scholarly journals Immunophenotype Expressions and Cytokine Profiles of Influenza A H1N1 Virus Infection in Pediatric Patients in 2009

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Shih-Min Wang ◽  
Yu-Ting Liao ◽  
Yu-Shiang Hu ◽  
Tzong-Shiann Ho ◽  
Ching-Fen Shen ◽  
...  

Background. A novel swine-origin influenza A H1N1 virus (S-OIV) caused human infection and acute respiratory illness in 2009, resulting in an influenza pandemic.Objectives. This study characterized the immune responses of S-OIV infection in pediatric patients at risk of pulmonary complications.Methods. All enrolled pediatric patients were confirmed virologically for S-OIV infection in 2009-2010, prospectively. Changes in cellular immunophenotypes were analyzed using flow cytometry. Plasma cytokine levels associated with S-OIV infection by pulmonary and without pulmonary complications were measured using cytokine cytometric bead assay kits.Results. A total of 85 patients with a mean age of 10.3 years were recruited. The level of C-reactive protein (CRP) was high in patients exhibiting pulmonary complications. The percentage of cellular immunophenotypes did not change between patients with and without pulmonary complications. The absolute numbers of peripheral blood mononuclear cells (PBMC), CD3, CD8, and CD16CD56 decreased with acute S-OIV pulmonary complications. Acute influenza infection with pulmonary complications was associated with high plasma concentrations of IL-1β, IL-6, IL-12, and IFN-γ.Conclusion. Immunophenotype studies have reported variability in immune response to the severity of S-OIV infections. Acute phase cytokine profiles of the 2009 S-OIV infection might have contributed to the pathogenesis of the pulmonary complications.

2010 ◽  
Vol 45 (10) ◽  
pp. 1014-1020 ◽  
Author(s):  
Soo Youn Shin ◽  
Joon Hyung Kim ◽  
Hyun Su Kim ◽  
Young A Kang ◽  
Ha Gyung Lee ◽  
...  

2010 ◽  
Vol 138 (11) ◽  
pp. 1542-1549 ◽  
Author(s):  
A. L. GREER ◽  
A. TUITE ◽  
D. N. FISMAN

SUMMARYThe world is currently confronting the first influenza pandemic of the 21st century [caused by a novel pandemic influenza A (H1N1) virus]. Earlier pandemics have been characterized by age distributions that are distinct from those observed with seasonal influenza epidemics, with higher attack rates (and correspondingly increased proportionate or relative mortality) in younger individuals. While the genesis of protection against infection in older individuals during a pandemic is uncertain, differential vulnerability to infection by age has important implications for disease dynamics and control, and for choice of optimal vaccination strategies. Age-related vulnerability to infection may explain differences between school- and community-derived estimates of the reproductive number (R) for a newly emerged pandemic strain, and may also help explain the failure of a newly emerged influenza A (H1N1) virus strain to cause a pandemic in 1977. Age-related factors may also help explain variability in attack rates, and the size and impact of influenza epidemics across jurisdictions and between populations. In Canada, such effects have been observed in the apparently increased severity of outbreaks on Indigenous peoples' reserves. The implications of these patterns for vaccine allocation necessitate targeted research to understand age-related vulnerabilities early in an influenza pandemic.


2009 ◽  
Vol 14 (39) ◽  
Author(s):  
E Pérez-Trallero ◽  
L Piñeiro ◽  
D Vicente ◽  
M Montes ◽  
G Cilla

