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All-cause mortality during COVID-19: No plague and a likely signature of mass homicide by government response
Abstract
The latest data of all-cause mortality by week does not show a winter-burden mortality that is statistically larger than for past winters. There was no plague. However, a sharp "COVID peak" is present in the data, for several jurisdictions in Europe and the USA. This all-cause-mortality "COVID peak" has unique characteristics: • Its sharpness, with a full-width at half-maximum of only approximately 4 weeks; • Its lateness in the infectious-season cycle, surging after week-11 of 2020, which is unprecedented for any large sharp-peak feature; • The synchronicity of the onset of its surge, across continents, and immediately following the WHO declaration of the pandemic; and • Its USA state-to-state absence or presence for the same viral ecology on the same territory, being correlated with nursing home events and government actions rather than any known viral strain discernment. These "COVID peak" characteristics, and a review of the epidemiological history, and of relevant knowledge about viral respiratory diseases, lead me to postulate that the "COVID peak" results from an accelerated mass homicide of immune-vulnerable individuals, and individuals made more immune-vulnerable, by government and institutional actions, rather than being an epidemiological signature of a novel virus, irrespective of the degree to which the virus is novel from the perspective of viral speciation.
... Following Rancourt's 2 June 2020 article critically assessing circumstances of the declared pandemic using all-cause mortality (ACM) (Rancourt, 2020), more and more researchers are recognizing that it is essential to examine ACM by time, and excess deaths from all causes compared with projections from historic trends, to help make sense of the events surrounding COVID-19 (Kontis et al., 2020;Rancourt, Baudin and Mercier, 2020;Villani et al., 2020;Mercier, 2021a, 2021b;Achilleos et al., 2021;Chan, Cheng and Martin, 2021;Faust et al., 2021;Islam, Jdanov, et al., 2021;Islam, Shkolnikov, et al., 2021;Jacobson and Jokela, 2021;Joffe, 2021;Karlinsky and Kobak, 2021;Kobak, 2021;Kontopantelis et al., 2021;Locatelli and Rousson, 2021;Sanmarchi et al., 2021;Woolf et al., 2021;Woolf, Masters and Aron, 2021;Kontopantelis et al., 2022;Ackley et al., 2022;Johnson and Rancourt, 2022;Lee et al., 2022;Wang et al., 2022). Rancourt (2020) argued that ACM by time and by jurisdiction data for many countries and states of the USA in the months that followed the WHO 11 March 2020 declaration of a pandemic: ...
... Following Rancourt's 2 June 2020 article critically assessing circumstances of the declared pandemic using all-cause mortality (ACM) (Rancourt, 2020), more and more researchers are recognizing that it is essential to examine ACM by time, and excess deaths from all causes compared with projections from historic trends, to help make sense of the events surrounding COVID-19 (Kontis et al., 2020;Rancourt, Baudin and Mercier, 2020;Villani et al., 2020;Mercier, 2021a, 2021b;Achilleos et al., 2021;Chan, Cheng and Martin, 2021;Faust et al., 2021;Islam, Jdanov, et al., 2021;Islam, Shkolnikov, et al., 2021;Jacobson and Jokela, 2021;Joffe, 2021;Karlinsky and Kobak, 2021;Kobak, 2021;Kontopantelis et al., 2021;Locatelli and Rousson, 2021;Sanmarchi et al., 2021;Woolf et al., 2021;Woolf, Masters and Aron, 2021;Kontopantelis et al., 2022;Ackley et al., 2022;Johnson and Rancourt, 2022;Lee et al., 2022;Wang et al., 2022). Rancourt (2020) argued that ACM by time and by jurisdiction data for many countries and states of the USA in the months that followed the WHO 11 March 2020 declaration of a pandemic: ...
... The initial surges in ACM are highly localized geographically (by jurisdiction) and are precisely synchronous (all starting immediately after the 11 March 2020 WHO declaration of a pandemic, across continents), which is contrary to model pandemic behaviour; but is consistent with the surges being caused by the known government and institutional responses (Rancourt, 2020;Rancourt, Baudin and Mercier, 2020, 2021a, 2021bJohnson and Rancourt, 2022 Figure 7). Above-decadal-trend mortality in the covid period is massive. ...
All-cause mortality by time is the most reliable data for detecting and epidemiologically characterizing events causing death, and for gauging the population-level impact of any surge or collapse in deaths from any cause. Such data is not susceptible to reporting bias or to any bias in attributing causes of death. We compare USA all-cause mortality by time (month, week), by age group and by state to number of vaccinated individuals by time (week), by injection sequence, by age group and by state, using consolidated data up to week-5 of 2022 (week ending on February 5, 2022), in order to detect temporal associations, which would imply beneficial or deleterious effects from the vaccination campaign. We also quantify total excess all-cause mortality (relative to historic trends) for the entire covid period (WHO 11 March 2020 announcement of a pandemic through week-5 of 2022, corresponding to a total of 100 weeks), for the covid period prior to the bulk of vaccine delivery (first 50 weeks of the defined 100-week covid period), and for the covid period when the bulk of vaccine delivery is accomplished (last 50 weeks of the defined 100-week covid period); by age group and by state. We find that the COVID-19 vaccination campaign did not reduce all-cause mortality during the covid period. No deaths, within the resolution of all-cause mortality, can be said to have been averted due to vaccination in the USA. The mass vaccination campaign was not justified in terms of reducing excess all-cause mortality. The large excess mortality of the covid period, far above the historic trend, was maintained throughout the entire covid period irrespective of the unprecedented vaccination campaign, and is very strongly correlated (r = +0.86) to poverty, by state; in fact, proportional to poverty. It is also correlated to several other socioeconomic and health factors, by state, but not correlated to population fractions (65+, 75+, 85+ years) of elderly state residents.
