oalib
Search Results: 1 - 10 of 100 matches for " "
All listed articles are free for downloading (OA Articles)
Page 1 /100
Display every page Item
The Anticipated Severity of a “1918-Like” Influenza Pandemic in Contemporary Populations: The Contribution of Antibacterial Interventions  [PDF]
Yu-Wen Chien, Bruce R. Levin, Keith P. Klugman
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0029219
Abstract: Recent studies have shown that most of deaths in the 1918 influenza pandemic were caused by secondary bacterial infections, primarily pneumococcal pneumonia. Given the availability of antibiotics and pneumococcal vaccination, how will contemporary populations fare when they are next confronted with pandemic influenza due to a virus with the transmissibility and virulence of that of 1918? To address this question we use a mathematical model and computer simulations. Our model considers the epidemiology of both the influenza virus and pneumonia-causing bacteria and allows for co-infection by these two agents as well as antibiotic treatment, prophylaxis and pneumococcal vaccination. For our simulations we use influenza transmission and virulence parameters estimated from 1918 pandemic data. We explore the anticipated rates of secondary pneumococcal pneumonia and death in populations with different prevalence of pneumococcal carriage and contributions of antibiotic prophylaxis, treatment, and vaccination to these rates. Our analysis predicts that in countries with lower prevalence of pneumococcal carriage and access to antibiotics and pneumococcal conjugate vaccines, there would substantially fewer deaths due to pneumonia in contemporary populations confronted with a 1918-like virus than that observed in the 1918. Our results also predict that if the pneumococcal carriage prevalence is less than 40%, the positive effects of antibiotic prophylaxis and treatment would be manifest primarily at of level of individuals. These antibiotic interventions would have little effect on the incidence of pneumonia in the population at large. We conclude with the recommendation that pandemic preparedness plans should consider co-infection with and the prevalence of carriage of pneumococci and other bacteria responsible for pneumonia. While antibiotics and vaccines will certainly reduce the rate of individual mortality, the factor contributing most to the relatively lower anticipated lethality of a pandemic with a 1918-like influenza virus in contemporary population is the lower prevalence of pneumococcal carriage.
The Relationship between Tuberculosis and Influenza Death during the Influenza (H1N1) Pandemic from 1918-19
Welling Oei,Hiroshi Nishiura
Computational and Mathematical Methods in Medicine , 2012, DOI: 10.1155/2012/124861
Abstract: The epidemiological mechanisms behind the W-shaped age-specific influenza mortality during the Spanish influenza (H1N1) pandemic 1918-19 have yet to be fully clarified. The present study aimed to develop a formal hypothesis: tuberculosis (TB) was associated with the W-shaped influenza mortality from 1918-19. Three pieces of epidemiological information were assessed: (i) the epidemic records containing the age-specific numbers of cases and deaths of influenza from 1918-19, (ii) an outbreak record of influenza in a Swiss TB sanatorium during the pandemic, and (iii) the age-dependent TB mortality over time in the early 20th century. Analyzing the data (i), we found that the W-shaped pattern was not only seen in mortality but also in the age-specific case fatality ratio, suggesting the presence of underlying age-specific risk factor(s) of influenza death among young adults. From the data (ii), TB was shown to be associated with influenza death (=0.09), and there was no influenza death among non-TB controls. The data (iii) were analyzed by employing the age-period-cohort model, revealing harvesting effect in the period function of TB mortality shortly after the 1918-19 pandemic. These findings suggest that it is worthwhile to further explore the role of TB in characterizing the age-specific risk of influenza death.
