Social media platforms like Twitter and Facebook provide risk communicators with the opportunity to quickly reach their constituents at the time of an emerging infectious disease. On these platforms, messages gain exposure through message passing (called "sharing" on Facebook and "retweeting" on Twitter). This raises the question of how to optimize risk messages for diffusion across networks and, as a result, increase message exposure. In this study we add to this growing body of research by identifying message-level strategies to increase message passing during high-ambiguity events. In addition, we draw on the extended parallel process model to examine how threat and efficacy information influence the passing of Zika risk messages. In August 2016, we collected 1,409 Twitter messages about Zika sent by U.S. public health agencies' accounts. Using content analysis methods, we identified intrinsic message features and then analyzed the influence of those features, the account sending the message, the network surrounding the account, and the saliency of Zika as a topic, using negative binomial regression. The results suggest that severity and efficacy information increase how frequently messages get passed on to others. Drawing on the results of this study, previous research on message passing, and diffusion theories, we identify a framework for risk communication on social media. This framework includes four key variables that influence message passing and identifies a core set of message strategies, including message timing, to increase exposure to risk messages on social media during high-ambiguity events.

Limited research has examined the messages produced about health-related crises on social media platforms and whether these messages contain content that would allow individuals to make sense of a crisis and respond effectively. This study uses the crisis and emergency risk communication (CERC) framework to evaluate the content of messages sent via Twitter during an emerging crisis. Using manual and computer-driven content analysis methods, the study analyzed 25,598 tweets about the H7N9 virus that were produced in April 2013. The study found that a large proportion of messages contained sensemaking information. However, few tweets contained efficacy information that would help individuals respond to the crisis appropriately. Implications and recommendations for practice and future study are discussed.

Lung cancer advocates, as well as patient and medical advocacy organizations, with an interest in expanding the reach and effectiveness of social media efforts should monitor the topical nature of public tweets across the cancer continuum and consider integrating cues to action as a strategy to increase engagement and behavioral activation pertaining to lung cancer reduction efforts.

The current study examines crisis communication on social media by observing how twelve National Weather Service (NWS) offices use Twitter to facilitate engagement with stakeholders during threat and nonthreat periods. Using content analytic methods, we examine message features related to content and structure during a 3‐month period in spring 2016. We conduct chi‐square analyses to determine how the prevalence of these features varies by time. Results indicate that NWS offices use Twitter for ongoing engagement communication through both the content and structure of their messages, where community building and action‐orientated messages are primarily used during nonthreat periods. When fair weather changes and storms approach, the offices shift to the communication of risk. Our findings underscore the need to examine organizational communication practices in a manner that recognizes the distinctions between long‐term engagement goals and short‐term goals related to the mission of the organization.

Aims/hypothesis CD40 expressed in Müller cells is a central driver of diabetic retinopathy. CD40 causes phospholipase Cγ1 (PLCγ1)-dependent ATP release in Müller cells followed by purinergic receptor (P2X7)-dependent production of proinflammatory cytokines in myeloid cells. In the diabetic retina, CD40 and P2X7 upregulate a broad range of inflammatory molecules that promote development of diabetic retinopathy. The molecular event downstream of CD40 that activates the PLCγ1–ATP–P2X7–proinflammatory cytokine cascade and promotes development of diabetic retinopathy is unknown. We hypothesise that disruption of the CD40-driven molecular events that trigger this cascade prevents/treats diabetic retinopathy in mice. Methods B6 and transgenic mice with Müller cell-restricted expression of wild-type (WT) CD40 or CD40 with mutations in TNF receptor-associated factor (TRAF) binding sites were made diabetic using streptozotocin. Leucostasis was assessed using FITC-conjugated concanavalin A. Histopathology was examined in the retinal vasculature. Expression of inflammatory molecules and phospho-Tyr783 PLCγ1 (p-PLCγ1) were assessed using real-time PCR, immunoblot and/or immunohistochemistry. Release of ATP and cytokines were measured by ATP bioluminescence and ELISA, respectively. Results Human Müller cells with CD40 ΔT2,3 (lacks TRAF2,3 binding sites) were unable to phosphorylate PLCγ1 and release ATP in response to CD40 ligation, and could not induce TNF-α/IL-1β secretion in bystander myeloid cells. CD40–TRAF signalling acted via Src to induce PLCγ1 phosphorylation. Diabetic mice in which WT CD40 in Müller cells was replaced by CD40 ΔT2,3 failed to exhibit phosphorylation of PLCγ1 in these cells and upregulate P2X7 and TNF-α in microglia/macrophages. P2x7 (also known as P2rx7), Tnf-α (also known as Tnf), Il-1β (also known as Il1b), Nos2, Icam-1 (also known as Icam1) and Ccl2 mRNA were not increased in these mice and the mice did not develop retinal leucostasis and capillary degeneration. Diabetic B6 mice treated intravitreally with a cell-permeable peptide that disrupts CD40–TRAF2,3 signalling did not exhibit either upregulation of P2X7 and inflammatory molecules in the retina or leucostasis. Conclusions/interpretation CD40–TRAF2,3 signalling activated the CD40–PLCγ1–ATP–P2X7–proinflammatory cytokine pathway. Src functioned as a link between CD40–TRAF2,3 and PLCγ1. Replacing WT CD40 with CD40 ΔT2,3 impaired activation of PLCγ1 in Müller cells, upregulation of P2X7 in microglia/macrophages, upregulation of a broad range of inflammatory molecules in the diabetic retina and the development of diabetic retinopathy. Administration of a peptide that disrupts CD40–TRAF2,3 signalling reduced retinal expression of inflammatory molecules and reduced leucostasis in diabetic mice, supporting the therapeutic potential of pharmacological inhibition of CD40–TRAF2,3 in diabetic retinopathy. Graphical abstract