... e all-cause mortality shows sharp surges in deaths that followed the 11 March 2020 WHO global recommendation for hospital clearing as "pandemic" response, across the world, in those jurisdictions that sent hospitalised infected elderly persons into the community, including locked down care homes.[2] [3][4] [5] e mechanism that made care homes and institutions for sick and elderly persons into killing elds includes the following elements:[2] ...
... The Great VIRAL Debate: Dr Rancourt's Closing Statement -OffGuardian https://off-guardian.org/2020/11/10/the-great-viral-debate-dr-rancourts-closing-statement/ 5/76 [3][4] [5] is was a mass crime. ...
... e post-March-11th "COVID-peaks" that I rst identi ed in the all-cause mortality data for the USA and Europe would not have occurred. [3] In the context of this debate, "herd/community immunity" refers to the business-as-usual natural coping of individuals and society constantly challenged by respiratory disease viruses, as has been the case for thousands of years. In technical terms, the concept of "herd immunity" was introduced by vaccine manufacturers as a pretext for universal vaccination programs, rather than individual personalchoice "protection". ...
Welcome to Closing Statements of The Great VIRAL Debate. Track this debate’s progress in our Coronavirus Debate Section. Dr Piers Robinson is our chair. Off-Guardian is your host.
-- The mechanism that made care homes and institutions for sick and elderly persons into killing fields includes the following elements:
* infection seeding by hospital transfers into the care homes
* universal lockdowns of the care homes
* denied specialized medical treatment to the residents of the care homes
* reduced staffing and staff abandonment in the care homes, and negligence
* collateral effects of the universal lockdown of the care homes: extreme social isolation, psychological stress, reduced aerosol-exhaust ventilation, lost oversight of the institutions by family-members
... Analysis of worldwide mortality data by Verduyn, Engler and Kenyon (2023a&b) indicates that 'Covid deaths should be categorized as part of the baseline of normal deaths, rather than as the driving force behind excess deaths'. Rancourt et al (2022) analyzed US all-cause mortality to show that its behaviour was inconsistent with 'pandemic behaviour caused by a new respiratory virus' (see also Rancourt, 2020;Rancourt, Hickey and Linard, 2024). ...
Major crisis events, such as the assassination of political leaders, terrorist attacks and public health emergencies, can be politically useful. Unfortunately, critical discussion of whether such events are exploited or even instigated in order to enable particular policy agendas is all too often dismissed as ‘conspiracism’. Fortunately, Peter Dale Scott’s structural deep event (SDE) and Lance deHaven-Smith’s state crime against democracy (SCAD) are concepts that provide a basis for critical exploration of major crisis events. This article builds upon these ideas, as well as that of propaganda and preliminary work by Kevin Ryan (2020), in order to develop a framework for identifying the key features, or ‘observable implications’, of a structural deep event. Utilizing the principles of a ‘structured focused comparison’ (George, 1979), the framework is then applied across two events — 9/11 and COVID-19 — claimed to have been manipulated for political purposes. It will be argued that both events share key features associated with SDEs — a) major policy drives associated with structural transformation of society, b) involvement of deep state actors, and c) the manipulation of an event and public perceptions of it — and that further research is warranted into these events. The paper concludes by discussing key implications of this study and makes suggestions for further research.
... Analysis of worldwide mortality data by Verduyn, Engler and Kenyon (2023a&b) indicates that 'Covid deaths should be categorized as part of the baseline of normal deaths, rather than as the driving force behind excess deaths'. Rancourt et al (2022) analyzed US all-cause mortality to show that its behaviour was inconsistent with 'pandemic behaviour caused by a new respiratory virus' (see also Rancourt, 2020;Rancourt, Hickey and Linard, 2024). ...
... No sooner was the "pandemic" declared than "Covid-19" cases and deaths began to surge worldwide at an unnaturally fast rate that cannot plausibly be accounted for by viral spread and the "extraordinary forecasting ability of the global health-monitoring system" (Rancourt, 2020a(Rancourt, , 2020b(Rancourt, , 2020c. As Engler (2022) writes of Lombardy: "A virus doesn't spread across thousands of kilometres within days [generating] peaks [of deaths] at the same time"; rather, like a 2003 heatwave in France that was blamed on neglect, the cause was probably attributable to the state. ...
