Background Eating disorders (EDs) lead to multiple psychiatric and somatic complications and thus constitute a major public health concern. Objectives The aim of this study was to give an exhaustive view of the studies reporting the prevalence of the different EDs or total EDs and to study their evolution. Methods A literature search following PRISMA Guidelines and limited to studies in English or French published between 2000 and 2018 was performed and relevant studies were included in this systematic review on the prevalence of EDs. The literature search revealed 94 studies with accurate ED diagnosis and 27 with broad ED diagnosis. Results In 94 studies with accurate ED diagnosis, the weighted means (ranges) of lifetime ED were 8.4% (3.3–18.6%) for women and 2.2% (0.8–6.5%) for men. The weighted means (ranges) of 12-month ED prevalence were 2.2% (0.8–13.1%) for women and 0.7% (0.3–0.9%) for men. The weighted means (ranges) of point prevalence were 5.7% (0.9–13.5%) for women and 2.2% (0.2–7.3%) for men. According to continents, the weighted means (ranges) of point prevalence were 4.6% (2.0–13.5%) in America, 2.2% (0.2–13.1%) in Europe, and 3.5% (0.6–7.8%) in Asia. In addition to the former, 27 other studies reported the prevalence of EDs as broad categories resulting in weighted means (ranges) of total point prevalence of any EDs of 19.4% (6.5–36.0%) for women and 13.8% (3.6–27.1%) for men. Conclusions Despite the complexity of integrating all ED prevalence data, the most recent studies confirm that EDs are highly prevalent worldwide, especially in women. Moreover, the weighted means of point ED prevalence increased over the study period from 3.5% for the 2000–2006 period to 7.8% for the 2013–2018 period. This highlights a real challenge for public health and healthcare providers.

The infection mechanism of vaccinia virus is largely unknown. Neither the attachment protein of extracellular enveloped virus (EEV), the biologically relevant infectious form of the virus, nor its cellular receptor has been identified. Surprisingly, all former attempts using antibodies to block EEV infection of cells in vitro had failed. Here, we report the production of an anti-envelope hyperimmune serum with EEV neutralizing activity and show that a polyclonal antiserum against the extraviral domain of protein B5R also inhibited EEV infection. In vivo, mice vaccinated with B5R protein were protected against a lethal vaccinia virus challenge. This protectivity is likely to be mediated by neutralizing antibodies. Protein A33R, but not A34R and A36R, also proved to be protective in active and passive vaccination experiments. However, in contrast to B5R, A33R protectivity did not correlate with antibody titers. Because anti-A33R antibodies did not neutralize EEV in vitro, the protectivity mediated by A33R protein probably involves a mechanism different from simple antibody binding. Taken together, our results suggest that antibodies to a specific protective epitope or epitopes on protein B5R are able to prevent EEV infection. The protein encoded by the B5R gene is therefore likely to play a crucial role in the initial steps of vaccinia virus infection-binding to a host cell and entry into its cytoplasm.

In human long-term marrow cultures connective tissue-forming stromal cells are an essential cellular component of the adherent layer where granulomonocytic progenitors are generated from week 2 onward. We have previously found that most stromal cells in confluent cultures were stained by monoclonal antibodies directed against smooth muscle- specific actin isoforms. The present study was carried out to evaluate the time course of alpha-SM-positive stromal cells and to search for other cytoskeletal proteins specific for smooth muscle cells. It was found that the expression of alpha-SM in stromal cells was time dependent. Most of the adherent spindle-shaped, vimentin-positive stromal cells observed during the first 2 weeks of culture were alpha- SM negative. On the contrary, from week 3 to week 7, most interdigitated stromal cells contained stress fibers whose backbone was made of alpha-SM-positive microfilaments. In addition, in confluent cultures, other proteins specific for smooth muscle were detected: metavinculin, h-caldesmon, smooth muscle myosin heavy chains, and calponin. This study confirms the similarity between stromal cells and smooth muscle cells. Moreover, our results reveal that cells in vivo with the phenotype closest to that of stromal cells are immature fetal smooth muscle cells and subendothelial intimal smooth muscle cells; a cell subset with limited development following birth but extensively recruited in atherosclerotic lesions. Stromal cells very probably derive from mesenchymal cells that differentiate along this distinctive vascular smooth muscle cell pathway. In humans, this differentiation seems crucial for the maintenance of granulomonopoiesis. These in vitro studies were completed by examination of trephine bone marrow biopsies from adults without hematologic abnormalities. These studies revealed the presence of alpha-SM-positive cells at diverse locations: vascular smooth muscle cells in the media of arteries and arterioles, pericytes lining capillaries, myoid cells lining sinuses at the abluminal side of endothelial cells or found within the hematopoietic logettes, and endosteal cells lining bone trabeculae. More or less mature cells of the granulocytic series were in intimate contact with the thin cytoplasmic extensions of myoid cells. Myoid cells may be the in vivo counterpart of stromal cells with the above-described vascular smooth muscle phenotype.