Abstract:This essay proposes that the ecologic association shown between the 20th century coronary heart disease epidemic and the 1918 influenza pandemic could shed light on the mechanism associated with the high lethality of the latter. It suggests that an autoimmune interference at the apoB-LDL interface could explain both hypercholesterolemia and inflammation (through interference with the cellular metabolism of arachidonic acid). Autoimmune inflammation, then, would explain the 1950s-60s acute coronary events (coro… Show more
“…Interestingly using a mouse model of atherosclerosis (Apolipoprotein E deficient mouse) injection of influenza A virus into the mice was associated with significant infiltration of inflammatory and smooth muscle cells in atherosclerotic plaques, superficial platelet aggregation, and occasional subocclusive fibrin thrombus [43], which may in part provide an explanation for the increase in cardiovascular deaths seen during influenza epidemics [44]. Interestingly, a cohort association exists between rates of vulnerability to influenza deaths in 1918 and CHD mortality among survivors from those vulnerable birth cohorts [45]. These researchers suggest that the 1918 influenza pandemic may have played a role in the future development of CHD in the survivors, through an effect secondary to the influenza priming of 1918 vulnerable individuals for late development of CHD potentially through mechanisms of endothelial dysfunction and lipid dysregulation.…”
Section: Influenza and Coronary Heart Diseasementioning
“…Interestingly using a mouse model of atherosclerosis (Apolipoprotein E deficient mouse) injection of influenza A virus into the mice was associated with significant infiltration of inflammatory and smooth muscle cells in atherosclerotic plaques, superficial platelet aggregation, and occasional subocclusive fibrin thrombus [43], which may in part provide an explanation for the increase in cardiovascular deaths seen during influenza epidemics [44]. Interestingly, a cohort association exists between rates of vulnerability to influenza deaths in 1918 and CHD mortality among survivors from those vulnerable birth cohorts [45]. These researchers suggest that the 1918 influenza pandemic may have played a role in the future development of CHD in the survivors, through an effect secondary to the influenza priming of 1918 vulnerable individuals for late development of CHD potentially through mechanisms of endothelial dysfunction and lipid dysregulation.…”
Section: Influenza and Coronary Heart Diseasementioning
“…Azambuja [4] suggested that the high pathogenicity of the (H1) influenza virus among young adults in 1918-1919 might have re-sulted from an immune response that went awry, in birth-cohorts originally primed by the influenza viruses emerging during the 1888-1890 Pandemic (according to sero-epidemiologic studies, possibly an H3 virus [5]). In 2009, severe cases and deaths have spared individuals born before 1957 (oldest than 60) [6][7][8], concentrating among those born in years of greater H3 (post-1968) and H2?…”
Current explanations to the high 1918-1919 mortality involve either a higher pathogenicity of the virus or bacterial super-infection in the absence of adequate therapeutic resources. However, neither of these hypotheses accounts for the age-distribution of severe cases and deaths, or for the geographic and other variations in rates and explosiveness of mortality during the Pandemic. It will be shown here that, alternatively, the epidemiology of the influenza lethality could be completely explained by a combination of two determinants: (1) acquired immune-differentiation of birth-cohorts, within populations, through developmental epigenetic adaptation (and selection) secondary to maternal or early-life episodes of influenza infection and (2) a triggering context - emergence of a new sub-type/strain, and its co-circulation (competition?) with seasonal viruses immunologically related to ones that had circulated in the past and primed particular population birth-cohorts. This article (1) presents age, geographic, and temporal variations in 1918-1919 and 2009 influenza severity, (2) presents and discusses ecologic evidence in favor of the hypothesis to influenza lethality advanced here, (3) suggests biologic mechanisms capable of explaining it, (4) retrospectively, proposes co-circulation between the Pandemic and a 1918 seasonal (H3?) influenza virus as the context for the increased lethality during the second wave of the 1918 Pandemic, and (5) predicts an increase in influenza severity in the northern hemisphere as the 2009-2010 season advances and H3 circulation increases.
“…In addition, morbidity and mortality associated with influenza infections may manifest as a decompensation of underlying chronic cardio‐pulmonary conditions leading to increased mortality 2 . It has previously been demonstrated that both influenza and other viral respiratory infections may cause an inflammatory state capable of destabilizing atherosclerotic plaques which in turn lead to fatal cardiovascular events 14–18 . Therefore, in this paper we have included medical diagnosis other than ‘ deaths attributable to respiratory infections’ to evaluate the impact on mortality of influenza and RSV.…”
Section: Introductionmentioning
confidence: 99%
“…2 It has previously been demonstrated that both influenza and other viral respiratory infections may cause an inflammatory state capable of destabilizing atherosclerotic plaques which in turn lead to fatal cardiovascular events. [14][15][16][17][18] Therefore, in this paper we have included medical diagnosis other than 'deaths attributable to respiratory infections' to evaluate the impact on mortality of influenza and RSV. The Centers for Disease Control and Prevention estimate that seasonal influenza viruses cause an average of 51 203 deaths per year in the United States, whereas RSV is thought to cause an average of 17 358 deaths per year.…”
Please cite this paper as: Comas‐García et al. (2011) Mortality attributable to pandemic influenza A (H1N1) 2009 in San Luis Potosí, Mexico. Influenza and Other Respiratory Viruses 5(2), 76–82.
Background Acute respiratory infections are a leading cause of morbidity and mortality worldwide. Starting in 2009, pandemic influenza A(H1N1) 2009 virus has become one of the leading respiratory pathogens worldwide. However, the overall impact of this virus as a cause of mortality has not been clearly defined.
Objectives To determine the impact of pandemic influenza A(H1N1) 2009 on mortality in a Mexican population.
Methods We assessed the impact of pandemic influenza virus on mortality during the first and second outbreaks in San Luis Potosí, Mexico, and compared it to mortality associated with seasonal influenza and respiratory syncytial virus (RSV) during the previous winter seasons.
Results We estimated that, on average, 8·1% of all deaths that occurred during the 2003–2009 seasons were attributable to influenza and RSV. During the first pandemic influenza A(H1N1) 2009 outbreak, there was an increase in mortality in persons 5–59 years of age, but not during the second outbreak (Fall of 2009). Overall, pandemic influenza A (H1N1) 2009 outbreaks had similar effects on mortality to those associated with seasonal influenza virus epidemics.
Conclusions The impact of influenza A(H1N1) 2009 virus on mortality during the first year of the pandemic was similar to that observed for seasonal influenza. The establishment of real‐time surveillance systems capable of integrating virological, morbidity, and mortality data may result in the timely identification of outbreaks so as to allow for the institution of appropriate control measures to reduce the impact of emerging pathogens on the population.
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