Western governments have long used manufactured fear as a means of keeping the population susceptible to propaganda. A “pandemic” is a powerful fear concept; yet, there is no credible evidence of a viral pandemic in 2020. “Covid-19” does not meet any credible (pre-2009) definition of a “pandemic,” and attempts to present “Covid-19” as a new “Spanish flu” are bogus. The exaggerated threat of “Covid-19” was a function of military-grade propaganda, emanating from governments and the media, involving a barrage of terrifying images, messages, and “alert levels.” The BBC played a particularly culpable role in spreading fear. Death statistics were manipulated. Propaganda about hospitals being overwhelmed by “Covid-19” admissions camouflaged a sinister attack on public health. The primary purpose of face masks and PCR tests was to spread fear. Waves of fear/terror were sent by “new variants,” “immunity escape,” and the open letter by Geert Vanden Bossche. The spurious concept of “long Covid” projects the danger out into the future.
... The "lockdowns" left behind a "legacy of harm for hundreds of millions of people in the years ahead" owing to a rise in non-Covid excess mortality, mental health deterioration, child abuse and domestic violence, widening global inequality, food insecurity, lost educational opportunities, unhealthy lifestyle behaviours, social polarization, soaring debt, democratic backsliding and declining human rights. (Bardosh, 2023) There is clear evidence of democide (Rancourt, 2020;Rancourt et al., 2021Rancourt et al., , 2023, state-sponsored euthanasia, and experimentation on human beings . Patterns of sadism and cruelty have been deliberately instigated, from locking elderly people up in care homes and not allowing relatives to visit (HART, 2022a), to forcing children to wear masks in schools all day, to persecuting those not complying with tyranny (see Chapter 7). ...
The transnational ruling class has no choice but to keep pushing for global technocracy, and the rest of humanity has no choice but to fight back. Knowing since 1968 at least that this moment was coming, the former has developed the CIA’s information-liquidation model used in Indonesia and Vietnam in the 1960s into a global digital surveillance dragnet. The “Covid-19 vaccines,” shot into as many people as possible for no sound medical reason, could form part of an advanced weapons system, not least in the context of the emergent “IT/Bio/Nano era” envisaged by NASA in 2001, involving the use of nanotechnologies to connect human beings to an external network. If the brain is the twenty-first-century battlescape, and given that syringe-injectable neural nets were a reality by 2018, the evil potential of weaponised neurotechnology knows no bounds. History teaches that as the old social order breaks down, a moment of revolutionary potential arises. Lest unimaginable horrors be allowed to manifest, as in previous world wars, that moment must be seized.
... Indeed, we consider COVID lethality records faulty by two main biases: a) Over-notification and/or under-notification of COVID deaths. As reported by Islam [17], a dropping of 73% of COVID-19 demises occurred in the official records when Public Health England changed its definition of COVID-19 deaths in July 2020. Furthermore, Rancourt [18] pointed out the all-cause mortality as the most useful parameter in investigating the epidemiology of the pandemic. ...
The temporal correlation structure between the profiles of all-causes mortality relative to Italian regions highlighted a largely, unexpected result. Notwithstanding the elimination of well-known seasonal effects, the time series of fluctuations in death rates with respect to the 2015-2019, showed a very high mutual correlation among the 20 Italian regions under scrutiny, ruling out any 'randomness' hypothesis. On the contrary, the standardized death rates dynamics was almost invariant along the years, giving rise to a major 'size' principal component correspondent to the among regions shared motion, and a second 'shape' component modelling the North-South antiphase behaviour. The COVID-19 epidemic, while affecting the breadth of mortality incidence, did not change the among regions correlation dynamics, thus suggesting that this contingency impinges on an intrinsic death rate dynamical mode. The exceptional increase in mortality in the Northern regions observed in 2020 was of the same entity of the North-South differences in mortality observed in 'normal' periods. A coherent and homogeneous distribution of mortality rates would had be expected if COVID-related death were to be attributed (solely) to the pathogenic potency of the virus. Conversely, differences in mortality trends across the North-South divide may likely reflect differences in health care availability or other societal features.
... Your closed-door statement of January 2017 is an indelible part of your professional legacy. 5 But the most graphic representation of your legacy could be the absurdity depicted here: ...
... Your closed-door statement of January 2017 is an indelible part of your professional legacy. 5 But the most graphic representation of your legacy could be the absurdity depicted here: ...
Alleged "COVID-19 Pandemic" mandated government enforced lockdowns of citizens, leading to massive but ignored K -12 suicide deaths of our children is connectable to Dr. Anthony Fauci.
