respiratory pathogen [78]. With the advent of the reverse genetics system for HPIV3, it has been utilized as a backbone for the generation of a viral vector vaccine for EBOV by incorporating the gene(s) for GP or GP and NP. The immunogenicity of HPIV3-EBOV vaccine was analyzed in NHPs and the vaccine was shown to be 88% protective with a single dose delivered intranasal/intratracheally, and 100% protective with two doses by the same route. Due to the respiratory route of immunization robust IgG and IgA were produced against EBOV GP as well as moderately activated CD8+ and CD4+ T cells (Figure 1) [79,80]. As with the case of the adenoviral vectors, preexisting immunity to HPIV3 was a concern for vaccine efficacy. To ablate this concern, a HPIV3/∆F-HN/EBOVGP was constructed to remove the primary antigenic regions of HPIV3, which demonstrated safety and 100% protection in small animal models, and a more robust EBOV GP-specific antibody response [81]. This construct was further tested to deduce if preexisting immunity to HPIV3 in NHPs negatively impacted the vaccines’ immunogenicity [82]. However, this study did not utilize a challenge model, and the production of antibodies does not always correlate with survival against EBOV infection. Due to the replication competent nature of the vaccine, additional safety concerns require further evaluation, such as the pathogenic potential in immunocompromised individuals.