Assessing the Quality and Behavior Change Potential of Vaping Cessation Apps: Systematic Search and Assessment.

Background: An increasing number of people are using vapes (e-cigarettes), and with growing evidence of associated harms, there is a need for acceptable cessation support and interventions. Smartphone apps for health and well-being have increased in popularity and use. Limited published literature assesses the potential of apps to support vaping cessation. Objective: A systematic search of vaping cessation apps currently available in Australia for iOS and Android platforms was conducted. Apps were assessed against established health app assessment tools for quality and behavior change potential. Methods: A systematic search through the Australian Apple iTunes and Google Play stores was conducted using the search terms "vape"; "vaping"; "e-cigarette"; and "cessation," "quit," or "quitting" in May 2023. Only apps that encouraged the cessation of vaping were included. App descriptions were reviewed to determine if they were relevant for inclusion in this study, and relevant apps were downloaded onto the appropriate mobile device for review. The Mobile App Rating Scale (MARS) was used to rate the quality (engagement, functionality, aesthetics, and information) of the apps using an overall score out of 5. The App Behavior Change Scale (ABACUS) was used to assess the behavior change potential of each app using a score out of 21. Results: An initial search of the app stores yielded 220 Android apps and 124 iOS apps. Screening against the inclusion criteria left 20 iOS apps and 10 Android apps for review. Six apps were available on both operating systems, and these were downloaded, reviewed, and reported separately for each operating system. The average MARS score for all apps assessed in this review was 3.1 (SD 0.41) out of 5. The reviewed apps overall performed well for the MARS elements relating to functionality, such as ease of use and navigation, but had the lowest scores for information-related elements, such as credibility. The number of ABACUS behavior change features per app ranged from 0 to 19 out of 21, with a mean of 8.9 (SD 4.51). The apps commonly included information-related features, such as requesting baseline information. The least common behavior change features were those relating to goal-setting, such as asking about the user's willingness for behavior change and providing feedback on current actions in comparison to future goals. Conclusions: The identified vaping cessation apps had moderate levels of quality and some behavior change components. Future vaping cessation apps could benefit from including more features that are known to support behavior change, such as goal-setting, to improve the potential benefit of these apps to support people to stop vaping. As guidelines for vaping cessation continue to be established, future apps need to reference these in their development.

Targeting cancer prevention and screening interventions to LGBTQ communities: A scoping review.

Although some people within LGBTQ communities are at risk of developing some cancers at higher rates than non-LGBTQ people, there is limited evidence of the outcomes of targeted cancer prevention and screening interventions for these communities. This scoping review examined key findings regarding the feasibility, acceptability and efficacy of evaluated intervention studies conducted in high income settings and published in peer reviewed literature (2014-2020) by combining evidence of both cancer risk-reducing behavioural interventions and screening and preventative practice interventions. While there is limited evidence of stronger outcomes from targeted interventions with cohorts of gender and sexuality diverse communities, compared with the use of mainstream or untailored interventions, there is stronger evidence that targeted interventions are more acceptable to these communities and may be more feasible in some contexts. Thus, there is benefit in understanding what targeting entails in these interventions, and to understand what influences acceptability, to inform the design and delivery of such interventions.

Human papillomavirus capsids preferentially bind and infect tumor cells.

We previously determined that human papillomavirus (HPV) virus-like particles (VLPs) and pseudovirions (PsV) did not, respectively, bind to or infect intact epithelium of the cervicovaginal tract. However, they strongly bound heparan sulfate proteoglycans (HSPG) on the basement membrane of disrupted epithelium and infected the keratinocytes that subsequently entered the disrupted site. We here report that HPV capsids (VLP and PsV) have the same restricted tropism for a wide variety of disrupted epithelial and mesothelial tissues, whereas intact tissues remain resistant to binding. However, the HPV capsids directly bind and infect most tumor-derived cell lines in vitro and have analogous tumor-specific properties in vivo, after local or intravenous injection, using orthotopic models for human ovarian and lung cancer, respectively. The pseudovirions also specifically infected implanted primary human ovarian tumors. Heparin and ι-carrageenan blocked binding and infection of all tumor lines tested, implying that tumor cell binding is HSPG-dependent. A survey using a panel of modified heparins indicates that N-sulfation and, to a lesser degree, O-6 sulfation of the surface HSPG on the tumors are important for HPV binding. Therefore, it appears that tumor cells consistently evolve HSPG modification patterns that mimic the pattern normally found on the basement membrane but not on the apical surfaces of normal epithelial or mesothelial cells. Consequently, appropriately modified HPV VLPs and/or PsV could be useful reagents to detect and potentially treat a remarkably broad spectrum of cancers.

