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The French Armed Forces Biomedical Research Institute (IRBA) deeply involved in research on SARS-COV-2, participated in the creation of the Obépine sentinel network in charge of detecting, qualifying and quantifying the virus genome in wastewater in France. During this pandemic, wastewater-based epidemiology has proven to be a first class public health tool for assessing viral dynamics in populations and environment. Obépine has also conducted research demonstrating the low infectivity of faeces and wastewater and allowed for early detection of epidemic waves linked to new variants. The IRBA has adapted this powerful tool to the monitoring of viral infections on board the aircraft carrier Charles-de-Gaulle in order to get an operational system for anticipation after the first local outbreak in 2020. The presence of this surveillance and anticipation tool has allowed a better management of SARS-CoV-2 contingent introductions on board during stopovers or crewmembers entries. The combination of a mandatory vaccination protocol and the surveillance of viral circulation in black waters has made it possible to identify and locate cases, and thus to continue the operational mission in the COVID-19 environment while limiting the spread and preserving the health of the crew. This innovative tool can easily be redirected to the search for any other pathogens in blackwater or even, in the long term, to ensure health surveillance of any military establishment, at sea or on land, in France or on overseas bases., (© 2022 l'Académie nationale de médecine. Published by Elsevier Masson SAS. All rights reserved.)

The existence of infectious agents smaller than bacteria was demonstrated already near the close of the 19th century by Martinus Beijerinck. After this discovery it took more than 60 years before a resilient definition of viruses could be given and an introduction to modern virology was established. Indeed, the major challenge was to conceive living submicrospic agents exclusively defined in opposition to the bacteriological criteria (non-observable, non-cultivable,). Progresses in biochemistry, electron microscopy, and in control of cell culture techniques have led to the conviction that the viruses were infectious agents entirely original. These last 20 years unrevealed molecular biology as a tool of choice for the discovery of new viral agents and analysis of pathologies of viral etiology., (Copyright © 2009 Elsevier Masson SAS. All rights reserved.)

HMGB1 (High Mobility group box 1) protein was originally identified as a DNA-binding protein that functions as a structural co-factor. Recent works demonstrated that HMGB1 can be released outside the cell, upon immune activation or primary cell necrosis. In the extracellular space, HMGB1 acts as a potent soluble factor that coordinates cellular events that are crucial for the amplification of inflammation, establishment of early immune responses and tissue repair. However, extracellular HMGB1 also acts as a potent pro-inflammatory cytokine that contributes to the pathogenesis of diverse inflammatory and infectious disorders., (Copyright © 2009 Elsevier Masson SAS. All rights reserved.)

In the 20th century dengue fever became one of the leading causes of morbidity and mortality throughout the tropics. The dengue virus is an arbovirus transmitted by Aedes mosquitoes. There are four distinct serotypes of dengue arbovirus (DENV-1, 2, 3, 4). According to the World Health Organization, a person infected by one of the dengue viruses can develop symptoms ranging from the classical self-limiting form characterized by high temperature, headache, myalgia, and arthralgia to the severe, potentially fatal, form known as dengue shock syndrome. For over 40 years the main explanation for the pathogenesis of dengue has been based on the "antibody-dependent enhancement" (ADE) concept stating that enhancing antibodies acquired during a primary infection increase the number of infected cells, and thus the level of viremia, during secondary infection. However the severity of dengue is not limited to dengue shock syndrome and there are many cases that do not conform to the ADE concept. A meta-analysis could provide crucial information for resolving this controversy and open the way for development of a monovalent vaccine against the dengue virus as for the closely related yellow fever virus.

Background: We conducted a prospective study to determine the prevalence of activated protein C resistance and anticardiolipin antibodies in leg ulcers, whatever venous, arterial or arteriovenous., Patients and Methods: One hundred fifteen patients hospitalized for leg ulcers, without antiphospholipid syndrome were included. The vascular abnormalities were studied by clinical examination, Doppler, duplex Doppler and, when required, arteriography. Activated protein C resistance was isolated by a "classic" test (normalized APTT ratio in PCa presence or absence) and by a "second generation test" (by preliminary dilution with deficient factor V plasma). All patients with abnormal results on the second test were screened for the factor V Leiden (by PCR amplication with use of restriction enzymes). Anticardiolipin antibodies were investigated with an ELISA method with Harris standards as reference, in which the positive threshold was established at 20 units., Results: Among these 115 patients, 50 venous (43.5 p. 100), 23 arterial (20 p. 100), 42 arteriovenous (36.5 p. 100) leg ulcers were identified. Activated protein C resistance was isolated in 12 cases (10.4 p. 100) (heterozygous carriers): 7 venous ulcers, 3 arteriovenous, 2 arterial. Anticardiolipin antibodies were measured at significant level in 49 cases (42.6 p. 100): 21 venous ulcers, 18 arteriovenous, 10 arterial., Discussion: In this study, there was no statistical difference between the activated protein C resistance prevalence in leg ulcers when compared with Lorraine population (p=0.27). Factor V Leiden or anticardiolipin antibodies abnormalities were isolated in 56 cases (48.7 p. 100) without statistical difference between the 3 types of ulcers. Finally, the pathophysiology of venous, arterial and arteriovenous leg ulcers remains complex, suggesting several coagulation perturbations.

The mdm2 cellular protooncogene is involved in many human tumors where it has been shown to be overexpressed, including sarcomas, osteosarcomas, gliomas and others. The Mdm2 protein is believed to be oncogenic by binding and inactivating the p53 and Rb tumor suppressor gene products and by activating the E2F-1/DP-1 transcription factors, thus promoting the G1 to S phase transition. The mdm2 gene is activated transcriptionally by p53, thus forming an autoregulatory negative feedback loop. This feedback loop is important in normal cells and when cells are exposed to various genotoxic agents. By activating its own negative regulator, p53 would signal the cells to resume proliferation after a p53-mediated G1 arrest in response to DNA damage. The review aims to detail the functions of Mdm2 in normal and tumor cells. We also discuss several recent data suggesting that Mdm2 may exhibit activities unrelated to its well known function as a negative regulator of p53 activities.

Epstein-Barr Virus (EBV) is the prototype member of the human herpesvirus subfamily Gammaherpesviridae. EBV establishes a latent infection in lymphoïd cell and replicates in epithelial cells. Infection of individuals with EBV is widespread in all human populations, as shown by the high proportion of individual with specific antibodies in their serum. EBV is the etiological agent of the infectious mononucleosis and has been implicated in the pathogenesis of an increasing number of human malignancies, the best characterized being endemic Burkitt's lymphomas, nasopharyngeal carcinomas (NPC), and polyclonal lymphomas in immunocompromised patients. EBV infection in vivo is a complex mixture of latent, reactivated, transforming, or replicative type of infection. EBV infection is characterized by sporadic viral excretion in the oropharynx and persistent latent infection in the bone marrow and peripheral blood lymphocytes. EBV infection includes an intense immune response. During primary infection, the humoral response is primarily directed toward antigens of the lytic cycle, membrane antigen complex, early antigen (EA), viral capsid antigen (VCA) while the antibodies response to EBNAs is delayed. The cell mediated response controls the proliferation of EBV-infected lymphocytes through two classes of cytotoxic cells, namely, natural killer and T8 cytotoxic cells. Laboratory diagnosis of EBV infection is recently based upon molecular biology techniques which provides a useful tool for direct identification of EBV and may allow to better understand the role of the virus in the pathogenesis of EBV associated disorders.