The 2009 pandemic influenza A(H1N1) virus has a higher incidence in children and young adults, a pattern that has also been reported in seasonal influenza caused by the influenza A(H1N1) virus. We analysed age at infection in symptomatic patients with influenza in the Basque Country (northern Spain), reported through the sentinel influenza surveillance system which monitors 2.2-2.5% of the population. Between September 1999 and August 2009, influenza A(H3N2) or seasonal influenza A(H1N1) was detected in 941 patients, and from April to August 2009, pandemic influenza A(H1N1) was detected in 112 patients. The H3/H1 seasonal influenza ratio was between 3.3 and 3.4 in the under 60 year-olds, but 9.8 in older individuals, suggesting that people born before 1950 have residual immunity against the influenza A H1N1 subtype (both seasonal and pandemic). Introduction In 1957, the Asian influenza pandemic was caused by influenza A(H2N2) virus, which circulated until 1968 when it was displaced by the influenza A(H3N2) virus which was responsible for the Hong Kong pandemic. Before 1957, direct descendants of the influenza A(H1N1) virus that had caused the 1918 pandemic (Spanish flu) had circulated. In 1977, an influenza A(H1N1) strain re-emerged, which, together with the dominant influenza A(H3N2) strain, has been the cause of seasonal human influenza for more than three decades [1]. Despite the prolonged co-circulation of both subtypes, few studies have analysed their ability to affect distinct age groups. The current pandemic influenza A(H1N1) virus, influenza A(H1N1)v, which emerged in the spring of 2009, has spread throughout the world. The aim of this study was to compare the distribution in distinct age groups of infections caused by the two subtypes of seasonal influenza in the past 10 seasons and refer therelate this to recent infections due to influenza A(H1N1)v.


1981 ◽  
Vol 87 (3) ◽  
pp. 383-392 ◽  
Author(s):  
N. Yamane ◽  
M. Hiratsuka ◽  
J. Arikawa ◽  
T. Odagiri ◽  
N. Ishida

SummaryAntibody responses to influenza virus immunizations were examined among junior high school students. The students received two doses of a commercial split-product vaccine containing influenza A H1N1 during a 2-year period following the first appearance of H1N1 virus in the winter of 1977–78. In haemagglutination-inhibition (HI) tests, the students who had been infected with H1N1 virus in 1977–78 showed a better response and wider cross-reactivity to the drift strain than the students who had not experienced earlier H1N1 influenza infection. Neuraminidase-inhibition (NAI) antibody titres after immunization depended upon a history of natural infection with H1N1 virus, since students not previously infected showed no significant NAI antibody rise after immunization.


mBio ◽  
2010 ◽  
Vol 1 (1) ◽  
Author(s):  
Brett W. Jagger ◽  
Matthew J. Memoli ◽  
Zong-Mei Sheng ◽  
Li Qi ◽  
Rachel J. Hrabal ◽  
...  

ABSTRACTThe swine-origin H1N1 influenza A virus emerged in early 2009 and caused the first influenza pandemic in 41 years. The virus has spread efficiently to both the Northern and the Southern Hemispheres and has been associated with over 16,000 deaths. Given the virus’s recent zoonotic origin, there is concern that the virus could acquire signature mutations associated with the enhanced pathogenicity of previous pandemic viruses or H5N1 viruses with pandemic potential. We tested the hypothesis that mutations in the polymerase PB2 gene at residues 627 and 701 would enhance virulence but found that influenza viruses containing these mutations in the context of the pandemic virus polymerase complex are attenuated in cell culture and mice.IMPORTANCEInfluenza A virus (IAV) evolution is characterized by host-specific lineages, and IAVs derived in whole or in part from animal reservoirs have caused pandemics in humans. Because IAVs are known to acquire host-adaptive genome mutations, and since the PB2 gene of the 2009 H1N1 virus is of recent avian derivation, there exists concern that the pathogenicity of the 2009 H1N1 influenza A pandemic virus could be potentiated by acquisition of the host-adaptive PB2-E627K or -D701N mutations, which have been shown to enhance the virulence of other influenza viruses. We present data from a mouse model of influenza infection showing that such mutations do not increase the virulence of viruses containing the 2009 H1N1 viral polymerase.


2010 ◽  
Vol 201 (3) ◽  
pp. 346-353 ◽  
Author(s):  
Patrick C. Y. Woo ◽  
Edward T. K. Tung ◽  
Kwok‐Hung Chan ◽  
Candy C. Y. Lau ◽  
Susanna K. P. Lau ◽  
...  

2019 ◽  
Vol 2019 ◽  
pp. 1-3 ◽  
Author(s):  
Camila D. Odio ◽  
Charisse Mandimika ◽  
Thiago A. Jabuonski ◽  
Maricar Malinis

Myositis is a rare and morbid complication of influenza infection that can rapidly progress to rhabdomyolysis with acute renal failure. Here, we describe a 35-year-old obese woman with severe influenza A(H1N1) virus infection complicated by myositis, refractory rhabdomyolysis, and compartment syndrome.


