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Molecular evolution and the global reemergence of enterovirus D68 by genome-wide analysis.

Gong YN, Yang SL, Shih SR, Huang YC, Chang PY, Huang CG, Kao KC, Hu HC, Liu YC, Tsao KC - Medicine (Baltimore) (2016)

Bottom Line: Here, all publically available sequences including 147 full and 1248 partial genomes from GenBank were collected and compared at the clade and subclade level; 11 whole genomes isolated in Taiwan (TW) in 2014 were also added to the database.Notably, severe cases isolated from Taiwan and China in 2014 were found in subclade B3.In summary, a new subclade, genetic indels, and polymorphisms in global strains were discovered elucidating evolutionary and epidemiological trends of EV-D68, and 11 genomes were added to the database.

View Article: PubMed Central - PubMed

Affiliation: aDepartment of Laboratory Medicine, Linkou Chang Gung Memorial Hospital bDepartment of Medical Biotechnology and Laboratory Science cResearch Center for Emerging Viral Infections, Chang Gung University dDepartment of Pediatrics, Linkou Chang Gung Memorial Hospital eCollege of Medicine, Chang Gung University fDepartment of Respiratory Therapy gDepartment of Pulmonary and Critical Care Medicine, Linkou Chang Gung Memorial Hospital hDepartment of Respiratory Therapy iDepartment of Pulmonary and Critical Care Medicine, Chang Gung University, Taoyuan, Taiwan.

ABSTRACT
Human enterovirus D68 (EV-D68) was first reported in the United States in 1962; thereafter, a few cases were reported from 1970 to 2005, but 2 outbreaks occurred in the Philippines (2008) and the United States (2014). However, little is known regarding the molecular evolution of this globally reemerging virus due to a lack of whole-genome sequences and analyses. Here, all publically available sequences including 147 full and 1248 partial genomes from GenBank were collected and compared at the clade and subclade level; 11 whole genomes isolated in Taiwan (TW) in 2014 were also added to the database. Phylogenetic trees were constructed to identify a new subclade, B3, and represent clade circulations among strains. Nucleotide sequence identities of the VP1 gene were 94% to 95% based on a comparison of subclade B3 to B1 and B2 and 87% to 91% when comparing A, C, and D. The patterns of clade circulation need to be clarified to improve global monitoring of EV-D68, even though this virus showed lower diversity among clades compared with the common enterovirus EV-71. Notably, severe cases isolated from Taiwan and China in 2014 were found in subclade B3. One severe case from Taiwan occurred in a female patient with underlying angioimmunoblastic T-cell lymphoma, from whom a bronchoalveolar lavage specimen was obtained. Although host factors play a key role in disease severity, we cannot exclude the possibility that EV-D68 may trigger clinical symptoms or death. To further investigate the genetic diversity of EV-D68, we reported 34 amino acid (aa) polymorphisms identified by comparing subclade B3 to B1 and B2. Clade D strains had a 1-aa deletion and a 2-aa insertion in the VP1 gene, and 1 of our TW/2014 strains had a shorter deletion in the 5' untranslated region than a previously reported deletion. In summary, a new subclade, genetic indels, and polymorphisms in global strains were discovered elucidating evolutionary and epidemiological trends of EV-D68, and 11 genomes were added to the database. Virus variants may contribute to disease severity and clinical manifestations, and further studies are needed to investigate the associations between genetic diversity and clinical outcomes.

No MeSH data available.


