In response to the outbreak of Zika virus (ZIKV) infection in the Western Hemisphere and the recognition of a causal association with fetal malformations, the Global Virus Network (GVN) assembled an international taskforce of virologists to promote basic research, recommend public health measures and encourage the rapid development of vaccines, antiviral therapies and new diagnostic tests. In this article, taskforce members and other experts review what has been learned about ZIKV-induced disease in humans, its modes of transmission and the cause and nature of associated congenital manifestations. After describing the make-up of the taskforce, we summarize the emergence of ZIKV in the Americas, Africa and Asia, its spread by mosquitoes, and current control measures. We then review the spectrum of primary ZIKV-induced disease in adults and children, sites of persistent infection and sexual transmission, then examine what has been learned about maternal-fetal transmission and the congenital Zika syndrome, including knowledge obtained from studies in laboratory animals. Subsequent sections focus on vaccine development, antiviral therapeutics and new diagnostic tests. After reviewing current understanding of the mechanisms of emergence of Zika virus, we consider the likely future of the pandemic.

Campylobacterjejuni is able to colonize the human intestinal mucosa and cause disease. For this reason, it was important to investigate mechanisms by which C. jejuni adheres to epithelial cells and intestinal mucus gel. All strains of C. jejuni used were able to adhere to INT 407 epithelial cells and mucus, but high adherence to one substrate did not necessarily indicate comparable adherence to the other. The adherence of C. jejuni to cells was inhibited partially by treating the bacterial cells with proteases or glutaraldehyde or by adding a certain carbohydrate (fucose or mannose) to the medium. The flagellum of C. jejuni was identified as a potential adhesin by comparing adherence of flagellated and aflagellated variants. Shearing of the bacterial cells to remove the flagella reduced bacterial adhesion, whereas immobilization of the flagellum with KCN increased adhesion. Purified flagella showed specific, fucose-resistant binding to epithelial cells but not to intestinal mucus. The presence of a second, nonproteinaceous adhesin was suggested because no single treatment of the bacteria completely inhibited adhesion. Lipopolysaccharide (LPS) was identified as another C. jejuni adhesin. [3H]LPS specifically bound to epithelial cells, and this phenomenon was inhibited by periodate oxidation of the LPS or glutaraldehyde fixation of the epithelial cells. LPS, unlike flagella, was fucose sensitive and inhibited binding of whole bacterial cells to INT 407 cells. LPS was also able to bind to intestinal mucus gel. These data indicate that both flagella and LPS are important in adhesion to the mucosal surface. Campylobacter jejuni is a frequent agent of diarrhea in humans (5), yet the interplay of its virulence factors in pathogenesis is poorly understood. The mechanisms by which C. jejuni interacts with the intestinal mucosa and initiates diarrhea are also unclear. Adhesion of bacteria to mucosal surfaces is necessary for colonization and subsequent pathogenesis. This process is mediated by chemotactic factors (9) and bacterial appendages (adhesins) which can include pili, flagella, capsules, glycocalyces, lipopolysaccharides, and cell-associated lectins (1, 2, 7). Complete evaluation of adhesion mechanisms of many organisms, however, has only recently begun. Newell and Pearson (24) used scanning electron microscopy to demonstrate in vitro adherence of C. jejuni to intestinal epithelial cells and saw morphologic evidence that this adhesion could be mediated by flagella. Later, flagellated organisms were shown to adhere in greater numbers to cells than did an aflagellated variant (23). Dijs and De Graaf (8) showed that C. jejuni cells do not possess fimbriae or pili but are able to agglutinate a variety of mammalian erythrocytes. Later, Naess et al. (22) were able to show in vitro adherence of C. jejuni strains to porcine small intestinal brush border preparations. Cinco et al. (6) also studied Campylobacter adherence to intestinal epithelial cells. The adhesion was inhibited partially by L-fuCose and D-mannose. This sug...

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100 years after the discovery of a bacterial 'endotoxin', 50 years after the introduction of antibiotics and 25 years after the routine use of intensive care units to support septic shock patients, Gram-negative infections continue to account for significant morbidity and mortality. In the coming decade, basic research on the structure/function of LPS, the cytokine cascade, and receptor-mediated intracellular signalling responses to LPS and cytokines will provide a greater understanding of the molecular, cellular and systemic responses to endotoxin and infection. New therapeutic agents now emerging from research, and better designed clinical trials to assess those agents will contribute to the next significant decline in sepsis- and shock-related morbidity and mortality. This article summarizes the findings of a workshop convened at the National Institutes of Health (NIH) to examine current research on endotoxin and Gram-negative septic shock.