scholarly journals Serological Response of Patients with Influenza A (H1N1) pdm09-Associated Pneumonia: An Observational Study

PLoS ONE ◽  
2013 ◽  
Vol 8 (11) ◽  
pp. e81436
Author(s):  
Nasikarn Angkasekwinai ◽  
Bualan Kaewnapha ◽  
Duangdao Waywa ◽  
Peerawong Werarak ◽  
Sasima Tongsai ◽  
...  
Vaccine ◽  
2012 ◽  
Vol 30 (52) ◽  
pp. 7630-7636 ◽  
Author(s):  
Wakaba Fukushima ◽  
Satoko Ohfuji ◽  
Masaaki Deguchi ◽  
Kazume Kawabata ◽  
Hideaki Hatayama ◽  
...  

2010 ◽  
Vol 22 (6) ◽  
pp. 428-430
Author(s):  
D. Curcio ◽  
L. Ferreira Cabrera ◽  
A. Duarte ◽  
E. Valencia ◽  
C.H. Paz Chávez ◽  
...  

1981 ◽  
Vol 87 (1) ◽  
pp. 139-146 ◽  
Author(s):  
M. Lebiush ◽  
L. Rannon ◽  
J. D. Kark

SummaryAn outbreak of influenza caused by the A(H1N1) subtype in military recruits in February 1978 afforded an opportunity to study the association of ABO blood groups with influenza morbidity and serological response. Fifty-eight per cent of 336 recruits became clinically ill. There was no differential distribution of clinical influenza by blood group. However, seroconversion to a titre of ≥ 20 was significantly and appreciably higher in groups A and B than O and AB. Also, among those with serologically confirmed clinical influenza, the occurrence was significantly higher in groups A and B than groups O and AB.


PLoS ONE ◽  
2010 ◽  
Vol 5 (8) ◽  
pp. e12474 ◽  
Author(s):  
Mark I. Chen ◽  
Ian G. Barr ◽  
Gerald C. H. Koh ◽  
Vernon J. Lee ◽  
Caroline P. S. Lee ◽  
...  

F1000Research ◽  
2015 ◽  
Vol 3 ◽  
pp. 221 ◽  
Author(s):  
Maria Cecilia Dignani ◽  
Patricia Costantini ◽  
Claudia Salgueira ◽  
Rosana Jordán ◽  
Graciela Guerrini ◽  
...  

Background: During March 2009 a novel Influenza A virus emerged in Mexico. We describe the clinical picture of the pandemic Influenza A (H1N1) Influenza in cancer patients during the 2009 influenza season.Methods: Twelve centers participated in a multicenter retrospective observational study of cancer patients with confirmed infection with the 2009 H1N1 Influenza A virus (influenza-like illness or pneumonia plus positive PCR for the 2009 H1N1 Influenza A virus  in respiratory secretions). Clinical data were obtained by retrospective chart review and analyzed. Results: From May to August 2009, data of 65 patients were collected. Median age was 51 years, 57 % of the patients were female. Most patients (47) had onco-hematological cancers and 18 had solid tumors. Cancer treatment mainly consisted of chemotherapy (46), or stem cell transplantation (SCT) (16). Only 19 of 64 patients had received the 2009 seasonal Influenza vaccine. Clinical presentation included pneumonia (43) and upper respiratory tract infection (22). Forty five of 58 ambulatory patients were admitted. Mechanical ventilation was required in 12 patients (18%). Treatment included oseltamivir monotherapy or in combination with amantadine for a median of 7 days. The global 30-day mortality rate was 18%. All 12 deaths were among the non-vaccinated patients. No deaths were observed among the 19 vaccinated patients. Oxygen saturation <96% at presentation was a predictor of mortality (OR 19.5; 95%CI: 2.28 to 165.9).Conclusions: In our cancer patient population, the pandemic 2009 Influenza A (H1N1) virus was associated with high incidence of pneumonia (66%), and 30-day mortality (18.5%). Saturation <96% was significantly associated with death. No deaths were observed among vaccinated patients.


1986 ◽  
Vol 96 (2) ◽  
pp. 335-343 ◽  
Author(s):  
E. A. Grilli ◽  
J. R. Davies ◽  
A. J. Smith

SUMMARYThree outbreaks of influenza caused by influenza A H1N1 occurred in a boys' boarding school in 1978, 1979 and 1983. The serological response to infection with variants of the H1N1 virus was studied by radial haemolysis and haemagglutination inhibition after primary infection and reinfection. The persistence of this antibody was also studied. Infection in 1978 resulted in the production of persistent antibody to both the haemagglutinin and neuraminidase of the homotypic strain. Antibody which cross-reacted with later variants of the virus was less frequently produced, the peak response was delayed and such antibody persisted less well. Infection in 1979 resulted in a similar response to that observed in 1978 after primary infection. Reinfection resulted in a broad response in all cases. In 1983 all infected boys produced antibody which reacted with the homotypic strain but only approximately one-third of primary infections produced antibody which reacted with the A/USSR/92/77 strain. The neuraminidase of the A/USSR strain failed to detect one third of the primary infections. Reinfection again resulted in a broad response.


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