Mouse model of cervicovaginal papillomavirus infection.

Virtually all cervical cancers are caused by human papillomavirus infections. The efficient assembly of pseudovirus (PsV) particles incorporating a plasmid expressing a reporter gene has been an invaluable tool in the development of in vitro neutralization assays and in studies of the early mechanisms of viral entry in vitro. Here, we describe a mouse model of human papillomavirus PsV infection of the cervicovaginal epithelium that recapitulates the early events of papillomavirus infection in vivo.

Active depletion of host cell inhibitor-of-apoptosis proteins triggers apoptosis upon baculovirus DNA replication.

Apoptosis is an important antivirus defense by virtue of its impact on virus multiplication and pathogenesis. To define molecular mechanisms by which viruses are detected and the apoptotic response is initiated, we examined the antiviral role of host inhibitor-of-apoptosis (IAP) proteins in insect cells. We report here that the principal IAPs, DIAP1 and SfIAP, of the model insects Drosophila melanogaster and Spodoptera frugiperda, respectively, are rapidly depleted and thereby inactivated upon infection with the apoptosis-inducing baculovirus Autographa californica multicapsid nucleopolyhedrovirus (AcMNPV). Virus-induced loss of these host IAPs triggered caspase activation and apoptotic death. Elevation of IAP levels by ectopic expression repressed caspase activation. Loss of host IAP in both species was triggered by AcMNPV DNA replication. By using selected inhibitors, we found that virus-induced IAP depletion was mediated in part by the proteasome but not by caspase cleavage. Consistent with this conclusion, mutagenic disruption of the SfIAP RING motif, which acts as an E3 ubiquitin ligase, stabilized SfIAP during infection. Importantly, SfIAP was also stabilized upon the removal of its 99-residue N-terminal leader, which serves as a critical determinant of IAP turnover. These data indicated that a host pathway initiated by virus DNA replication and acting through instability motifs embedded within IAP triggers IAP depletion and thereby causes apoptosis. Taken together, the results of our study suggest that host modulation of cellular IAP levels is a conserved mechanism by which insects mount an apoptotic antiviral response. Thus, host IAPs may function as critical sentinels of virus invasion in insects.

Host insect inhibitor-of-apoptosis SfIAP functionally replaces baculovirus IAP but is differentially regulated by Its N-terminal leader.

The inhibitor-of-apoptosis (IAP) proteins encoded by baculoviruses bear a striking resemblance to the cellular IAP homologs of their invertebrate hosts. By virtue of the acquired selective advantage of blocking virus-induced apoptosis, baculoviruses may have captured cellular IAP genes that subsequently evolved for virus-specific objectives. To compare viral and host IAPs, we defined antiapoptotic properties of SfIAP, the principal cellular IAP of the lepidopteran host Spodoptera frugiperda. We report here that SfIAP prevented virus-induced apoptosis as well as viral Op-IAP3 (which is encoded by the Orgyia pseudotsugata nucleopolyhedrovirus) when overexpressed from the baculovirus genome. Like Op-IAP3, SfIAP blocked apoptosis at a step prior to caspase activation. Both of the baculovirus IAP repeats (BIRs) were required for SfIAP function. Moreover, deletion of the C-terminal RING motif generated a loss-of-function SfIAP that interacted and dominantly interfered with wild-type SfIAP. Like Op-IAP3, wild-type SfIAP formed intracellular homodimers, suggesting that oligomerization is a functional requirement for both cellular and viral IAPs. SfIAP possesses a ∼100-residue N-terminal leader domain, which is absent among all viral IAPs. Remarkably, deletion of the leader yielded a fully functional SfIAP with dramatically increased protein stability. Thus, the SfIAP leader contains an instability motif that may confer regulatory options for cellular IAPs that baculovirus IAPs have evolved to bypass for maximal stability and antiapoptotic potency. Our findings that SfIAP and viral IAPs have common motifs, share multiple biochemical properties including oligomerization, and act at the same step to block apoptosis support the hypothesis that baculoviral IAPs were derived by acquisition of host insect IAPs.