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Recent translational data suggest that deep brain stimulation (DBS) of the cortico-striato-thalamo-cortical (CSTC) loops improves sensorimotor gating in psychiatric disorders that show deficient prepulse inhibition (PPI), a robust operational measure of sensorimotor gating. To our knowledge we are the first to investigate this effect in patients with Tourette syndrome (TS). We measured PPI of the acoustic startle reflex in patients with TS (N = 10) or Obsessive-Compulsive Disorder (OCD) (N = 8) treated with DBS of the centromedian and ventro-oral internal thalamic nucleus and the anterior limb of internal capsule-nucleus accumbens area respectively, and aged- and gender-matched healthy controls (HC). PPI of the DBS groups was measured in randomized order in the ON and OFF stimulation condition. Statistical analysis revealed no significant difference in PPI (%) of patients with TS between ON (M = 20.5, SD = 14.9) and OFF (M = 25.2, SD = 29.7) condition. There were significantly reduced PPI levels in patients with TS in the ON condition compared to HC (M = 49.2, SD = 10.7), but no significant difference in PPI between TS in the OFF condition and HC. Furthermore, we found no significant stimulation or group effect for OCD and HC (OCD ON: M = 57.0, SD = 8.3; OCD OFF: 67.8, SD = 19.6; HC: M = 63.0, SD = 24.3). Our study has a number of limitations. Sample sizes are small due to the restricted patient collective. The study was not controlled for use of psychoactive medication or nicotine. Furthermore, we were not able to assess presurgical PPI measurements. In conclusion, we were able to show that PPI is impaired in patients with TS. This finding is in line with recent translational work. With respect to the OCD cohort we were not able to replicate our previously published data. A disability in sensorimotor gating plays a pivotal role in many psychiatric disorders therefore more research should be conducted to disentangle the potential and limitations of modulating sensorimotor gating via brain stimulation techniques.

Summary The PALM trial in the Democratic Republic of the Congo identified a statistically significant survival benefit for two monoclonal antibody-based therapeutics in the treatment of acute Ebola virus disease; however, substantial gaps remain in improving the outcomes of acute Ebola virus disease and for the survivors. Ongoing efforts are needed to develop more effective strategies, particularly for individuals with severe disease, for prevention and treatment of viral persistence in immune-privileged sites, for optimisation of post-exposure prophylaxis, and to increase therapeutic breadth. As antibody-based approaches are identified and advanced, promising small-molecule antivirals currently in clinical stage development should continue to be evaluated for filovirus diseases, with consideration of their added value in combination approaches with bundled supportive care, their penetration in tissues of interest, the absence of interaction with glycoprotein-based vaccines, and filoviral breadth.

In 1998, Mike Bray and colleagues published the first immunocompetent laboratory mouse model of Ebola virus disease. Often labeled by peer reviewers as inferior to nonhuman primate efforts, this model initially laid the foundation for the recent establishment of panel-derived cross-bred and humanized mouse models and a golden hamster model. Nonhuman primate research has always been associated with ethical concerns and is sometimes deemed scientifically questionable due to the necessarily low animal numbers in individual studies. Independent of these concerns, the now-global severe shortage of commercially available nonhuman primates may pragmatically push research toward increased and improved rodent modeling that may altogether replace nonhuman primate studies in the short-term as well as in an optimal future.

Simian arteriviruses are endemic in some African primates and can cause fatal hemorrhagic fevers when they cross into primate hosts of new species. We find that CD163 acts as an intracellular receptor for simian hemorrhagic fever virus (SHFV; a simian arterivirus), a rare mode of virus entry that is shared with other hemorrhagic fever-causing viruses (e.g., Ebola and Lassa viruses). Further, SHFV enters and replicates in human monocytes, indicating full functionality of all of the human cellular proteins required for viral replication. Thus, simian arteriviruses in nature may not require major adaptations to the human host. Given that at least three distinct simian arteriviruses have caused fatal infections in captive macaques after host-switching, and that humans are immunologically naive to this family of viruses, development of serology tests for human surveillance should be a priority.

