scholarly journals Virome of respiratory secretion from children with unknown etiological acute respiratory disease revealed recombinant human parechovirus and other significant viruses

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Ying Liu ◽  
Hao Wang ◽  
Jie Yang ◽  
Jian Zeng ◽  
Guang-Ming Sun
Keyword(s):  
Respiratory Disease ◽  
Foot And Mouth Disease ◽  
Viral Metagenomics ◽  
Clinical Samples ◽  
Acute Respiratory Disease ◽  
Human Parechovirus ◽  
Respiratory Sample ◽  
Respiratory Secretion ◽  
Separate Branch ◽  
Human Parainfluenza Virus

AbstractUsing viral metagenomics, viral nucleic acid in 30 respiratory secretion samples collected from children with unknown etiological acute respiratory disease were investigated. Sequences showing similarity to human parainfluenza virus 1, anellovirus, bocavirus, coxsackievirus A4, human parechovirus (HPeV), and alphaflexivirus were recovered from these samples. Complete genomes of one anellovirus, one coxsackievirus A4, three parechoviruses were determined from these libraries. The anellovirus (MW267851) phylogenetically clustered with an unpublished anellovirus (MK212032) from respiratory sample of a Vietnamese patient, forming a separate branch neighboring to strains within the genus Betatorquevirus. The genome of coxsackievirus A4 (MW267852) shares the highest sequence identity of 96.4% to a coxsackievirus A4 (MN964079) which was identified in clinical samples from children with Hand, Foot, and Mouth Disease (HFMD). Two (MW267853 and MW267854) of the three parechoviruses belong to HPeV-1 and the other one (MW267855) belongs to HPeV-6. Recombination analysis indicated that an HPeV-1 (MW267854) identified in this study is a putative recombinant occurred between HPeV-1 and HPeV-3. Whether these viruses have association with specific respiratory disease calls for further investigation.

scholarly journals Complete Genome Sequences of Two Human Parainfluenza Virus Type 3 Isolates Collected in Brazil

2017 ◽  
Vol 5 (49) ◽  
Author(s):  
Nicholas Di Paola ◽  
Marielton dos Passos Cunha ◽  
Giuliana Stravinskas Durigon ◽  
Eitan Naaman Berezin ◽  
Edison Durigon ◽  
...  
Keyword(s):  
Respiratory Disease ◽  
Virus Type ◽  
Complete Genome ◽  
Parainfluenza Virus ◽  
Acute Respiratory Disease ◽  
Genome Sequences ◽  
Human Parainfluenza Virus ◽  
Type 3

ABSTRACT Here, we present the complete genome sequences of two human parainfluenza virus type 3 (HPIV-3) isolates collected from hospitalized infants suffering from acute respiratory disease. These are the first complete genome sequences of HPIV-3 originating from Brazil.

Acute Respiratory Disease and Adenovirus Infection Among U.S Army Basic Trainees At Ft. Jackson, South Carolina 1998

2000 ◽  
Author(s):  
Shellie Kolavic ◽  
Jose Sanchez ◽  
Leonard Binn ◽  
Marcela Echavarria ◽  
Bruce Innis
Keyword(s):  
South Carolina ◽  
Respiratory Disease ◽  
Adenovirus Infection ◽  
Acute Respiratory Disease

scholarly journals Selected nonvaccine interventions to prevent infectious acute respiratory disease

2005 ◽  
Vol 28 (3) ◽  
pp. 305-316 ◽  
Author(s):  
Terrence Lee ◽  
Nikki N. Jordan ◽  
Jose L. Sanchez ◽  
Joel C. Gaydos
Keyword(s):  
Respiratory Disease ◽  
Acute Respiratory Disease

scholarly journals Isolation and Characterization of Novel Human Parechovirus from Clinical Samples

2007 ◽  
Vol 13 (6) ◽  
pp. 889-895 ◽  
Author(s):  
Kanako Watanabe ◽  
Masayasu Oie ◽  
Masaya Higuchi ◽  
Makoto Nishikawa ◽  
Masahiro Fujii
Keyword(s):  
Clinical Samples ◽  
Human Parechovirus ◽  
Isolation And Characterization

scholarly journals Viral Entry Properties Required for Fitness in Humans Are Lost through Rapid Genomic Change during Viral Isolation

mBio ◽  
2018 ◽  
Vol 9 (4) ◽  
Author(s):  
Sho Iketani ◽  
Ryan C. Shean ◽  
Marion Ferren ◽  
Negar Makhsous ◽  
Dolly B. Aquino ◽  
...  
Keyword(s):  
Primary Culture ◽  
Parainfluenza Virus ◽  
Clinical Samples ◽  
Genomic Change ◽  
Viral Isolation ◽  
Dimer Interface ◽  
Genome Wide ◽  
A Genome ◽  
Immortalized Cells ◽  
Human Parainfluenza Virus

ABSTRACTHuman parainfluenza viruses cause a large burden of human respiratory illness. While much research relies upon viruses grown in cultured immortalized cells, human parainfluenza virus 3 (HPIV-3) evolves in culture. Cultured viruses differ in their properties compared to clinical strains. We present a genome-wide survey of HPIV-3 adaptations to culture using metagenomic next-generation sequencing of matched pairs of clinical samples and primary culture isolates (zero passage virus). Nonsynonymous changes arose during primary viral isolation, almost entirely in the genes encoding the two surface glycoproteins—the receptor binding protein hemagglutinin-neuraminidase (HN) or the fusion protein (F). We recovered genomes from 95 HPIV-3 primary culture isolates and 23 HPIV-3 strains directly from clinical samples. HN mutations arising during primary viral isolation resulted in substitutions at HN’s dimerization/F-interaction site, a site critical for activation of viral fusion. Alterations in HN dimer interface residues known to favor infection in culture occurred within 4 days (H552 and N556). A novel cluster of residues at a different face of the HN dimer interface emerged (P241 and R242) and imply a role in HPIV-3-mediated fusion. Functional characterization of these culture-associated HN mutations in a clinical isolate background revealed acquisition of the fusogenic phenotype associated with cultured HPIV-3; the HN-F complex showed enhanced fusion and decreased receptor-cleaving activity. These results utilize a method for identifying genome-wide changes associated with brief adaptation to culture to highlight the notion that even brief exposure to immortalized cells may affect key viral properties and underscore the balance of features of the HN-F complex required for fitness by circulating viruses.IMPORTANCEHuman parainfluenza virus 3 is an important cause of morbidity and mortality among infants, the immunocompromised, and the elderly. Using deep genomic sequencing of HPIV-3-positive clinical material and its subsequent viral isolate, we discover a number of known and novel coding mutations in the main HPIV-3 attachment protein HN during brief exposure to immortalized cells. These mutations significantly alter function of the fusion complex, increasing fusion promotion by HN as well as generally decreasing neuraminidase activity and increasing HN-receptor engagement. These results show that viruses may evolve rapidly in culture even during primary isolation of the virus and before the first passage and reveal features of fitness for humans that are obscured by rapid adaptation to laboratory conditions.

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