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On both sides of the Atlantic, in Anglo-Saxon countries, the issue of excess mortality due to Covid-19 among members of minorities has emerged as a central social justice issue. Outside the Anglo-Saxon countries, where race and ethnicity are generally recorded, it is difficult to address this issue. However, in France, data for the period up to the end of confinement, mentioning country of birth and place of death, from "état-civil" files, allow comparisons to be made on the determinants of the severity of Covid-19 integrating ethnicity. Regression analyses based on the difference in death counts between the spring of 2020 and the same period of previous years, show that the interweaving of health status, household size and ethnicity accurately reflects the disparities between departmental mortality rates due to Covid-19. People born in Black Africa clearly appear to be in a worse position than those born in the Maghreb, in Asian and European countries, not to mention the natives, in terms of risk of death.

The European response to COVID-19 has revealed an inconvenient truth. Despite having integrated public health concerns across all its policies – be it agriculture, consumer protection, or security –, the Union cannot directly act to save people’s lives. Only member states can do so. Yet when they adopted unilateral measures to counter the spread of the virus, those proved not only ineffective but also disruptive on vital supply chains, by ultimately preventing the flow of essential goods and people across the Union. These fragmented efforts in tackling cross-border health threats have almost immediately prompted political calls for the urgent creation of a European Health Union. Yet this call raises more questions than answers. With the aim to offer a rigorous and timely blueprint to decision-makers and the public at large, this Special Issue of the European Journal of Risk Regulation contextualizes such a new political project within the broader constitutional and institutional framework of EU public health law and policy. By introducing the Special, this paper argues that unless the envisaged Health Union will tackle the root causes of what prevented the Union from effectively responding to COVID-19 – the divergent health capacity across the Union –, it might fall short of its declared objective of strengthening the EU’resilience for cross-border health threats.

SARS-CoV-2 outbreak is the first pandemic of the century. SARS-CoV-2 infection is transmitted through droplets; other transmission routes are hypothesized but not confirmed. So far, it is unclear whether and how SARS-CoV-2 can be transmitted from the mother to the fetus. We demonstrate the transplacental transmission of SARS-CoV-2 in a neonate born to a mother infected in the last trimester and presenting with neurological compromise. The transmission is confirmed by comprehensive virological and pathological investigations. In detail, SARS-CoV-2 causes: (1) maternal viremia, (2) placental infection demonstrated by immunohistochemistry and very high viral load; placental inflammation, as shown by histological examination and immunohistochemistry, and (3) neonatal viremia following placental infection. The neonate is studied clinically, through imaging, and followed up. The neonate presented with neurological manifestations, similar to those described in adult patients. Congenital infection of SARS-CoV-2 has been described, but the transmission routes remain unclear. Here, the authors report evidence of transplacental transmission of SARS-CoV-2 in a neonate born to a mother infected in the last trimester and presenting with neurological compromise.

The first case of coronavirus disease 2019 (COVID-19) in Algeria was reported on 25 February 2020. Since then, it has progressed rapidly and the number of cases grow exponentially each day. In this article, we utilize SEIR modelling to forecast COVID-19 outbreak in Algeria under two scenarios by using the real-time data from March 01 to April 10, 2020. In the first scenario: no control measures are put into place, we estimate that the basic reproduction number for the epidemic in Algeria is 2.1, the number of new cases in Algeria will peak from around late May to early June and up to 82% of the Algerian population will likely contract the coronavirus. In the second scenario, at a certain date T, drastic control measures are taken, people are being advised to self-isolate or to quarantine and will be able to leave their homes only if necessary. We use SEIR model with fast change between fully protected and risky states. We prove that the final size of the epidemic depends strongly on the cumulative number of cases at the date when we implement intervention and on the fraction of the population in confinement. Our analysis shows that the longer we wait, the worse the situation will be and this very quickly produces.

AbstractBluetongue virus (BTV) is an arbovirus transmitted by blood-feeding midges to a wide range of wild and domestic ruminants. In this report, we showed that BTV, through its virulence non-structural protein NS3 (BTV-NS3), is able to activate the MAPK/ERK pathway. In response to growth factors, the MAPK/ERK pathway activates cell survival, differentiation, proliferation and protein translation but can also lead to the production of several inflammatory cytokines. By combining immunoprecipitation of BTV-NS3 and mass spectrometry analysis from both BTV-infected and NS3-transfected cells, we identified the serine/threonine-protein kinase B-Raf (BRAF), a crucial player of the MAPK/ERK pathway, as a new cellular interactor of BTV-NS3. BRAF silencing led to a significant decrease of the MAPK/ERK activation by BTV supporting a model where BTV-NS3 interacts with BRAF to activate this signaling cascade. Furthermore, the intrinsic ability of BTV-NS3 to bind BRAF and activate the MAPK/ERK pathway is conserved throughout multiple serotypes/strains but appears to be specific to BTV compared to other members ofOrbivirusgenus. Inhibition of MAPK/ERK pathway with U0126 reduced viral titers, suggesting that BTV manipulates this pathway for its own replication. Therefore, the activation of the MAPK/ERK pathway by BTV-NS3 could benefit to BTV replication by promoting its own viral protein synthesis but could also explain the deleterious inflammation associated with tissue damages as already observed in severe cases of BT disease. Altogether, our data provide molecular mechanisms to explain the role of BTV-NS3 as a virulence factor and determinant of pathogenesis.ImportanceBluetongue Virus (BTV) is responsible of the non-contagious arthropod-borne disease Bluetongue (BT) transmitted to ruminants by blood-feeding midges. Despite the fact that BTV has been extensively studied, we still have little understanding of the molecular determinants of BTV virulence. In this report, we found that the virulence protein NS3 interacts with BRAF, a key component of the MAPK/ERK pathway. In response to growth factors, this pathway promotes cell survival, increases protein translation but also contributes to the production of inflammatory cytokines. We showed that BTV-NS3 enhances the MAPK/ERK pathway and this activation is BRAF-dependent. Our results demonstrate, at the molecular level, how a single virulence factor has evolved to target a cellular function to ensure its viral replication. On the other hand, our findings could also explain the deleterious inflammation associated with tissue damages as already observed in severe cases of BT disease.