Effect of 1918 PB1-F2 Expression on Influenza A Virus Infection Kinetics  [PDF]
Amber M. Smith,Frederick R. Adler,Julie L. McAuley,Ryan N. Gutenkunst,Ruy M. Ribeiro,Jonathan A. McCullers,Alan S. Perelson
PLOS Computational Biology , 2011, DOI: 10.1371/journal.pcbi.1001081
Abstract: Relatively little is known about the viral factors contributing to the lethality of the 1918 pandemic, although its unparalleled virulence was likely due in part to the newly discovered PB1-F2 protein. This protein, while unnecessary for replication, increases apoptosis in monocytes, alters viral polymerase activity in vitro, enhances inflammation and increases secondary pneumonia in vivo. However, the effects the PB1-F2 protein have in vivo remain unclear. To address the mechanisms involved, we intranasally infected groups of mice with either influenza A virus PR8 or a genetically engineered virus that expresses the 1918 PB1-F2 protein on a PR8 background, PR8-PB1-F2(1918). Mice inoculated with PR8 had viral concentrations peaking at 72 hours, while those infected with PR8-PB1-F2(1918) reached peak concentrations earlier, 48 hours. Mice given PR8-PB1-F2(1918) also showed a faster decline in viral loads. We fit a mathematical model to these data to estimate parameter values. The model supports a higher viral production rate per cell and a higher infected cell death rate with the PR8-PB1-F2(1918) virus. We discuss the implications these mechanisms have during an infection with a virus expressing a virulent PB1-F2 on the possibility of a pandemic and on the importance of antiviral treatments.
A Single Mutation in the PB1-F2 of H5N1 (HK/97) and 1918 Influenza A Viruses Contributes to Increased Virulence  [PDF]
Gina M Conenello,Dmitriy Zamarin,Lucy A Perrone,Terrence Tumpey,Peter Palese
PLOS Pathogens , 2007, DOI: 10.1371/journal.ppat.0030141
Abstract: The proapoptotic PB1-F2 protein of influenza A viruses has been shown to contribute to pathogenesis in the mouse model. Expression of full-length PB1-F2 increases the pathogenesis of the influenza A virus, causing weight loss, slower viral clearance, and increased viral titers in the lungs. After comparing viruses from the Hong Kong 1997 H5N1 outbreak, one amino acid change (N66S) was found in the PB1-F2 sequence at position 66 that correlated with pathogenicity. This same amino acid change (N66S) was also found in the PB1-F2 protein of the 1918 pandemic A/Brevig Mission/18 virus. Two isogenic recombinant chimeric viruses were created with an influenza A/WSN/33 virus background containing the PB1 segment from the HK/156/97: WH and WH N66S. In mice infected with WH N66S virus there was increased pathogenicity as measured by weight loss and decreased survival, and a 100-fold increase in virus replication when compared to mice infected with the WH virus. The 1918 pandemic strain A/Brevig Mission/18 was reconstructed with a pathogenicity-reducing mutation in PB1-F2 (S66N). The resultant 1918 S66N virus was attenuated in mice having a 3-log lower 50% lethal dose and caused less morbidity and mortality in mice than the wild-type virus. Viral lung titers were also decreased in 1918 S66N–infected mice compared with wild-type 1918 virus–infected mice. In addition, both viruses with an S at position 66 (WH N66S and wt 1918) induced elevated levels of cytokines in the lungs of infected mice. Together, these data show that a single amino acid substitution in PB1-F2 can result in increased viral pathogenicity and could be one of the factors contributing to the high lethality seen with the 1918 pandemic virus.