We investigate why the USA, unlike Canada and Western European countries, has a sustained exceedingly large mortality in the “COVID-era” occurring from March 2020 to present (October 2021). All-cause mortality by time is the most reliable data for detecting true catastrophic events causing death, and for gauging the population-level impact of any surge in deaths from any cause. The behaviour of the USA all-cause mortality by time (week, year), by age group, by sex, and by state is contrary to pandemic behaviour caused by a new respiratory disease virus for which there is no prior natural immunity in the population. Its seasonal structure (summer maxima), age-group distribution (young residents), and large state-wise heterogeneity are unprecedented and are opposite to viral respiratory disease behaviour, pandemic or not. We conclude that a pandemic did not occur. We infer that persistent chronic psychological stress induced by the long-lasting government-imposed societal and economic transformations during the COVID-era converted the existing societal (poverty), public-health (obesity) and hot-climate risk factors into deadly agents, largely acting together, with devastating population-level consequences against large pools of vulnerable and disadvantaged residents of the USA, far above preexisting pre-COVID-era mortality in those pools. We also find a large COVID-era USA pneumonia epidemic that is not mentioned in the media or significantly in the scientific literature, which was not adequately addressed. Many COVID-19-assigned deaths may be misdiagnosed bacterial pneumonia deaths. The massive vaccination campaign (380 M administered doses, 178 M fully vaccinated individuals, mainly January-August 2021 and March-August 2021, respectively) had no detectable mitigating effect, and may have contributed to making the younger population more vulnerable (35-64 years, summer-2021 mortality).
A vile new mantra is on the lips of every public health official and politician in the global campaign to force universal masking on the general public: “there is a growing body of evidence”.
This propagandistic phrase is a vector designed to achieve five main goals:
- Give the false impression that a balance of evidence now proves that masks reduce the transmission of COVID-19
- Falsely assimilate commentary made in scientific venues with “evidence”
- Hide the fact that a decade’s worth of policy-grade evidence proves the opposite: that masks are ineffective with viral respiratory diseases
- Hide the fact that there is now direct observational proof that cloth masks do not prevent exhalation of clouds of suspended aerosol particles; above, below and through the masks
- Deter attention away from the considerable known harms and risks due to face masks, applied to entire populations
The said harms and risks include that a cloth mask becomes a culture medium for a large variety of bacterial pathogens, and a collector of viral pathogens; given the hot and humid environment and the constant source, where home fabrics are hydrophilic whereas medical masks are hydrophobic.
In short, I argue: op-eds are not “evidence”, irrelevance does not help, and more bias does not remove bias. Their mantra of “a growing body of evidence” is a self-serving contrivance that impedes good science and threatens public safety.
I prove that there is no policy-grade evidence to support forced masking on the general population, and that all the latest-decade’s policy-grade evidence points to the opposite: NOT recommending forced masking of the general population. Therefore, the politicians and health authorities are acting without legitimacy and recklessly.
Significance
Ecological scaling laws are intensively studied for their predictive power and universal nature but often fail to unify biodiversity across domains of life. Using a global-scale compilation of microbial and macrobial data, we uncover relationships of commonness and rarity that scale with abundance at similar rates for microorganisms and macroscopic plants and animals. We then show a unified scaling law that predicts the abundance of dominant species across 30 orders of magnitude to the scale of all microorganisms on Earth. Using this scaling law combined with the lognormal model of biodiversity, we predict that Earth is home to as many as 1 trillion (10 ¹² ) microbial species.
Author Summary
The immune response is energetically costly and often requires adaption of the whole organism to ensure it receives enough energy. It is not well understood how distribution of energy resources within the organism is regulated during an immune response. To understand this better, we used parasitoid wasp infection of fruit fly larvae—the host larvae have 48 h before they pupate to destroy the infecting “alien” or face destruction by the parasitoid that will consume the developing pupa. Here we find a signal, generated by the host immune cells, which mediates a systemic energy switch. This signal—adenosine—suppresses processes driving larval to pupal development of the host, thereby freeing up energy for the immune system. We show that the resulting developmental delay in the fruit fly larvae is crucial for an efficient immune response; without the adenosine signal, resistance to the parasitoid drops drastically. Generation of this signal by immune cells demonstrates that in response to external stressors, the immune system can mobilize reallocation to itself of energy and nutrients from the rest of the organism.
Cardiovascular diseases (CVD) mortality has been shown to follow a seasonal pattern. Several studies suggested several possible determinants of this pattern, including misclassification of causes of deaths. We aimed at assessing seasonality in overall, CVD, cancer and non-CVD/non-cancer mortality using data from 19 countries from different latitudes.
Monthly mortality data were compiled from 19 countries, amounting to over 54 million deaths. We calculated ratios of the observed to the expected numbers of deaths in the absence of a seasonal pattern. Seasonal variation (peak to nadir difference) for overall and cause-specific (CVD, cancer or non-CVD/non-cancer) mortality was analyzed using the cosinor function model. Mortality from overall, CVD and non-CVD/non-cancer showed a consistent seasonal pattern. In both hemispheres, the number of deaths was higher than expected in winter. In countries close to the Equator the seasonal pattern was considerably lower for mortality from any cause. For CVD mortality, the peak to nadir differences ranged from 0.185 to 0.466 in the Northern Hemisphere, from 0.087 to 0.108 near the Equator, and from 0.219 to 0.409 in the Southern Hemisphere. For cancer mortality, the seasonal variation was nonexistent in most countries.
In countries with seasonal variation, mortality from overall, CVD and non-CVD/non-cancer show a seasonal pattern with mortality being higher in winter than in summer. Conversely, cancer mortality shows no substantial seasonality.
