[This corrects the article DOI 10.1371/journal.pone.0202450.].The genus Vitivirus in the family Betaflexiviridae includes eleven viruses known to infect grapevine grapevine vitiviruses A, B, D, E, F, G, H, I, J, L and M (GVA-GVM). Three of these viruses, GVA, GVB and GVD, have been associated with the etiology of rugose wood disease in grapevine and cause agronomically significant losses. The other vitiviruses were more recently discovered and their effects on grapevine are undetermined. To certify grape material for propagation as virus tested, an updated reverse transcription PCR (RT-PCR) assay to detect all known vitiviruses is desirable. To accomplish this, multiple grapevine vitivirus sequences were aligned at the amino acid level to search for conserved motifs. Two highly conserved motifs were found at an ideal distance for RT-PCR detection in the RNA-dependent RNA polymerase region of the replicase protein. The amino acid motifs were back translated to create degenerate primers and used to successfully amplify all eleven grapevine vitiviruses. The RT-PCR primers were used to test a panel of vitivirus-infected vines for inclusivity as well as vines infected with closely related viruses in the Betaflexiviridae family (i.e. grapevine pinot gris virus and grapevine rupestris stem pitting-associated virus) for exclusivity. Broader use of these primers to detect vitiviruses in other plant hosts was investigated. In summary, an end-point RT-PCR assay that detects all the known grapevine vitiviruses and potentially other members of the genus Vitivirus has been developed. The universal assay represents an alternative to individual assays to reduce the work associated with the diagnosis of vitiviruses, including for regulatory purposes. Improving health outcomes for Indigenous people by strengthening the cultural safety of care is a vital challenge for the health sector, both in Australia and internationally. Although Indigenous people have long requested to have Indigenous practitioners involved in their health care, many health services report difficulties with recruiting and retaining Indigenous staff. This article describes Indigenous workforce policies and strategies from two Australian health services, as well as cancer-service specific strategies. Services were identified as part of a national study designed to identify and assess innovative services for Indigenous cancer patients and their families. In-depth interviews were conducted in a small number of identified services. The interviews from two services, which stood out as particularly high performing, were analysed through the lens of Indigenous health workforce. Twenty-four hospital staff (Indigenous and non-Indigenous), five Indigenous people with cancer and three family own policies and programs to support building their Indigenous workforce. These two cancer services and their affiliated hospitals show how positive patient outcomes and a strong Indigenous health workforce can be achieved when a health service has strong leadership, commits to an inclusive and enabling culture, facilitates two-way learning and develops specific support structures appropriate for Indigenous staff. It is hoped that the strategies captured in this study will be used by health services and cancer services to inform their own policies and programs to support building their Indigenous workforce.Social distancing, a non-pharmaceutical tactic aimed at reducing the spread of COVID-19, can arise because individuals voluntarily distance from others to avoid contracting the disease. Alternatively, it can arise because of jurisdictional restrictions imposed by local authorities. We run reduced form models of social distancing as a function of county-level exogenous demographic variables and jurisdictional fixed effects for 49 states to assess the relative contributions of demographic and jurisdictional effects in explaining social distancing behavior. To allow for possible spatial aspects of a contagious disease, we also model the spillovers associated with demographic variables in surrounding counties as well as allow for disturbances that depend upon those in surrounding counties. We run our models weekly and examine the evolution of the estimated coefficients over time since the onset of the COVID-19 pandemic in the United States. These estimated coefficients express the revealed preferences of individus and coldspots of social distance, which has implications for disease spread and mitigation.Enzymatic inactivation of Rho-family GTPases by the glucosyltransferase domain of Clostridioides difficile Toxin B (TcdB) gives rise to various pathogenic effects in cells that are classically thought to be responsible for the disease symptoms associated with C. difficile infection (CDI). Recent in vitro studies have shown that TcdB can, under certain circumstances, induce cellular toxicities that are independent of glucosyltransferase (GT) activity, calling into question the precise role of GT activity. Here, to establish the importance of GT activity in CDI disease pathogenesis, we generated the first described mutant strain of C. difficile producing glucosyltransferase-defective (GT-defective) toxin. Using allelic exchange (AE) technology, we first deleted tcdA in C. difficile 630Δerm and subsequently introduced a deactivating D270N substitution in the GT domain of TcdB. To examine the role of GT activity in vivo, we tested each strain in two different animal models of CDI pathogenesis. In the non-lethal murine model of infection, the GT-defective mutant induced minimal pathology in host tissues as compared to the profound caecal inflammation seen in the wild-type and 630ΔermΔtcdA (ΔtcdA) strains. https://www.selleckchem.com/products/brequinar.html In the more sensitive hamster model of CDI, whereas hamsters in the wild-type or ΔtcdA groups succumbed to fulminant infection within 4 days, all hamsters infected with the GT-defective mutant survived the 10-day infection period without primary symptoms of CDI or evidence of caecal inflammation. These data demonstrate that GT activity is indispensable for disease pathogenesis and reaffirm its central role in disease and its importance as a therapeutic target for small-molecule inhibition.