2013 ◽  
Vol 79 (7) ◽  
pp. 2148-2155 ◽  
Author(s):  
A. D. Coulliette ◽  
K. A. Perry ◽  
J. R. Edwards ◽  
J. A. Noble-Wang

ABSTRACTIn the United States, the 2009 pandemic influenza A (H1N1) virus (pH1N1) infected almost 20% of the population and caused >200,000 hospitalizations and >10,000 deaths from April 2009 to April 2010. On 24 April 2009, the CDC posted interim guidance on infection control measures in health care settings explicitly for pH1N1 and recommended using filtering face respirators (FFRs) when in close contact with a suspected- or confirmed-to-be-infected individual, particularly when performing aerosol-generating procedures. The persistence and infectivity of pH1N1 were evaluated on FFRs, specifically N95 respirators, under various conditions of absolute humidity (AH) (4.1 × 105mPa, 6.5 × 105mPa, and 14.6 × 105mPa), sample matrices (2% fetal bovine serum [FBS], 5 mg/ml mucin, and viral medium), and times (4, 12, 24, 48, 72, and 144 h). pH1N1 was distributed onto N95 coupons (3.8 to 4.2 cm2) and extracted by a vortex-centrifugation-filtration process, and the ability of the remaining virus to replicate was quantified using an enzyme-linked immunosorbent assay (ELISA) to determine the log10concentration of the infectious virus per coupon. Overall, pH1N1 remained infectious for 6 days, with an approximately 1-log10loss of virus concentrations over this time period. Time and AH both affected virus survival. We found significantly higher (P≤ 0.01) reductions in virus concentrations at time points beyond 24 to 72 h (−0.52-log10reduction) and 144 h (−0.74) at AHs of 6.5 × 105mPa (−0.53) and 14.6 × 105mPa (−0.47). This research supports discarding respirators after close contact with a person with suspected or confirmed influenza infection due to the virus's demonstrated ability to persist and remain infectious.


2009 ◽  
Vol 21 (6) ◽  
pp. 987-989 ◽  
Author(s):  
Sandra S. Chan ◽  
Linda C. W. Lam ◽  
Helen F. K. Chiu

The emergence of the novel swine-origin influenza A (H1N1) virus in humans has aroused great concern among medical professionals about the possible evolution of a full-blown influenza pandemic, one on the scale of the “Spanish” influenza pandemic of 1918–19 (Belshe, 2009). It has been speculated that the return of a pandemic virus equivalent in pathogenicity to the virus of 1918 would likely kill more than 100 million people worldwide, including a large number of economically active young people (Taubenberger and Morens, 2006). Health administrations worldwide have stepped up reporting and surveillance of the deaths and illnesses associated with H1N1, and most countries have national strategies to fight the outbreak, though skeptics doubt how such plans could be operationalized, especially in developing countries (Coker, 2009). As of 6 July 2009, the cumulative total of H1N1 cases exceeds 90,000 in over 100 countries, with over 400 deaths directly related to the infection (World Health Organization, 2009a). Optimists might believe this pandemic is not going to match the scale of the historical 1918 pandemic given the relatively low fatality rate observed thus far. However, the World Health Organization has cautioned that we have just entered Phase 6 of the pandemic – i.e. we are in the early days of the 2009 flu pandemic (Chan, 2009). The course of the pandemic is thus unpredictable at this stage but it is evident that international multilateral plans and agreements have enabled much greater coordination of communication and action than ever before. The guidance behind these multilateral international actions, rooted in the World Health Organization's International Health Regulations (IHR) 2005, only came into being five years ago in response to the threat of emerging infectious diseases and particularly by the events related to the emergence of Severe Acute Respiratory Syndrome (SARS) (Katz, 2009). The morbidity and mortality directly resulting from this novel influenza A H1N1 outbreak are in the center of the world media's spotlight, but the potential impact of the pandemic on global mental health has not yet received the attention it deserves.


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