BackgroundGlobal HIV-1 genetic diversity and evolution form a major challenge to treatment and prevention efforts. An increasing number of distinct HIV-1 recombinants have been identifiedworldwide, but their contribution to the global epidemic is unknown. We aimed to estimate the global and regional distribution of HIV-1 recombinant forms during 1990-2015. MethodsWe assembled a global HIV-1 molecular epidemiology database through a systematic literature review and a global survey. We searched PubMed, EMBASE (Ovid), CINAHL (Ebscohost), and Global Health (Ovid) for HIV-1 subtyping studies published from Jan 1, 1990, to Dec 31, 2015. Unpublished original HIV-1 subtyping data was collected through a survey among experts in the field who were members of the WHO-UNAIDS Network for HIV Isolation and Characterisation. We included prevalence studies with HIV-1 subtyping data collected during 1990-2015. Countries were grouped into 14 regions and analyses conducted for four time periods (1990-99, 2000-04, 2005-09 and 2010-15). The distribution of circulating recombinant forms (CRFs), and unique recombinant forms (URFs) in individual countries was weighted according to the UNAIDS estimates of the number of people living with HIV in each country to generate regional and global estimates of numbers and proportions of HIV-1 recombinants in each time period. The systematic review is registered with PROSPERO, number CRD42017067164.

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Rabies virus (RABV), the causative agent for rabies disease is still presenting a major public health concern causing approximately 60,000 deaths annually. This neurotropic virus (genus Lyssavirus, family Rhabdoviridae) induces an acute and almost always fatal form of encephalomyelitis in humans. Despite the lethal consequences associated with clinical symptoms of rabies, RABV limits neuro-inflammation without causing major histopathological lesions in humans. Nevertheless, information about the mechanisms of infection and cellular response in the central nervous system (CNS) remain scarce. Here, we investigated the expression of inflammatory genes involved in immune response to RABV (dog-adapted strain Tha) in mice, the most common animal model used to study rabies. To better elucidate the pathophysiological mechanisms during natural RABV infection, we compared the inflammatory transcriptome profile observed at the late stage of infection in the mouse brain (cortex and brain stem/cerebellum) with the ortholog gene expression in post-mortem brain biopsies of rabid patients. Our data indicate that the inflammatory response associated with rabies is more pronounced in the murine brain compared to the human brain. In contrast to murine transcription profiles, we identified CXC motif chemokine ligand 16 (CXCL16) as the only significant differentially expressed gene in post-mortem brains of rabid patients. This result was confirmed in vitro, in which Tha suppressed interferon alpha (IFN-α)-induced CXCL16 expression in human CNS cell lines but induced CXCL16 expression in IFN-α-stimulated murine astrocytes. We hypothesize that RABV-induced modulation of the CXCL16 pathway in the brain possibly affects neurotransmission, natural killer (NK) and T cell recruitment and activation. Overall, we show species-specific differences in the inflammatory response of the brain, highlighted the importance of understanding the potential limitations of extrapolating data from animal models to humans.

Les hantavirus sont des virus appartenant à la famille des Bunyaviridae. Vingt-trois espèces sont officiellement rapportées mais plus de 70 taxons sont en attente de classification. Chaque taxon a pour réservoir une espèce de rongeurs ou d'insectivores (Ordre Soricomorpha). Des séquences de nouveaux hantavirus ont été très récemment détectées chez des chauves-souris. Certains des hantavirus associés aux rongeurs sont zoonotiques La transmission s'effectue généralement par l'inhalation d'aérosols d'excrétats ou de sécrétions de rongeurs contaminés. Ces virus sont alors responsables d'une fièvre hémorragique avec syndrome rénal (FHSR) ou d'un syndrome cardio pulmonaire (SCP). Le traitement de ces maladies est symptomatique. Trois de ces virus zoonotiques ont été détectés en France métro-politaine. Le virus Puumala, associé au rongeur Myodes glareolus, a la plus grande importance médi-cale. Environ un millier de cas de FHSR ont été détectés au cours des dix dernières années, dans le quart Nord-Est de la France qui est la zone d'endémie. Des épidémies sont observées tous les deux à trois ans avec un pic survenant généralement à la fin du printemps. Les adultes et particulièrement les hommes sont les plus atteints. La manipulation du bois, l'ouverture et le nettoyage de local non utilisé, les activités en forêt sont des occupations favorisant l'exposition. Le virus Seoul a été détecté chez Rattus norvegicus à Lyon. Des cas humains étaient suspectés mais la preuve virologique d'un premier cas de FHSR due à ce virus n'a été faite qu'en 2012. Le virus Tula a été détecté chez son hôte Microtus arvalis dans le Jura. Aucun cas humain n'a pour le moment été observé. Enfin, le virus Maripa a été décrit pour la première fois en Guyane française. Il a été responsable de trois cas de SCP dont deux mortels. Trente ans après la détection des premiers cas humains d'infection par un hantavirus en France, il reste encore beaucoup à découvrir sur la circulation de ces virus dans le pays.

