Predictors of adherence to a brief sleep extension protocol in emerging adults.

OBJECTIVES: This study examined how mental health symptoms (i.e., depression, anxiety, stress) and baseline sleep characteristics (i.e., sleep quality and levels of daytime sleepiness) predicted adherence to and initial success of a brief sleep extension research protocol in emerging adults. METHODS: 184 emerging adults (ages 18-25; M = 20.96, SD = 2.04) were asked to extend their nightly sleep opportunity to 8 hr for 1 week and to anchor bedtime and waketime. Sleep outcomes (adherence and initial protocol success) were tracked using actigraphy. Baseline sleep quality, daytime sleepiness, depression, anxiety, and stress were assessed using self-report questionnaires. RESULTS: Poorer baseline sleep quality predicted better adherence to the protocol (p = .002). Other baseline sleep characteristics and mental health were not predictive of adherence (ps>.50). Lower levels of baseline daytime sleepiness approached significance in predicting greater initial protocol success following the protocol (p = .05). Baseline sleep quality and mental health did not predict initial protocol success (ps > 0.34). CONCLUSIONS: Mental health symptoms did not significantly predict adherence to or the success of a sleep extension protocol. Surprisingly, individuals with poor baseline sleep quality were more likely to adhere to the extension protocol, perhaps suggesting heightened motivation for change or increased risk for sleep problems. This research provides valuable insight into factors that predict adherence to sleep extension protocols in emerging adults.

The impact of experimentally shortened sleep on timing of eating occasions in adolescents: A brief report.

Short sleep increases the risk for obesity in adolescents. One potential mechanism relates to when eating occurs in the day. This study investigated the impact of shortened sleep on eating occasion timing in adolescents. Ninety-three healthy 14- to 17-year-olds (62% female) completed a within-subject experimental sleep manipulation, engaging in 5-night spans of Short Sleep (6.5-hr sleep opportunity) or Healthy Sleep (9.5-hr sleep opportunity), with order randomized. During each condition, adolescents completed three 24-hr diet recall interviews. Repeated-measure t-tests assessed the sleep manipulation effect on each adolescent's number of meals, first and last eating occasion (relative to the clock and time since sleep onset/offset), feeding window (timespan from first to last eating), and the midpoint of feeding. The timing of the first eating occasion was similar across conditions, relative to the clock (Short = 08:51, Healthy = 08:52) and to time since waking (Short = 2.0 hr, Healthy = 2.2 hr). The timing of the last eating occasion was later relative to the clock (Short = 20:34, Healthy = 19:39; p < 0.001), resulting in a longer feeding window (Short = 11.7 hr, Healthy = 10.8 hr, p < 0.001) and a later midpoint in the feeding window (Short = 14:41, Healthy = 14:18, p = 0.002). The gap between last eating occasion and sleep onset was larger in Short (4.2 hr) than Healthy Sleep (2.9 hr; p < 0.001), though the last eating occasion was much earlier than when they fell asleep during either condition. Shortened sleep resulted in adolescents eating later and lengthening the daily feeding window. These findings may help explain the link between shortened sleep and increased obesity risk in adolescents.

African horse sickness virus NS4 protein is an important virulence factor and interferes with JAK-STAT signaling during viral infection.

African horse sickness virus (AHSV) non-structural protein NS4 is a nucleocytoplasmic protein that is expressed in the heart, lung, and spleen of infected horses, binds dsDNA, and colocalizes with promyelocytic leukemia nuclear bodies (PML-NBs). The aim of this study was to investigate the role of AHSV NS4 in viral replication, virulence and the host immune response. Using a reverse genetics-derived virulent strain of AHSV-5 and NS4 deletion mutants, we showed that knockdown of NS4 expression has no impact in cell culture, but results in virus attenuation in infected horses. RNA sequencing (RNA-seq) was used to investigate the transcriptional response in these horses, to see how the lack of NS4 mediates the transition of the virus from virulent to attenuated. The presence of NS4 was shown to result in a 24 hour (h) delay in the transcriptional activation of several immune system processes compared to when the protein was absent. Included in these processes were the RIG-I-like, Toll-like receptor, and JAK-STAT signaling pathways, which are key pathways involved in innate immunity and the antiviral response. Thus, it was shown that AHSV NS4 suppresses the host innate immune transcriptional response in the early stages of the infection cycle. We investigated whether AHSV NS4 affects the innate immune response by impacting the JAK-STAT signaling pathway specifically. Using confocal laser scanning microscopy (CLSM) we showed that AHSV NS4 disrupts JAK-STAT signaling by interfering with the phosphorylation and/or translocation of STAT1 and pSTAT1 into the nucleus. Overall, these results showed that AHSV NS4 is a key virulence factor in horses and allows AHSV to overcome host antiviral responses in order to promote viral replication and spread.

Natural Bluetongue virus infection in alpacas in South Africa.

Bluetongue virus (BTV) was sporadically isolated over a four year period (2010-2014) from several alpaca carcasses that were presented for necropsy at the Western Cape Provincial Veterinary Laboratory, South Africa. Typically, the a ected animals had a history of acute dyspnoea and progressive weakness before death. Consistent hydrothorax and severe lung oedema in all lead to a preliminary diagnosis of Bluetongue, despite the absence of ulceration and hyperaemia of the oral mucosa which is characteristic of this viral infection in sheep. The diagnosis was con rmed by virus isolation in embryonated eggs and subsequent sequencing of the extracted RNA. Assembled sequences were subjected to Blast analysis and two of the isolates could be veri ed as BTV 3. These cases, originating from the Western Cape Province of South Africa, represents the rst o cial report of BTV infection in alpacas in Africa and demonstrates the susceptibility of the species to this disease when maintained in BTV endemic areas.

Consensus Sequence of 27 African Horse Sickness Virus Genomes from Viruses Collected over a 76-Year Period (1933 to 2009).

We announce the complete consensus genome sequence of 27 African horse sickness viruses, representing all nine African horse sickness virus (AHSV) serotypes from historical and recent isolates collected over a 76-year period (1933 to 2009). The data set includes the sequence of the virulent Office International des Epizooties AHSV reference strains which are not adapted to cell culture.

Structural insight into African horsesickness virus infection.

African horsesickness (AHS) is a devastating disease of horses. The disease is caused by the double-stranded RNA-containing African horsesickness virus (AHSV). Using electron cryomicroscopy and three-dimensional image reconstruction, we determined the architecture of an AHSV serotype 4 (AHSV-4) reference strain. The structure revealed triple-layered AHS virions enclosing the segmented genome and transcriptase complex. The innermost protein layer contains 120 copies of VP3, with the viral polymerase, capping enzyme, and helicase attached to the inner surface of the VP3 layer on the 5-fold axis, surrounded by double-stranded RNA. VP7 trimers form a second, T=13 layer on top of VP3. Comparative analyses of the structures of bluetongue virus and AHSV-4 confirmed that VP5 trimers form globular domains and VP2 trimers form triskelions, on the virion surface. We also identified an AHSV-7 strain with a truncated VP2 protein (AHSV-7 tVP2) which outgrows AHSV-4 in culture. Comparison of AHSV-7 tVP2 to bluetongue virus and AHSV-4 allowed mapping of two domains in AHSV-4 VP2, and one in bluetongue virus VP2, that are important in infection. We also revealed a protein plugging the 5-fold vertices in AHSV-4. These results shed light on virus-host interactions in an economically important orbivirus to help the informed design of new vaccines.