Similarities in mortality patterns from influenza in the first half of the 20th century and the rise and fall of ischemic heart disease in the United States: a new hypothesis concerning the coronary heart disease epidemic
Azambuja, Maria Inês Reinert;Duncan, Bruce B.;
Cadernos de Saúde Pública , 2002, DOI: 10.1590/S0102-311X2002000300002
Abstract: the classic risk factors for developing coronary heart disease (chd) explain less than 50% of the decrease in mortality observed since 1950. the transition currently under way, from the degenerative to the infectious-inflammatory paradigm, requires a new causal interpretation of temporal trends. the following is an ecological study based on data from the united states showing that in men and women an association between the age distribution of mortality due to influenza and pneumonia (i&p) associated with the influenza pandemic in 1918-1919 in the 10-49-year age bracket and the distribution of chd mortality from 1920 to 1985 in survivors from the corresponding birth cohorts. it further shows a significant negative correlation (r = -0.68, p = 0.042) between excess mortality from i&p accumulated in epidemics from 1931 to 1940 (used as indicator for persistent circulation of h1n1 virus combined with vulnerability to infection) and the order of the beginning in the decline in chd mortality in nine geographic divisions in the united states. in light of current biological knowledge, the data suggest that the 1918 influenza pandemic and the subsequent epidemics up to 1957 might have played a determinant role in the epidemic of chd mortality registered in the 20th century.
Similarities in mortality patterns from influenza in the first half of the 20th century and the rise and fall of ischemic heart disease in the United States: a new hypothesis concerning the coronary heart disease epidemic
Azambuja Maria Inês Reinert,Duncan Bruce B.
Cadernos de Saúde Pública , 2002,
Abstract: The classic risk factors for developing coronary heart disease (CHD) explain less than 50% of the decrease in mortality observed since 1950. The transition currently under way, from the degenerative to the infectious-inflammatory paradigm, requires a new causal interpretation of temporal trends. The following is an ecological study based on data from the United States showing that in men and women an association between the age distribution of mortality due to influenza and pneumonia (I&P) associated with the influenza pandemic in 1918-1919 in the 10-49-year age bracket and the distribution of CHD mortality from 1920 to 1985 in survivors from the corresponding birth cohorts. It further shows a significant negative correlation (r = -0.68, p = 0.042) between excess mortality from I&P accumulated in epidemics from 1931 to 1940 (used as indicator for persistent circulation of H1N1 virus combined with vulnerability to infection) and the order of the beginning in the decline in CHD mortality in nine geographic divisions in the United States. In light of current biological knowledge, the data suggest that the 1918 influenza pandemic and the subsequent epidemics up to 1957 might have played a determinant role in the epidemic of CHD mortality registered in the 20th century.
Did 20th century physics have the means to reveal the nature of inertia and gravitation?  [PDF]
Vesselin Petkov
Physics , 2000,
Abstract: At the beginning of the 20th century the classical electron theory (or, perhaps more appropriately, the classical electromagnetic mass theory) - the first physical theory that dared ask the question of what inertia and mass were - was gaining momentum and there were hopes that physics would be finally able to explain their origin. It is argued in this paper that if that promising research path had not been inexplicably abandoned after the advent of relativity and quantum mechanics, the contemporary physics would have revealed not only the nature of inertia, mass, and gravitation, but most importantly would have outlined the ways of their manipulation. Another goal of the paper is to try to stimulate the search for the mechanism responsible for inertia and gravitation by outlining a research direction, which demonstrates that the classical electromagnetic mass theory in conjunction with the principle of equivalence offers such a mechanism.