The model descibes the epidemic dynamics of Covid-19 in a population after vaccination. Using the maximum principale, our goal is to prove the existence of an optimal strategy such that it minimize the number of infected people after vaccination. Finally, some numerical results are provided.

Mortality inequalities remain substantial in many countries, and large shocks such as pandemics could amplify them further. The unequal distribution of COVID-19 confirmed cases suggests that this is the case. Yet, evidence on the causal effect of the epidemic on mortality inequalities remains scarce. In this paper, we exploit exhaustive municipality-level data in France, one of the most severely hit country in the world, to identify a negative relationship between income and excess mortality within urban areas, that persists over COVID-19 waves. Over the year 2020, the poorest municipalities experienced a 30% higher increase in excess mortality. Our analyses can rule out an independent contribution of lockdown policies to this heterogeneous impact. Finally, we find evidence that both labour-market exposure and housing conditions are major determinants of the epidemic-induced effects of COVID-19 on mortality inequalities, but that their respective role depends on the state of the epidemic.

Little is known about the general equilibrium impact COVID-19 induces on different gender groups. This paper addresses the problem of relatively few general equilibrium studies focusing on gender impacts of COVID-19. The analysis uses a gendered Computable General Equilibrium model linked to a microsimulation model that analyses a mild and severe scenario of the pandemic on economic and distributional outcomes for females. Irrespective of scenario, findings show that because women employment tend to have unskilled labour which is more concentrated in sectors that are hurt the most by COVID-19 response measures, they suffer disproportionately more from higher unemployment than their male counterparts. The poverty outcomes show worsened vulnerability for female-headed households given that, even prior to the pandemic, poverty was already higher amongst women. These simulated results are consistent with recently observed impacts and address research gaps important for well-designed public policies to reverse these trends.On connait peu les impacts d’équilibre général induits par la Covid-19 sur les groupes de genre différents. Cette étude adresse le problème de la pénurie d’études en équilibre général s’intéressant aux impacts de la COVID-19 sur le genre. L’analyse te combine un modèle d’équilibre général calculable sexo-spécifique avec un modèle de micro-simulation et évalue deux scenarios de la pandémie, l’un modéré et l’autre sévère, et leurs effets sur les résultats économiques et distributionnels des femmes. Quel que soit le scenario, les résultats démontrent que les femmes souffrent du chômage d’une manière disproportionée comparé aux hommes, puisque le travail des femmes tend à être du travail non qualifié, concentré dans les secteurs qui sont les plus frappés par les mesures de réponse à la COVID-19. En termes de pauvreté, les foyers dirigés par des femmes sont plus vulnérables, étant donné que même avant la pandémie, la pauvreté était déjà plus élevée chez les femmes. Les résultats simulés par cette étude concordent avec les impacts récemment observés, et abordent les lacunes de recherche nécessaires pour modéliser des politiques publiques bien conçues afin de renverser ces tendances.

Even though much has been learned about the new pathogen SARS-CoV-2 since the beginning of the COVID-19 pandemic, a lot of uncertainty remains. In this paper we argue that what is important to know under uncertainty is whether harm accelerates and whether health policies achieve deceleration of harm. For this, we need to see cases in relation to diagnostic effort and not to look at indicators based on cases only, such as a number of widely used epidemiological indicators, including the reproduction number, do. To do so overlooks a crucial dimension, namely the fact that the best we can know about cases will depend on some welldefined strategy of diagnostic effort, such as testing in the case of COVID-19. We will present a newly developed indicator to observe harm, the acceleration index, which is essentially an elasticity of cases in relation to tests. We will discuss what efficiency of testing means and propose that the corresponding health policy goal should be to find ever fewer cases with an ever-greater diagnostic effort. Easy and low-threshold testing will also be a means to give back people’s sovereignty to lead their life in an “open” as opposed to “locked-down” society.

ABSTRACTClinical manifestations of COVID-19 caused by the novel coronavirus SARS-CoV-2 are associated with age. While children are largely spared from severe respiratory disease, they can present with a SARS-CoV-2-associated multisystem inflammatory syndrome (MIS-C) similar to Kawasaki’s disease. Here, we show distinct antibody (Ab) responses in children with MIS-C compared to adults with severe COVID-19 causing acute respiratory distress syndrome (ARDS), and those who recovered from mild disease. There was a reduced breadth and specificity of anti-SARS-CoV-2-specific antibodies in MIS-C patients compared to the COVID patient groups; MIS-C predominantly generated IgG Abs specific for the Spike (S) protein but not for the nucleocapsid (N) protein, while the COVID-19 cohorts had anti-S IgG, IgM and IgA Abs, as well as anti-N IgG Abs. Moreover, MIS-C patients had reduced neutralizing activity compared to both COVID-19 cohorts, indicating a reduced protective serological response. These results suggest a distinct infection course and immune response in children and adults who develop severe disease, with implications for optimizing treatments based on symptom and age.