Swedish Institute

About: Swedish Institute is a government organization based out in Stockholm, Sweden. It is known for research contribution in the topics: Population & Health care. The organization has 1657 authors who have published 2301 publications receiving 103682 citations. The organization is also known as: Svenska Institutet.

Waterborne norovirus outbreak in a municipal drinking-water supply in Sweden

Abstract: During Easter 2009, almost 200 people resident in a small Swedish village fell ill with gastrointestinal symptoms. We conducted a retrospective cohort study and a molecular investigation in order to identify the source of the outbreak. Residents living in households connected to the public water network were at an increased risk of developing disease (relative risk 4·80, 95% confidence interval 1·68-13·73) compared to those with no connection to the public network. Norovirus genotype GI.3 was identified in stool samples from six patients and in a sample from the public water network. Contamination of one of the wells supplying the public water network was thought to be the source of the outbreak. This is a description of a norovirus outbreak linked to a municipal drinking-water supply in Sweden. Information from epidemiological and molecular investigations is of utmost importance to guide outbreak control measures and to prevent future outbreaks.

Occurrence of thin membranes in the structure of wool.

Abstract: WOOL keratin is considered to be completely soluble in sodium sulphide. 30 ml. of 0·3 M sodium sulphide was added to 1 gm. carefully purified, wool, and this mixture was allowed to stand for about a month. After this time a light green solution was obtained, but the solution showed a slight opalescence. The particles causing this opalescence (estimated to be not more than 0·1 per cent of the Wool) could be separated from the solution by centrifuging. After separating and washing with water, the solid matter was examined under the electron microscope. The specimen was mounted on collodion and observed directly. The solids proved to consist mainly of thin membranes, mostly rolled or folded, as is seen in Fig. 1. In order to determine the thickness of the membrane itself a collodion replica was made and gold-shadowed at a declination of 1 : 10. Fig. 2. shows how the thin membranes are rolled and the rolls flattened, probably by the surface tension during the drying. From the length of the shadows the thickness is calculated to be something between 50 and 100 A. Fig. 3. is a shadow-cast replica, where part of the wool membrane has stuck to the collodion. In part it shows both the membrane and the corresponding impression and is in that way interesting purely from the electron-micrograph point of view.

Cross-Protection against Challenge with Puumala Virus after Immunization with Nucleocapsid Proteins from Different Hantaviruses

Abstract: Hantaviruses are rodent-borne agents that cause hemorrhagic fever with renal syndrome or hantavirus pulmonary syndrome in humans. The nucleocapsid protein (N) is relatively conserved among hantaviruses and highly immunogenic in both laboratory animals and humans, and it has been shown to induce efficient protective immunity in animal models. To investigate the ability of recombinant N (rN) from different hantaviruses to elicit cross-protection, we immunized bank voles with rN from Puumala (PUUV), Topografov (TOPV), Andes (ANDV), and Dobrava (DOBV) viruses and subsequently challenged them with PUUV. All animals immunized with PUUV and TOPV rN were completely protected. In the group immunized with DOBV rN, 7 of 10 animals were protected, while only 3 of 8 animals were protected in the group immunized with ANDV rN, which is more closely related to PUUV rN than DOBV rN. Humoral and cellular immune responses after rN immunization were also investigated. The highest cross-reactive humoral responses against PUUV antigen were detected in sera from ANDV rN-immunized animals, followed by those from TOPV rN-immunized animals, and only very low antibody cross-reactivity was observed in sera from DOBV rN-immunized animals. In proliferation assays, T lymphocytes from animals immunized with all heterologous rNs were as efficiently recalled in vitro by PUUV rN as were T lymphocytes from animals immunized with homologous protein. In summary, this study has shown that hantavirus N can elicit cross-protective immune responses against PUUV, and the results suggest a more important role for the cellular arm of the immune response than for the humoral arm in cross-protection elicited by rN. Viruses belonging to the genus Hantavirus, family Bunyaviridae, are a diverse group of rodent-borne viruses that cause hemorrhagic fever with renal syndrome (HFRS) or hantavirus pulmonary syndrome (HPS) in humans (17). Hantaviruses are present worldwide, but the majority of the approximately 200,000 HFRS cases that are reported annually occur in Asia, where the prototype hantavirus, Hantaan virus (HTNV) causes a severe form of the disease. Seoul virus (SEOV) causes a moderate form of HFRS, mainly in Asia. In Europe, HFRS is caused by Dobrava (DOBV) and Puumala (PUUV) viruses (reviewed in reference 31). The latter is associated with a milder form of HFRS, nephropathia epidemica. In addition, the DOBV-like Saaremaa virus, representing a unique hantavirus serotype, has recently been shown to cause HFRS in Europe (3, 5, 35; A. Lundkvist, unpublished data). HPS is caused by several viruses in the Americas, with Sin Nombre virus and Andes virus (ANDV) being the most well known in North and South America, respectively. Topografov virus (TOPV) was discovered in Siberia but has not yet been associated with any disease (39). Hantaviruses are associated with specific rodent species, which act as hosts for the virus and in

Migratory Activation of Primary Cortical Microglia upon Infection with Toxoplasma gondii

Abstract: Disseminated toxoplasmosis in the central nervous system (CNS) is often accompanied by a lethal outcome. Studies with murine models of infection have focused on the role of systemic immunity in control of toxoplasmic encephalitis, while knowledge remains limited on the contributions of resident cells with immune functions in the CNS. In this study, the role of glial cells was addressed in the setting of recrudescent Toxoplasma infection in mice. Activated astrocytes and microglia were observed in the close vicinity of foci with replicating parasites in situ in the brain parenchyma. Toxoplasma gondii tachyzoites were allowed to infect primary microglia and astrocytes in vitro. Microglia were permissive to parasite replication, and infected microglia readily transmigrated across transwell membranes and cell monolayers. Thus, infected microglia, but not astrocytes, exhibited a hypermotility phenotype reminiscent of that recently described for infected dendritic cells. In contrast to gamma interferon-activated microglia, Toxoplasma-infected microglia did not upregulate major histocompatibility complex (MHC) class II molecules and the costimulatory molecule CD86. Yet Toxoplasma-infected microglia and astrocytes exhibited increased sensitivity to T cell-mediated killing, leading to rapid parasite transfer to effector T cells in vitro. We hypothesize that glial cells and T cells, besides their role in triggering antiparasite immunity, may also act as “Trojan horses,” paradoxically facilitating dissemination of Toxoplasma within the CNS. To our knowledge, this constitutes the first report of migratory activation of a resident CNS cell by an intracellular parasite.