5'PPP-RNA induced RIG-I activation inhibits drug-resistant avian H5N1 as well as 1918 and 2009 pandemic influenza virus replication
Priya Ranjan, Lakshmi Jayashankar, Varough Deyde, Hui Zeng, William G Davis, Melissa B Pearce, John B Bowzard, Mary A Hoelscher, Victoria Jeisy-Scott, Mayim E Wiens, Shivaprakash Gangappa, Larisa Gubareva, Adolfo García-Sastre, Jacqueline M Katz, Terrence M Tumpey, Takashi Fujita, Suryaprakash Sambhara
Virology Journal , 2010, DOI: 10.1186/1743-422x-7-102
Abstract: In the present investigation, using real time RT-PCR, immunofluorescence, immunoblot, and plaque assay we show that 5'PPP-containing single stranded RNA (5'PPP-RNA), a ligand for the intracytoplasmic RNA sensor, RIG-I can be used as a prophylactic agent against known drug-resistant avian H5N1 and pandemic influenza viruses. 5'PPP-RNA treatment of human lung epithelial cells inhibited replication of drug-resistant avian H5N1 as well as 1918 and 2009 pandemic influenza viruses in a RIG-I and type 1 interferon dependant manner. Additionally, 5'PPP-RNA treatment also inhibited 2009 H1N1 viral replication in vivo in mice.Our findings suggest that 5'PPP-RNA mediated activation of RIG-I can suppress replication of influenza viruses irrespective of their genetic make-up, pathogenicity, and drug-sensitivity status.Annual influenza epidemics caused by influenza A and B viruses result in three to five million cases of severe illness with about 250,000 to 500,000 deaths globally every year. In the United States, complications from influenza infections result in approximately 250,000 hospitalizations and 36,000 deaths in an average year, with majority of the fatalities occurring among the elderly population [1]. Influenza A viruses are further sub typed based on hemagglutinin (HA) and neuraminidase (NA) proteins present on the virion envelope and there are 16 HA and 9 NA types known among influenza A viruses [2,3]. Frequent minor genetic changes, known as antigenic drift and the emergence of influenza A viruses with novel NA and/or HA subtypes, known as antigenic shift result in epidemics and pandemics respectively. In the 20th century, only viruses of the H1, H2 or H3 and N1 or N2 subtypes have caused sustained epidemics in humans. However, other subtypes namely H7, H9, and H5 which primarily cause infections and death among avian species have crossed the species barrier and caused mild to severe or fatal disease in humans [4]. Since 2003, highly pathogenic avian influenza (HPA
Epidemia y perplejidades médicas: Uruguay, 1918-1919
Serrón, Víctor;
História, Ciências, Saúde-Manguinhos , 2011, DOI: 10.1590/S0104-59702011000300006
Abstract: this article seeks to establish the type of connection that existed between the responses implemented by the uruguayan state and dominant medical knowledge in the form of health policies during the influenza epidemic of 1918-1919. the problem can be split into two aspects: what were the most salient lines of medical thought on confronting the influenza epidemic of 1918-1919? and how was medical knowledge linked to the actions undertaken by the uruguayan state? answers will be sought through an indicial inquiry for two reasons. firstly, the sources consulted present a very high degree of dispersion and heterogeneity and secondly, the writer is in an exploratory phase of the problem.
Transmissibility of the Influenza Virus in the 1918 Pandemic  [PDF]
Laura Forsberg White, Marcello Pagano
PLOS ONE , 2008, DOI: 10.1371/journal.pone.0001498
Abstract: Background With a heightened increase in concern for an influenza pandemic we sought to better understand the 1918 Influenza pandemic, the most devastating epidemic of the previous century. Methodology/Principal Findings We use data from several communities in Maryland, USA as well as two ships that experienced well-documented outbreaks of influenza in 1918. Using a likelihood-based method and a nonparametric method, we estimate the serial interval and reproductive number throughout the course of each outbreak. This analysis shows the basic reproductive number to be slightly lower in the Maryland communities (between 1.34 and 3.21) than for the enclosed populations on the ships (R0 = 4.97, SE = 3.31). Additionally the effective reproductive number declined to sub epidemic levels more quickly on the ships (within around 10 days) than in the communities (within 30–40 days). The mean serial interval for the ships was consistent (3.33, SE = 5.96 and 3.81, SE = 3.69), while the serial intervals in the communities varied substantially (between 2.83, SE = 0.53 and 8.28, SE = 951.95). Conclusions/Significance These results illustrate the importance of considering the population dynamics when making statements about the epidemiological parameters of Influenza. The methods that we employ for estimation of the reproductive numbers and the serial interval can be easily replicated in other populations and with other diseases.
Page 1 /100
Display every page Item


Home
Copyright © 2008-2017 Open Access Library. All rights reserved.