Epidemiological and virological differences in human clustered and sporadic infections with avian influenza A H7N9

Background: Previous research has suggested that avian influenza A H7N9 has a greater potential pandemic risk than influenza A H5N1. This research investigated the difference in human clustered and sporadic cases of H7N9 virus and estimated the relative risk of clustered infections. Methods: Comparative epidemiology and virology studies were performed among 72 sporadic confirmed cases, 17 family clusters (FCs) caused by human-to-human transmission, and eight live bird market clusters (LCs) caused by co-exposure to the poultry environment. Results: The case fatality of FCs, LCs and sporadic cases (36%, 26%, and 29%, respectively) did not differ among the three groups (p > 0.05). The average age (36 years, 60 years, and 58 years), co-morbidities (31%, 60%, and 54%), exposure to birds (72%, 100%, and 83%), and H7N9-positive rate (20%, 64%, and 35%) in FCs, LCs, and sporadic cases, respectively, differed significantly (p  0.05). However, exposure to a person with confirmed avian influenza A H7N9 (primary 12% vs. secondary 95%), history of visiting a live bird market (100% vs. 59%), multiple exposures (live bird exposure and human-to-human transmission history) (12% vs. 55%), and median days from onset to antiviral treatment (6 days vs. 3 days) differed significantly between primary and secondary cases in FCs (p < 0.05). Mild cases were found in 6% of primary cases vs. 32% of secondary cases in FCs (p < 0.05). Twenty-five isolates from the three groups showed 99.1–99.9% homology and increased human adaptation. Conclusions: There was no statistical difference in the case fatality rate and limited transmission between FCs and LCs. However, the severity of the primary cases in FCs was much higher than that of the secondary cases due to the older age and greater underlying disease of the latter patients

Nontypeable induces COX-2 and PGE2 expression in lung epithelial cells via activation of p38 MAPK and NF-kappa B-1

, specific inhibitors of COX-1 and COX-2, and expression levels of PGE2 were measured by ELISA assay. Data are means ± SEM (n = 4), *. Mock group; **. NTHi group at 50 MOI.<p><b>Copyright information:</b></p><p>Taken from "Nontypeable induces COX-2 and PGE2 expression in lung epithelial cells via activation of p38 MAPK and NF-kappa B"</p><p>http://respiratory-research.com/content/9/1/16</p><p>Respiratory Research 2008;9(1):16-16.</p><p>Published online 31 Jan 2008</p><p>PMCID:PMC2270828.</p><p></p

Nontypeable induces COX-2 and PGE2 expression in lung epithelial cells via activation of p38 MAPK and NF-kappa B-0

of COX-1 and COX-2 was measured by RT-PCR analysis.<p><b>Copyright information:</b></p><p>Taken from "Nontypeable induces COX-2 and PGE2 expression in lung epithelial cells via activation of p38 MAPK and NF-kappa B"</p><p>http://respiratory-research.com/content/9/1/16</p><p>Respiratory Research 2008;9(1):16-16.</p><p>Published online 31 Jan 2008</p><p>PMCID:PMC2270828.</p><p></p

Nontypeable induces COX-2 and PGE2 expression in lung epithelial cells via activation of p38 MAPK and NF-kappa B-3

Ot analysis. A549 cells were inoculated with 50 MOI of NTHi with or without 20 μM of SB203580, and phosphorayltion of p38 MAPK was detected by Immunoblot analysis. representative blots from three independent experiments.<p><b>Copyright information:</b></p><p>Taken from "Nontypeable induces COX-2 and PGE2 expression in lung epithelial cells via activation of p38 MAPK and NF-kappa B"</p><p>http://respiratory-research.com/content/9/1/16</p><p>Respiratory Research 2008;9(1):16-16.</p><p>Published online 31 Jan 2008</p><p>PMCID:PMC2270828.</p><p></p

Nontypeable induces COX-2 and PGE2 expression in lung epithelial cells via activation of p38 MAPK and NF-kappa B-4

Y of NF-kappa B was measured by EMSA analysis. A representative gel from three independent experiments with similar results is shown in figure.<p><b>Copyright information:</b></p><p>Taken from "Nontypeable induces COX-2 and PGE2 expression in lung epithelial cells via activation of p38 MAPK and NF-kappa B"</p><p>http://respiratory-research.com/content/9/1/16</p><p>Respiratory Research 2008;9(1):16-16.</p><p>Published online 31 Jan 2008</p><p>PMCID:PMC2270828.</p><p></p

Nontypeable induces COX-2 and PGE2 expression in lung epithelial cells via activation of p38 MAPK and NF-kappa B-5

Sis 4 h after NTHi inoculation. A549 cells were inoculated with p38 inhibitors SB203580 or SB202190, and COX-2 mRNA expression was measured by RT-PCR analysis 4 h after NTHi inoculation. A549 cells were inoculated with NTHi with or without PDTC, SB203580, and SB202190, and expression levels of PGE2 were measured by ELISA assay 16 h after NTHi inoculation. Data are means ± SEM (n = 3). *< 0.05 . Mock; **< 0.05 . 50 MOI of NTHi.<p><b>Copyright information:</b></p><p>Taken from "Nontypeable induces COX-2 and PGE2 expression in lung epithelial cells via activation of p38 MAPK and NF-kappa B"</p><p>http://respiratory-research.com/content/9/1/16</p><p>Respiratory Research 2008;9(1):16-16.</p><p>Published online 31 Jan 2008</p><p>PMCID:PMC2270828.</p><p></p

Nontypeable induces COX-2 and PGE2 expression in lung epithelial cells via activation of p38 MAPK and NF-kappa B-6

of COX-1 and COX-2 was measured by RT-PCR analysis.<p><b>Copyright information:</b></p><p>Taken from "Nontypeable induces COX-2 and PGE2 expression in lung epithelial cells via activation of p38 MAPK and NF-kappa B"</p><p>http://respiratory-research.com/content/9/1/16</p><p>Respiratory Research 2008;9(1):16-16.</p><p>Published online 31 Jan 2008</p><p>PMCID:PMC2270828.</p><p></p

Nontypeable induces COX-2 and PGE2 expression in lung epithelial cells via activation of p38 MAPK and NF-kappa B-2

Ured by Q-PCR analysis. Data are means ± SEM (n = 3). *. CON; **. NTHi in HEK293-pcDNA. NS:non-significant . NTHi in HEK293-pcDNA; CON: control. Wild-type and TLR2 and TLR4 knock-out mice were intratracheally inoculated with 1 × 10CFU of NTHi, and mRNA expression of COX-2 was measured from the lungs of inoculated mice 6 h after inoculation. Data are means ± SEM (n = 3). *< 0.05 . CON in wild-type mice; **< 0.05 . NTHi in wild-type mice. NS: non-significant . NTHi in wild-type mice; CON: control.<p><b>Copyright information:</b></p><p>Taken from "Nontypeable induces COX-2 and PGE2 expression in lung epithelial cells via activation of p38 MAPK and NF-kappa B"</p><p>http://respiratory-research.com/content/9/1/16</p><p>Respiratory Research 2008;9(1):16-16.</p><p>Published online 31 Jan 2008</p><p>PMCID:PMC2270828.</p><p></p