Related in: MedlinePlus

The 29 nonconserved residues of 11 Taiwan/2014 genomes. Twenty-nine nonconserved residues were identified, including 7 in VP3, 5 in VP1, 4 in 2C, 3 each in VP2, 2A, 2B, and 3D, and 1 in 3A. These residues in the same aligned column were identical to the first sequence TW-02795-2014 and are masked by dots. Position 474 was the most divergent site, with 7 F's and 4 L's, followed by positions 558, 868, 1031, 1141, and 1190 with 3 substitutions, positions 377, 551, 849, and 2161 with 2 substitutions, and another 19 sites with only 1 substitution. Positions 558, 868, 1031, 1141, and 1190 are marked in red; they exhibit residues “G,” “A,” “S,” “T,” and “F” in 3 Linkou CGMH cases, but “A,” “V,” “N,” “N,” and “Y” in the other 8 TW cases and subclades B1 and B2, except for position 1141 in subclade B1. CDC = Centers for Disease Control and Prevention, CGMH = Chang Gung Memorial Hospital.
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Figure 3: The 29 nonconserved residues of 11 Taiwan/2014 genomes. Twenty-nine nonconserved residues were identified, including 7 in VP3, 5 in VP1, 4 in 2C, 3 each in VP2, 2A, 2B, and 3D, and 1 in 3A. These residues in the same aligned column were identical to the first sequence TW-02795-2014 and are masked by dots. Position 474 was the most divergent site, with 7 F's and 4 L's, followed by positions 558, 868, 1031, 1141, and 1190 with 3 substitutions, positions 377, 551, 849, and 2161 with 2 substitutions, and another 19 sites with only 1 substitution. Positions 558, 868, 1031, 1141, and 1190 are marked in red; they exhibit residues “G,” “A,” “S,” “T,” and “F” in 3 Linkou CGMH cases, but “A,” “V,” “N,” “N,” and “Y” in the other 8 TW cases and subclades B1 and B2, except for position 1141 in subclade B1. CDC = Centers for Disease Control and Prevention, CGMH = Chang Gung Memorial Hospital.

Mentions: As described in Table 3, clade B strains showed high sequence identities. Figure 3 presents 29 nonconserved residues from the 11 complete genomes provided in this study. Among them, position 474 had the highest diversity with 7 F's and 4 L's, followed by 5 positions (i.e., 558, 868, 1031, 1141, and 1190) with 3 substitutions, 4 positions (i.e., 377, 551, 849, and 2161) with 2 substitutions, and another 19 sites with only 1 substitution. Furthermore, positions 558, 868, 1031, 1141, and 1190 in 3 Linkou CGMH cases had residues “G,” “A,” “S,” “T,” and “F,” respectively, which diverged from the other 8 TW strains that had residues “A,” “V,” “N,” “N,” and “Y.” One death occurred among the 3 Linkou CGMH patients, associated with underlying AITL.


Molecular evolution and the global reemergence of enterovirus D68 by genome-wide analysis.

Gong YN, Yang SL, Shih SR, Huang YC, Chang PY, Huang CG, Kao KC, Hu HC, Liu YC, Tsao KC - Medicine (Baltimore) (2016)

The 29 nonconserved residues of 11 Taiwan/2014 genomes. Twenty-nine nonconserved residues were identified, including 7 in VP3, 5 in VP1, 4 in 2C, 3 each in VP2, 2A, 2B, and 3D, and 1 in 3A. These residues in the same aligned column were identical to the first sequence TW-02795-2014 and are masked by dots. Position 474 was the most divergent site, with 7 F's and 4 L's, followed by positions 558, 868, 1031, 1141, and 1190 with 3 substitutions, positions 377, 551, 849, and 2161 with 2 substitutions, and another 19 sites with only 1 substitution. Positions 558, 868, 1031, 1141, and 1190 are marked in red; they exhibit residues “G,” “A,” “S,” “T,” and “F” in 3 Linkou CGMH cases, but “A,” “V,” “N,” “N,” and “Y” in the other 8 TW cases and subclades B1 and B2, except for position 1141 in subclade B1. CDC = Centers for Disease Control and Prevention, CGMH = Chang Gung Memorial Hospital.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4979813&req=5