Segmentation of the influenza A virus (IAV) genome enables rapid gene reassortment at the cost of complicating the task of
assembling the full viral genome. By simultaneously probing for the expression of multiple viral proteins in MDCK cells infected
at a low multiplicity with IAV, we observe that the majority of infected cells lack detectable expression of one or more essential
viral proteins. Consistent with this observation, up to 90% of IAV-infected cells fail to release infectious progeny, indicating
that many IAV virions scored as noninfectious by traditional infectivity assays are capable of single-round infection. This
fraction was not significantly affected by target or producer cell type but varied widely between different IAV strains. These
data indicate that IAV exists primarily as a swarm of complementation-dependent semi-infectious virions, and thus traditional,
propagation-dependent assays of infectivity may drastically misrepresent the true infectious potential of a virus population.
Viruses are a significant cause of morbidity and mortality around the world. Determining the minimum dose of virus particles
that can initiate infection, termed the minimum infective dose (MID), is important for the development of risk assessment
models in the fields of food and water treatment and the implementation of appropriate infection control strategies in healthcare
settings. Both respiratory and enteric viruses can be shed at high titers from infected individuals even when the infection
is asymptomatic. Presence of pre-existing antibodies has been shown to affect the infectious dose and to be protective against
reinfection for many, but not all viruses. Most respiratory viruses appear to be as infective in humans as in tissue culture.
Doses of <1 TCID50 of influenza virus, rhinovirus, and adenovirus were reported to infect 50% of the tested population. Similarly, low doses
of the enteric viruses, norovirus, rotavirus, echovirus, poliovirus, and hepatitis A virus, caused infection in at least some
of the volunteers tested. A number of factors may influence viruses’ infectivity in experimentally infected human volunteers.
These include host and pathogen factors as well as the experimental methodology. As a result, the reported infective doses
of human viruses have to be interpreted with caution.
KeywordsMinimum infectious dose–Respiratory viruses–Enteric viruses–Infection
Author Summary
The origin of seasonality in influenza transmission is both of palpable public health importance and basic scientific interest. Here, we present statistical analyses and a mathematical model of epidemic influenza transmission that provide strong epidemiological evidence for the hypothesis that absolute humidity (AH) drives seasonal variations of influenza transmission in temperate regions. We show that the onset of individual wintertime influenza epidemics is associated with anomalously low AH conditions throughout the United States. In addition, we use AH to modulate the basic reproductive number of influenza within a mathematical model of influenza transmission and compare these simulations with observed excess pneumonia and influenza mortality. These simulations capture key details of the observed seasonal cycle of influenza throughout the US. The results indicate that AH affects both the seasonality of influenza incidence and the timing of individual wintertime influenza outbreaks in temperate regions. The association of anomalously low AH conditions with the onset of wintertime influenza outbreaks suggests that skillful, short-term probabilistic forecasts of epidemic influenza could be developed.
The 'independent action hypothesis' (IAH) states that each pathogen individual has a non-zero probability of causing host death and that pathogen individuals act independently. IAH has not been rigorously tested. In this paper, we (i) develop a probabilistic framework for testing IAH and (ii) demonstrate that, in two out of the six virus-insect pathosystems tested, IAH is supported by the data. We first show that IAH inextricably links host survivorship to the number of infecting pathogen individuals, and develop a model to predict the frequency of single- and dual-genotype infections when a host is challenged with a mixture of two genotypes. Model predictions were tested using genetically marked, near-identical baculovirus genotypes, and insect larvae from three host species differing in susceptibility. Observations in early-instar larvae of two susceptible host species support IAH, but observations in late-instar larvae of susceptible host species and larvae of a less susceptible host species were not in agreement with IAH. Hence the model is experimentally supported only in pathosystems in which the host is highly susceptible. We provide, to our knowledge, the first qualitative experimental evidence that, in such pathosystems, the action of a single virion is sufficient to cause disease.
Baseline levels of mortality in the United States in the absence of influenza epidemics were estimated using cyclical regression models applied to national vital statistics from October 1972 to May 1985. Models were developed by age and by region. Results from 1983 to 1985 are preliminary. More mortality than predicted by the theoretical baseline occurred during nine influenza seasons. Epidemics with high morbidity in children and young adults occurred in 1976/77 and 1978/79. Regional differences in the impact of influenza occurred occasionally. Total influenza-associated excess mortality in six epidemics from the winters of 1972/73 to 1980/81 was about 200,000. About 80-90 per cent of excess mortality occurred in persons over 64 years old.
Seasonal cycles of infectious diseases have been variously attributed to changes in atmospheric conditions, the prevalence or virulence of the pathogen, or the behavior of the host. Some observations about seasonality are difficult to reconcile with these explanations. These include the simultaneous appearance of outbreaks across widespread geographic regions of the same latitude; the detection of pathogens in the off-season without epidemic spread; and the consistency of seasonal changes, despite wide variations in weather and human behavior. In contrast, an increase in susceptibility of the host population, perhaps linked to the annual light/dark cycle and mediated by the pattern of melatonin secretion, might account for many heretofore unexplained features of infectious disease seasonality. Ample evidence indicates that photoperiod-driven physiologic changes are typical in mammalian species, including some in humans. If such physiologic changes underlie human resistance to infectious diseases for large portions of the year and the changes can be identified and modified, the therapeutic and preventive implications may be considerable.