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Hepatitis B virus (HBV) surface antigen (HBsAg) decay was explored in HIV-1-and HBV-coinfected patients beginning antiretroviral (ARV) therapy containing tenofovir disoproxil fumarate (TDF). The mean HBsAg decay was 0.38 log 10 IU/ml/year (95% confidence interval [CI], 0.71 to 0.05) in 18 patients with sustained plasma HIV-1 RNA suppression and 0.15 log 10 IU/ml/year (0.21 to 0.09) in 12 patients experiencing HIV-1 virologic failure due to suboptimal adherence to ARV (P ‫؍‬ 0.17). We estimated that six of these 18 patients will attain HBsAg values below 10 IU/ml after 10 years of treatment. Hepatitis B virus (HBV) suppression maintained by treatment with lamivudine (3TC), emtricitabine (FTC), and tenofovir disoproxil fumarate (TDF) reduces the progression of disease to liver failure and the development of hepatocellular carcinoma in HIV-1-infected patients. In some patients, therapy induces a complete loss of HBV surface antigen (HBsAg), indicating control of chronic HBV infection. HBsAg clearance was observed in 3% of HBV envelope antigen (HBeAg)-positive patients uninfected by HIV-1 after 1 year of treatment with 3TC (6), in 8% of HBeAgpositive patients after 3 years of treatment with TDF (5), and in 5% of HBeAg-negative patients after 5 years of treatment with adefovir (4). We conducted a longitudinal analysis of HBsAg concentration in HIV-1-and HBV-coinfected patients to explore the long-term evolution of HBsAg concentration after initiation of antiretroviral therapy (ART) containing TDF. The impact of imperfect adherence to ART on HBsAg decay was also explored.Ethical approval for this study was given by the local ethics committee (Comité de Protection des Personnes Sud Méditer-ranée IV), under the reference Q2011.12.01. Thirty HIV-1/HBVcoinfected subjects monitored in the Montpellier University Teaching Hospital were tested for HBsAg concentration after providing written informed consent. Patients had chronic hepatitis B infection, defined as detectable serum HBsAg for more than 6 months. TDF was initiated as a part of an ARV therapy regimen containing 3TC or FTC and a nonnucleoside reverse transcriptase inhibitor (11 of 30) or protease inhibitors (19 of 30). A mean (standard deviation [SD]) of 8 (Ϯ4) samples were quantified for HBsAg concentration per individual during a mean (SD) follow-up under ART of 6.5 years (Ϯ3).To address the potential impact of suboptimal adherence to ART on HBsAg clearance, we included in the group with suboptimal compliance with therapy 12 subjects that experienced HIV-1 RNA rebound exceeding 3 months during the follow-up and identified regular missed doses during interviews. Subjects who had detectable HIV-1 plasma RNA loads 9 months after initiation of ART were also included in this group. The other 18 individuals were categorized as being optimally treated. At the time of therapeutic initiation, the mean age was 40 years (Ϯ9); CD4 T cell count was 387/mm 3 (Ϯ100); the median (interquartile range[IQR]) HIV-1 RNA level was 4.48 (3.69 to 5.21) log 10 copies/ml, HBV DNA 5.62 (4.9...

We aimed to estimate the seroprevalence of Puumala orthohantavirus (PUUV) among forestry workers in northern France, and to explore sociodemographic risk factors. We conducted a random cross-sectional seroprevalence survey among 1777 forestry workers in 2019–2020. The presence of immunoglobulin G against PUUV antigens in serum was assessed using enzyme-linked immunosorbent assay and confirmed using immunofluorescence assay. Poisson regression models were used to explore factors associated with seropositivity. Weighted seroprevalence was 5% (3–6) in northeastern France, 4% (2–6) in north central France, and 1% in two regions located in the center of the country (Auvergne and Limousin). There were no seropositive workers detected in northwestern France. Seropositivity was associated with age, sex, and cumulative seniority in the forestry sector. Seroprevalence was highest in known endemic areas of the northeast and lowest in the northwest. Nevertheless, we found serological evidence of PUUV infection in two regions located in the center of the country, suggesting circulation of the virus in these regions, previously thought to be non-endemic.

Acute kidney injury (AKI) caused by hantavirus infections is rare but should be suspected in any patient presenting with flu-like symptoms, signs of haemolytic–uraemic syndrome or presence of anti-glomerular basement membrane (anti-GBM) antibodies. We report the first case of Dobrava–Belgrade virus in France imported from southeastern Europe. The characteristic macroscopic appearance of the fresh renal biopsy specimen, displaying a haemorrhagic appearance of the medulla, suggested hantavirus infection. AKI caused by hantavirus infections remains a diagnostic challenge, especially outside endemic areas.