Vaccination Status and Attitude among Measles Cluster Cases in Austria, 2019

On 21 January 2019, public health authorities of two neighboring Austrian provinces reported an increase in measles cases. We investigated this occurrence to identify clusters of epidemiologically linked cases and the associated vaccination status in order to generate hypotheses on those factors explaining the size of the measles clusters. Probable cases were residents of the provinces of Styria or Salzburg with clinical presentation of measles after 1 January 2019 who were linked to a confirmed case using RNA virus detection. We collected data on age, rash onset, certificate-based vaccination status and reasons for being unvaccinated. Contact history was used to identify chains of transmission. By 11 March, we identified 47 cases, with 40 (85.1%) in unvaccinated patients. A cluster of 35 cases with a median age of seven years (IQR: 1–11) occurred between 9 January and 20 February in the province of Styria due to one transmission chain with four case generations. Of 31 vaccine-eligible cases, 25 (80.6%) were unvaccinated, of which 13 refused vaccination. Between 10 January and 1 March, we identified 12 cases as part of five unlinked clusters in the province of Salzburg. Each of these five clusters consisted of two generations: the primary case and the successive cases (median age: 22 years, IQR: 11–35). Eleven of 12 cases occurred in unvaccinated patients, with none of the 11 having a vaccination-refusing attitude. An extended measles cluster in a vaccination-refusing community, compared to five short-lived clusters concurrently occurring in the neighboring province, illustrates how vaccine refusal may hamper control of transmission

A genome-wide Drosophila epithelial tumorigenesis screen identifies Tetraspanin 29Fb as an evolutionarily conserved suppressor of Ras-driven cancer.

Oncogenic mutations in the small GTPase Ras contribute to ~30% of human cancers. However, Ras mutations alone are insufficient for tumorigenesis, therefore it is paramount to identify cooperating cancer-relevant signaling pathways. We devised an in vivo near genome-wide, functional screen in Drosophila and discovered multiple novel, evolutionarily-conserved pathways controlling Ras-driven epithelial tumorigenesis. Human gene orthologs of the fly hits were significantly downregulated in thousands of primary tumors, revealing novel prognostic markers for human epithelial tumors. Of the top 100 candidate tumor suppressor genes, 80 were validated in secondary Drosophila assays, identifying many known cancer genes and multiple novel candidate genes that cooperate with Ras-driven tumorigenesis. Low expression of the confirmed hits significantly correlated with the KRASG12 mutation status and poor prognosis in pancreatic cancer. Among the novel top 80 candidate cancer genes, we mechanistically characterized the function of the top hit, the Tetraspanin family member Tsp29Fb, revealing that Tsp29Fb regulates EGFR signaling, epithelial architecture and restrains tumor growth and invasion. Our functional Drosophila screen uncovers multiple novel and evolutionarily conserved epithelial cancer genes, and experimentally confirmed Tsp29Fb as a key regulator of EGFR/Ras induced epithelial tumor growth and invasion