As a transmissible infectious disease, severe acute respiratory syndrome (SARS) was successfully contained globally by instituting widespread quarantine measures. Although these measures were successful in terminating the outbreak in all areas of the world, the adverse effects of quarantine have not previously been determined in a systematic manner. In this hypothesis-generating study supported by a convenience sample drawn in close temporal proximity to the period of quarantine, we examined the psychological effects of quarantine on persons in Toronto, Canada. The 129 quarantined persons who responded to a Web-based survey exhibited a high prevalence of psychological distress. Symptoms of posttraumatic stress disorder (PTSD) and depression were observed in 28.9% and 31.2% of respondents, respectively. Longer durations of quarantine were associated with an increased prevalence of PTSD symptoms. Acquaintance with or direct exposure to someone with a diagnosis of SARS was also associated with PTSD and depressive symptoms.
The first pandemic season of A/H3N2 influenza virus (1968/1969) resulted in significant mortality in the United States, but it was the second pandemic season of A/H3N2 influenza virus (1969/1970) that caused the majority of deaths in England. We further explored the global pattern of mortality caused by the pandemic during this period.
We estimated the influenza-related excess mortality in 6 countries (United States, Canada, England and Wales, France, Japan, and Australia) using national vital statistics by age for 1967-1978. Geographical and temporal pandemic patterns in mortality were compared with the genetic drift of the influenza viruses by analyzing hemagglutinin and neuraminidase sequences from GenBank.
In North America, the majority of influenza-related deaths in 1968/1969 and 1969/1970 occurred during the first pandemic season (United States, 70%; Canada, 54%). Conversely, in Europe and Asia, the pattern was reversed: 70% of deaths occurred during the second pandemic season. The second pandemic season coincided with a drift in the neuraminidase antigen.
We found a consistent pattern of mortality being delayed until the second pandemic season of A/H3N2 circulation in Europe and Asia. We hypothesize that this phenomenon may be explained by higher preexisting neuraminidase immunity (from the A/H2N2 era) in Europe and Asia than in North America, combined with a subsequent drift in the neuraminidase antigen during 1969/1970.
Influenza A virus is well known for its capability for genetic changes either through antigen drift or antigen shift. Antigen shift is derived from reassortment of gene segments between viruses, and may result in an antigenically novel virus that is capable of causing a worldwide pandemic. As we trace backwards through the history of influenza pandemics, a repeating pattern can be observed, namely, a limited wave in the first year followed by global spread in the following year. In the 20th century alone, there were three overwhelming pandemics, in 1918, 1957 and 1968, caused by H1N1 (Spanish flu), H2N2 (Asian flu) and H3N2 (Hong Kong flu), respectively. In 1957 and 1968, excess mortality was noted in infants, the elderly and persons with chronic diseases, similar to what occurred during interpandemic periods. In 1918, there was one distinct peak of excess death in young adults aged between 20 and 40 years old; leukopenia and hemorrhage were prominent features. Acute pulmonary edema and hemorrhagic pneumonia contributed to rapidly lethal outcome in young adults. Autopsies disclosed multiple-organ involvement, including pericarditis, myocarditis, hepatitis and splenomegaly. These findings are, in part, consistent with clinical manifestations of human infection with avian influenza A H5N1 virus, in which reactive hemophagocytic syndrome was a characteristic pathologic finding that accounted for pancytopenia, abnormal liver function and multiple organ failure. All the elements of an impending pandemic are in place. Unless effective measures are implemented, we will likely observe a pandemic in the coming seasons. Host immune response plays a crucial role in disease caused by newly emerged influenza virus, such as the 1918 pandemic strain and the recent avian H5N1 strain. Sustained activation of lymphocytes and macrophages after infection results in massive cytokine response, thus leading to severe systemic inflammation. Further investigations into how the virus interacts with the host's immune system will be helpful in guiding future therapeutic strategies in facing influenza pandemics.
Currently, little is known about the viral kinetics of influenza A during infection within an individual. We utilize a series of mathematical models of increasing complexity, which incorporate target cell limitation and the innate interferon response, to examine influenza A virus kinetics in the upper respiratory tracts of experimentally infected adults. The models were fit to data from an experimental H1N1 influenza A/Hong Kong/123/77 infection and suggest that it is important to include the eclipse phase of the viral life cycle in viral dynamic models. Doing so, we estimate that after a delay of approximately 6 h, infected cells begin producing influenza virus and continue to do so for approximately 5 h. The average lifetime of infected cells is approximately 11 h, and the half-life of free infectious virus is approximately 3 h. We calculated the basic reproductive number, R(0), which indicated that a single infected cell could produce approximately 22 new productive infections. This suggests that antiviral treatments have a large hurdle to overcome in moderating symptoms and limiting infectiousness and that treatment has to be initiated as early as possible. For about 50% of patients, the curve of viral titer versus time has two peaks. This bimodal behavior can be explained by incorporating the antiviral effects of interferon into the model. Our model also compared well to an additional data set on viral titer after experimental infection and treatment with the neuraminidase inhibitor zanamivir, which suggests that such models may prove useful in estimating the efficacies of different antiviral therapies for influenza A infection.