Figure 3: The 29 nonconserved residues of 11 Taiwan/2014 genomes. Twenty-nine nonconserved residues were identified, including 7 in VP3, 5 in VP1, 4 in 2C, 3 each in VP2, 2A, 2B, and 3D, and 1 in 3A. These residues in the same aligned column were identical to the first sequence TW-02795-2014 and are masked by dots. Position 474 was the most divergent site, with 7 F's and 4 L's, followed by positions 558, 868, 1031, 1141, and 1190 with 3 substitutions, positions 377, 551, 849, and 2161 with 2 substitutions, and another 19 sites with only 1 substitution. Positions 558, 868, 1031, 1141, and 1190 are marked in red; they exhibit residues “G,” “A,” “S,” “T,” and “F” in 3 Linkou CGMH cases, but “A,” “V,” “N,” “N,” and “Y” in the other 8 TW cases and subclades B1 and B2, except for position 1141 in subclade B1. CDC = Centers for Disease Control and Prevention, CGMH = Chang Gung Memorial Hospital.
Mentions: As described in Table 3, clade B strains showed high sequence identities. Figure 3 presents 29 nonconserved residues from the 11 complete genomes provided in this study. Among them, position 474 had the highest diversity with 7 F's and 4 L's, followed by 5 positions (i.e., 558, 868, 1031, 1141, and 1190) with 3 substitutions, 4 positions (i.e., 377, 551, 849, and 2161) with 2 substitutions, and another 19 sites with only 1 substitution. Furthermore, positions 558, 868, 1031, 1141, and 1190 in 3 Linkou CGMH cases had residues “G,” “A,” “S,” “T,” and “F,” respectively, which diverged from the other 8 TW strains that had residues “A,” “V,” “N,” “N,” and “Y.” One death occurred among the 3 Linkou CGMH patients, associated with underlying AITL.

Bottom Line: Here, all publically available sequences including 147 full and 1248 partial genomes from GenBank were collected and compared at the clade and subclade level; 11 whole genomes isolated in Taiwan (TW) in 2014 were also added to the database.Notably, severe cases isolated from Taiwan and China in 2014 were found in subclade B3.In summary, a new subclade, genetic indels, and polymorphisms in global strains were discovered elucidating evolutionary and epidemiological trends of EV-D68, and 11 genomes were added to the database.

View Article: PubMed Central - PubMed

Affiliation: aDepartment of Laboratory Medicine, Linkou Chang Gung Memorial Hospital bDepartment of Medical Biotechnology and Laboratory Science cResearch Center for Emerging Viral Infections, Chang Gung University dDepartment of Pediatrics, Linkou Chang Gung Memorial Hospital eCollege of Medicine, Chang Gung University fDepartment of Respiratory Therapy gDepartment of Pulmonary and Critical Care Medicine, Linkou Chang Gung Memorial Hospital hDepartment of Respiratory Therapy iDepartment of Pulmonary and Critical Care Medicine, Chang Gung University, Taoyuan, Taiwan.

ABSTRACT
Human enterovirus D68 (EV-D68) was first reported in the United States in 1962; thereafter, a few cases were reported from 1970 to 2005, but 2 outbreaks occurred in the Philippines (2008) and the United States (2014). However, little is known regarding the molecular evolution of this globally reemerging virus due to a lack of whole-genome sequences and analyses. Here, all publically available sequences including 147 full and 1248 partial genomes from GenBank were collected and compared at the clade and subclade level; 11 whole genomes isolated in Taiwan (TW) in 2014 were also added to the database. Phylogenetic trees were constructed to identify a new subclade, B3, and represent clade circulations among strains. Nucleotide sequence identities of the VP1 gene were 94% to 95% based on a comparison of subclade B3 to B1 and B2 and 87% to 91% when comparing A, C, and D. The patterns of clade circulation need to be clarified to improve global monitoring of EV-D68, even though this virus showed lower diversity among clades compared with the common enterovirus EV-71. Notably, severe cases isolated from Taiwan and China in 2014 were found in subclade B3. One severe case from Taiwan occurred in a female patient with underlying angioimmunoblastic T-cell lymphoma, from whom a bronchoalveolar lavage specimen was obtained. Although host factors play a key role in disease severity, we cannot exclude the possibility that EV-D68 may trigger clinical symptoms or death. To further investigate the genetic diversity of EV-D68, we reported 34 amino acid (aa) polymorphisms identified by comparing subclade B3 to B1 and B2. Clade D strains had a 1-aa deletion and a 2-aa insertion in the VP1 gene, and 1 of our TW/2014 strains had a shorter deletion in the 5' untranslated region than a previously reported deletion. In summary, a new subclade, genetic indels, and polymorphisms in global strains were discovered elucidating evolutionary and epidemiological trends of EV-D68, and 11 genomes were added to the database. Virus variants may contribute to disease severity and clinical manifestations, and further studies are needed to investigate the associations between genetic diversity and clinical outcomes.

No MeSH data available.


Related in: MedlinePlus