tetano
Editor, Senior Moderator
PLoS One. 2014 Nov 3;9(11):e111640. doi: 10.1371/journal.pone.0111640. eCollection 2014.
Patient-based transcriptome-wide analysis identify interferon and ubiquination pathways as potential predictors of influenza a disease severity.
Hoang LT1, Tolfvenstam T2, Ooi EE3, Khor CC1, Naim AN1, Ho EX1, Ong SH1, Wertheim HF4, Fox A4, Van Vinh Nguyen C5, Nghiem NM5, Ha TM6, Thi Ngoc Tran A6, Tambayah P7, Lin R7, Sangsajja C8, Manosuthi W8, Chuchottaworn C9, Sansayunh P9, Chotpitayasunondh T10, Suntarattiwong P10, Chokephaibulkit K11, Puthavathana P11, de Jong MD12, Farrar J13, van Doorn HR13, Hibberd ML1.
Author information
Abstract
BACKGROUND:
The influenza A virus is an RNA virus that is responsible for seasonal epidemics worldwide with up to five million cases of severe illness and 500,000 deaths annually according to the World Health Organization estimates. The factors associated with severe diseases are not well defined, but more severe disease is more often seen among persons aged >65 years, infants, pregnant women, and individuals of any age with underlying health conditions.
METHODOLOGY/PRINCIPAL FINDINGS:
Using gene expression microarrays, the transcriptomic profiles of influenza-infected patients with severe (N = 11), moderate (N = 40) and mild (N = 83) symptoms were compared with the febrile patients of unknown etiology (N = 73). We found that influenza-infected patients, regardless of their clinical outcomes, had a stronger induction of antiviral and cytokine responses and a stronger attenuation of NK and T cell responses in comparison with those with unknown etiology. More importantly, we found that both interferon and ubiquitination signaling were strongly attenuated in patients with the most severe outcomes in comparison with those with moderate and mild outcomes, suggesting the protective roles of these pathways in disease pathogenesis.
CONCLUSION/SIGNIFICANCES:
The attenuation of interferon and ubiquitination pathways may associate with the clinical outcomes of influenza patients.
PMID:
25365328
[PubMed - in process]
PMCID:
PMC4218794
Free PMC Article
http://www.ncbi.nlm.nih.gov/pubmed/25365328
Patient-based transcriptome-wide analysis identify interferon and ubiquination pathways as potential predictors of influenza a disease severity.
Hoang LT1, Tolfvenstam T2, Ooi EE3, Khor CC1, Naim AN1, Ho EX1, Ong SH1, Wertheim HF4, Fox A4, Van Vinh Nguyen C5, Nghiem NM5, Ha TM6, Thi Ngoc Tran A6, Tambayah P7, Lin R7, Sangsajja C8, Manosuthi W8, Chuchottaworn C9, Sansayunh P9, Chotpitayasunondh T10, Suntarattiwong P10, Chokephaibulkit K11, Puthavathana P11, de Jong MD12, Farrar J13, van Doorn HR13, Hibberd ML1.
Author information
Abstract
BACKGROUND:
The influenza A virus is an RNA virus that is responsible for seasonal epidemics worldwide with up to five million cases of severe illness and 500,000 deaths annually according to the World Health Organization estimates. The factors associated with severe diseases are not well defined, but more severe disease is more often seen among persons aged >65 years, infants, pregnant women, and individuals of any age with underlying health conditions.
METHODOLOGY/PRINCIPAL FINDINGS:
Using gene expression microarrays, the transcriptomic profiles of influenza-infected patients with severe (N = 11), moderate (N = 40) and mild (N = 83) symptoms were compared with the febrile patients of unknown etiology (N = 73). We found that influenza-infected patients, regardless of their clinical outcomes, had a stronger induction of antiviral and cytokine responses and a stronger attenuation of NK and T cell responses in comparison with those with unknown etiology. More importantly, we found that both interferon and ubiquitination signaling were strongly attenuated in patients with the most severe outcomes in comparison with those with moderate and mild outcomes, suggesting the protective roles of these pathways in disease pathogenesis.
CONCLUSION/SIGNIFICANCES:
The attenuation of interferon and ubiquitination pathways may associate with the clinical outcomes of influenza patients.
PMID:
25365328
[PubMed - in process]
PMCID:
PMC4218794
Free PMC Article
http://www.ncbi.nlm.nih.gov/pubmed/25365328