Using the guinea pig as a model host, we show that aerosol spread of influenza virus is dependent upon both ambient relative humidity and temperature. Twenty experiments performed at relative humidities from 20% to 80% and 5 degrees C, 20 degrees C, or 30 degrees C indicated that both cold and dry conditions favor transmission. The relationship between transmission via aerosols and relative humidity at 20 degrees C is similar to that previously reported for the stability of influenza viruses (except at high relative humidity, 80%), implying that the effects of humidity act largely at the level of the virus particle. For infected guinea pigs housed at 5 degrees C, the duration of peak shedding was approximately 40 h longer than that of animals housed at 20 degrees C; this increased shedding likely accounts for the enhanced transmission seen at 5 degrees C. To investigate the mechanism permitting prolonged viral growth, expression levels in the upper respiratory tract of several innate immune mediators were determined. Innate responses proved to be comparable between animals housed at 5 degrees C and 20 degrees C, suggesting that cold temperature (5 degrees C) does not impair the innate immune response in this system. Although the seasonal epidemiology of influenza is well characterized, the underlying reasons for predominant wintertime spread are not clear. We provide direct, experimental evidence to support the role of weather conditions in the dynamics of influenza and thereby address a long-standing question fundamental to the understanding of influenza epidemiology and evolution.
Sequelae frequently seen in patients with chronic inflammatory diseases, such as fatigue, depressed mood, sleep alterations, loss of appetite, muscle wasting, cachectic obesity, bone loss and hypertension, can be the result of energy shortages caused by an overactive immune system. These sequelae can also be found in patients with chronic inflammatory diseases that are in remission and in ageing individuals, despite the immune system being less active in these situations. This Perspectives article proposes a new way of understanding situations of chronic inflammation (such as rheumatic diseases) and ageing based on the principles of evolutionary medicine, energy regulation and neuroendocrine–immune crosstalk. A conceptual framework is provided to enable physicians and scientists to better understand the signs and symptoms of chronic inflammatory diseases and long-term disease consequences resulting from physical and mental inactivity.
It is a truism that the brain influences the body and that peripheral physiology influences the brain. Never is this clearer than during stress, where the subtlest emotions or the most abstract thoughts can initiate stress responses, with consequences throughout the body, and the endocrine transducers of stress alter cognition, affect and behavior. For a fervent materialist, few things in life bring more pleasure than contemplating the neurobiology of stress.
The reevaluation of drinking water treatment practices in a desire to minimize the formation of disinfection byproducts while assuring minimum levels of public health protection against infectious organisms has caused it to become necessary to consider the problem of estimation of risks posed from exposure to low levels of microorganisms, such as virus or protozoans, found in treated drinking water. This paper outlines a methodology based on risk assessment principles to approach the problem. The methodology is validated by comparison with results obtained in a prospective epidemiological study. It is feasible to produce both point and interval estimates of infection, illness and perhaps mortality by this methodology. Areas of uncertainty which require future data are indicated.
The on-going debate about the health burden of the 2009 influenza pandemic and discussions about the usefulness of vaccine recommendations has been hampered by an absence of directly comparable measures of mortality impact. Here we set out to generate an "apples-to-apples" metric to compare pandemic and epidemic mortality. We estimated the mortality burden of the pandemic in the US using a methodology similar to that used to generate excess mortality burden for inter-pandemic influenza seasons. We also took into account the particularly young age distribution of deaths in the 2009 H1N1 pandemic, using the metric "Years of Life Lost" instead of numbers of deaths. Estimates are based on the timely pneumonia and influenza mortality surveillance data from 122 US cities, and the age distribution of laboratory-confirmed pandemic deaths, which has a mean of 37 years. We estimated that between 7,500 and 44,100 deaths are attributable to the A/H1N1 pandemic virus in the US during May-December 2009, and that between 334,000 and 1,973,000 years of life were lost. The range of years of life lost estimates includes in its lower part the impact of a typical influenza epidemic dominated by the more virulent A/H3N2 subtype, and the impact of the 1968 pandemic in its upper bound. We conclude that the 2009 A/H1N1 pandemic virus had a substantial health burden in the US over the first few months of circulation in terms of years of life lost, justifying the efforts to protect the population with vaccination programs. Analysis of historic records from three other pandemics over the last century suggests that the emerging pandemic virus will continue to circulate and cause excess mortality in unusually young populations for the next few years. Continuing surveillance for indicators of increased mortality is of key importance, as pandemics do not always cause the majority of associated deaths in the first season of circulation.
