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Abstract Lateral-shaking inducing neuro-degenerative agent virus (LindaV) is a novel member of the highly diverse genus Pestivirus within the family Flaviviridae. LindaV was first detected in Austria in 2015 and was associated with congenital tremor in piglets. Since then, the virus or specific antibodies have been found in a few further pig farms in Austria. However, the actual spatial distribution and the existence of reservoir hosts is largely unknown. Since other pestiviruses of pigs such as classical swine fever virus or atypical porcine pestivirus can also infect wild boar, the question arises whether LindaV is likewise present in the wild boar population. Therefore, we investigated the presence of neutralizing antibodies against LindaV in 200 wild boar samples collected in Southern Germany, which borders Austria. To establish a serological test system, we made use of the interchangeability of the surface glycoproteins and created a chimeric pestivirus using Bungowannah virus (species Pestivirus australiaense) as synthetic backbone. The E1 and E2 glycoproteins were replaced by the heterologous E1 and E2 of LindaV resulting in the chimera BV_E1E2_LV. Viable virus could be rescued and was subsequently applied in a neutralization test. A specific positive control serum generated against the E2 protein of LindaV gave a strong positive result, thereby confirming the functionality of the test system. All wild boar samples, however, tested negative. Hence, there is no evidence that LindaV has become highly prevalent in the wild boar population in Southern Germany.

Sequence learning in serial reaction time tasks (SRTT) is an established, lab-based experimental paradigm to study acquisition and transfer of skill based on the detection of predictable stimulus and motor response sequences. Sequence learning has been mainly studied in key presses using visual target stimuli and is demonstrated by better performance in predictable sequences than in random sequences. In this study, we investigated sequence learning in the context of more complex locomotor responses. To this end, we developed a novel goal-directed stepping SRTT with auditory target stimuli in order to subsequently assess the effect of aging on sequence learning in this task, expecting that age-related performance reductions in postural control might disturb the acquisition of the sequence. We used pressure-sensitive floor mats to characterise performance across ten blocks of trials. In Experiment 1, 22 young adults demonstrated successful acquisition of the sequence in terms of the time to step on the target mat and percent error and thus validated our new paradigm. In Experiment 2, in order to contrast performance improvements in the stepping SRTT between 27 young and 22 old adults, motion capture of the feet was combined with the floor mat system to delineate individual movement phases during stepping onto a target mat. The latencies of several postural events as well as other movement parameters of a step were assessed. We observed significant learning effects in the latency of step initiation, the time to step on the target mat, and motion parameters such as stepping amplitude and peak stepping velocity, as well as in percent error. The data showed general age-related slowing but no significant performance differences in procedural locomotor sequence learning between young and old adults. The older adults also had comparable conscious representations of the sequence of stimuli as the young adults. We conclude that sequence learning occurred in this locomotor learning task that is much more complex than typical finger-tapping sequence learning tasks, and that healthy older adults showed similar learning effects compared to young adults, suggesting intact locomotor sequence learning capabilities despite general slowing and normal age-related decline in sensorimotor function.

The clinical outcomes of short interruptions of PI-based ART regimens remains undefined.A 2-arm non-inferiority trial was conducted on 53 HIV-1 infected South African participants with viral load 450 cells/µl on stavudine (or zidovudine), lamivudine and lopinavir/ritonavir. Subjects were randomized to a) sequential 2, 4 and 8-week ART interruptions or b) continuous ART (cART). Primary analysis was based on the proportion of CD4 count >350 cells(c)/ml over 72 weeks. Adherence, HIV-1 drug resistance, and CD4 count rise over time were analyzed as secondary endpoints.The proportions of CD4 counts >350 cells/µl were 82.12% for the intermittent arm and 93.73 for the cART arm; the difference of 11.95% was above the defined 10% threshold for non-inferiority (upper limit of 97.5% CI, 24.1%; 2-sided CI: -0.16, 23.1). No clinically significant differences in opportunistic infections, adverse events, adherence or viral resistance were noted; after randomization, long-term CD4 rise was observed only in the cART arm.We are unable to conclude that short PI-based ART interruptions are non-inferior to cART in retention of immune reconstitution; however, short interruptions did not lead to a greater rate of resistance mutations or adverse events than cART suggesting that this regimen may be more forgiving than NNRTIs if interruptions in therapy occur.ClinicalTrials.gov NCT00100646.

Background Advanced HIV infection can result in lipoatrophy and wasting, even in the absence of ongoing opportunistic infections, suggesting that HIV may directly affect adipose tissue amount and distribution. Methods We assessed the relationship of fat (measured using anthropometry, DEXA, MRI scans) or markers related to glucose and lipid metabolism with viral load in a cross‐sectional sample of 83 antiretroviral‐naïve HIV‐1‐infected South African women. A multivariable linear model was fitted to log10VL to assess the combined effect of these variables. Results In addition to higher T cell activation, women with viral load greater than the population median had lower waist circumference, body mass index and subcutaneous abdominal fat, as well as lower serum leptin. We demonstrate that leptin serum levels are inversely associated with viral replication, independent of the amount of adipose tissue. This association is maintained after adjusting for multiple variables associated with disease progression (i.e., cellular activation and innate immunity effector levels). Conclusions Our results demonstrate that serum leptin levels are inversely associated with viral replication, independent of disease progression: we postulate that leptin may affect viral replication.