Langmuir, A. D.(Department of Preventive and Social Medicine, Harvard and Medical School, 25 Shattuck Street, Boston, Massachusetts 02115, USA). William Far: founder of modern concepts of surveillance. International Journal of Epidemiology 1976. 5: 13–18.
Considerable confusion surrounds the use of the term surveillance in the context of public health but the principles underlying all uses are as old as epidemiology itself. William Farr has contributed more than anyone else to the development of these principles and to the demonstration of their value in practice on a large scale. This paper re-examines the basic tenets which guided him and the methods and techniques which he developed in the hope of reviving insights and resetting standards that modern epidemiologists might, with benefit, strive to emulate.
Airborne virus particles of vaccinia, influenza, Venezuelan equine encephalomyelitis, and poliomyelitis have been tested for viable survival in the dark at controlled temperatures and relative humidity (R.H.) for up to 23 hr. after spraying.
Viable survival at each R.H. level was better at lower temperature than at higher temperature. Poliomyelitis virus showed best survival at high R.H.; the other three viruses survived best at low R.H.
Dominance hierarchies occur in numerous social species, and rank within them can greatly influence the quality of life of an animal. In this review, I consider how rank can also influence physiology and health. I first consider whether it is high- or low-ranking animals that are most stressed in a dominance hierarchy; this turns out to vary as a function of the social organization in different species and populations. I then review how the stressful characteristics of social rank have adverse adrenocortical, cardiovascular, reproductive, immunological, and neurobiological consequences. Finally, I consider how these findings apply to the human realm of health, disease, and socioeconomic status.
There are important gaps in our current understanding of the influenza virus behavior. In particular, it remains unclear why some inter-pandemic seasons are associated with unusually high mortality impact, sometimes comparable to that of pandemics. Here we compare the epidemiological patterns of the unusually deadly 1951 influenza epidemic (A/H1N1) in England and Wales and Canada with those of surrounding epidemic and pandemic seasons, in terms of overall mortality impact and transmissibility. Based on the statistical and mathematical analysis of vital statistics and morbidity epidemic curves in these two countries, we show that the 1951 epidemic was associated with both higher mortality impact and higher transmissibility than the 1957 and 1968 pandemics. Surprisingly in Liverpool, considered the 'epicenter' of the severe 1951 epidemic, the mortality impact and transmissibility even surpassed the 1918 pandemic.
The 'massacre' of Italy's elderly nursing home residents: Covid-19 patients in Italy's virus epicentre of Lombardy were transferred to nursing homes by an official resolution with catastrophic consequences
• "The 'massacre' of Italy's elderly nursing home residents: Covid-19 patients in Italy's
virus epicentre of Lombardy were transferred to nursing homes by an official resolution
with catastrophic consequences", by Maria Tavernini and Alessandro Di Rienzo, TRT
World, 20 April 2020.
CDC: 80,000 people died of flu last winter in U.S., highest death toll in 40 years
• "CDC: 80,000 people died of flu last winter in U.S., highest death toll in 40 years", by
Associated Press, STAT News, 26 September 2018.
Rethinking the Virus Species Concept
- Egor Alimpiev
Alimpiev, Egor (2019) "Rethinking the Virus Species Concept", dated 15 March 2019, posted to
stanford.edu
http://stanford.edu/~alimpiev/thnk_ppr.pdf
COVID-19 Antibody Seroprevalence
- Bendavid
Bendavid et al. (2020) "COVID-19 Antibody Seroprevalence in Santa Clara County, California",
medRxiv 2020.04.14.20062463; doi: https://doi.org/10.1101/2020.04.14.20062463
Charter 1a -Epidemiology: Epidemic theory (effective & basic reproduction numbers, epidemic thresholds) & techniques for analysis of infectious disease data (construction & use of epidemic curves, generation numbers, exceptional reporting & identification of significant clusters)
- Healthknowlege-Uk
HealthKnowlege-UK (2020) "Charter 1a -Epidemiology: Epidemic theory (effective & basic
reproduction numbers, epidemic thresholds) & techniques for analysis of infectious disease
data (construction & use of epidemic curves, generation numbers, exceptional reporting &
identification of significant clusters)", HealthKnowledge.org.uk, accessed on 2020-04-10.
https://www.healthknowledge.org.uk/public-health-textbook/research-methods/1a-epidemiology/epidemic-theory
The impact of influenza epidemics on mortality: introducing a severity index
- L Simonsen
Simonsen, L. et al. (1997) "The impact of influenza epidemics on mortality: introducing a
severity index", Am J Public Health. 87(12):1944-1950. doi:10.2105/ajph.87.12.1944
https://pubmed.ncbi.nlm.nih.gov/9431281/
Concentrations and size distributions of airborne influenza A viruses measured indoors at a health centre, a day-care centre and on aeroplanes
- W Yang
Yang, W. et al. (2011) "Concentrations and size distributions of airborne influenza A viruses
measured indoors at a health centre, a day-care centre and on aeroplanes", Journal of the Royal
Society, Interface. 2011 Aug;8(61):1176-1184. DOI: 10.1098/rsif.2010.0686.
https://royalsocietypublishing.org/doi/10.1098/rsif.2010.0686