Summary Background The 2018 Ebola virus disease (EVD) outbreak in Equateur Province, Democratic Republic of the Congo, began on May 8, and was declared over on July 24; it resulted in 54 documented cases and 33 deaths. We did a retrospective genomic characterisation of the outbreak and assessed potential therapeutic agents and vaccine (medical countermeasures). Methods We used target-enrichment sequencing to produce Ebola virus genomes from samples obtained in the 2018 Equateur Province outbreak. Combining these genomes with genomes associated with known outbreaks from GenBank, we constructed a maximum-likelihood phylogenetic tree. In-silico analyses were used to assess potential mismatches between the outbreak strain and the probes and primers of diagnostic assays and the antigenic sites of the experimental rVSVΔG-ZEBOV-GP vaccine and therapeutics. An in-vitro flow cytometry assay was used to assess the binding capability of the individual components of the monoclonal antibody cocktail ZMapp. Findings A targeted sequencing approach produced 16 near-complete genomes. Phylogenetic analysis of these genomes and 1011 genomes from GenBank revealed a distinct cluster, confirming a new Ebola virus variant, for which we propose the name “Tumba”. This new variant appears to have evolved at a slower rate than other Ebola virus variants (0·69 × 10−3 substitutions per site per year with “Tumba” vs 1·06 × 10−3 substitutions per site per year without “Tumba”). We found few sequence mismatches in the assessed assay target regions and antigenic sites. We identified nine amino acid changes in the Ebola virus surface glycoprotein, of which one resulted in reduced binding of the 13C6 antibody within the ZMapp cocktail. Interpretation Retrospectively, we show the feasibility of using genomics to rapidly characterise a new Ebola virus variant within the timeframe of an outbreak. Phylogenetic analysis provides further indications that these variants are evolving at differing rates. Rapid in-silico analyses can direct in-vitro experiments to quickly assess medical countermeasures. Funding Defense Biological Product Assurance Office .

Spumaretroviruses, commonly referred to as foamy viruses, are complex retroviruses belonging to the subfamily Spumaretrovirinae, family Retroviridae, which naturally infect a variety of animals including nonhuman primates (NHPs). Additionally, cross-species transmissions of simian foamy viruses (SFVs) to humans have occurred following exposure to tissues of infected NHPs. Recent research has led to the identification of previously unknown exogenous foamy viruses, and to the discovery of endogenous spumaretrovirus sequences in a variety of host genomes. Here, we describe an updated spumaretrovirus taxonomy that has been recently accepted by the International Committee on Taxonomy of Viruses (ICTV) Executive Committee, and describe a virus nomenclature that is generally consistent with that used for other retroviruses, such as lentiviruses and deltaretroviruses. This taxonomy can be applied to distinguish different, but closely related, primate (e.g., human, ape, simian) foamy viruses as well as those from other hosts. This proposal accounts for host-virus co-speciation and cross-species transmission.

Summary Bundibugyo virus (BDBV) is one of four ebolaviruses known to cause disease in humans. Bundibugyo virus disease (BVD) outbreaks occurred in 2007–2008 in Bundibugyo District, Uganda, and in 2012 in Isiro, Province Orientale, Democratic Republic of the Congo. The 2012 BVD outbreak resulted in 38 laboratory-confirmed cases of human infection, 13 of whom died. However, only 4 BDBV specimens from the 2012 outbreak have been sequenced. Here, we provide BDBV sequences from seven additional patients. Analysis of the molecular epidemiology and evolutionary dynamics of the 2012 outbreak with these additional isolates challenges the current hypothesis that the outbreak was the result of a single spillover event. In addition, one patient record indicates that BDBV’s initial emergence in Isiro occurred 50 days earlier than previously accepted. Collectively, this work demonstrates how retrospective sequencing can be used to elucidate outbreak origins and provide epidemiological contexts to a medically relevant pathogen., Graphical abstract, Highlights In 2012, BDBV was circulating earlier than previously appreciated BDBV genomes from seven additional patients are sequenced Molecular analyses indicate that multiple spillover events fueled the BVD outbreak, Elucidation of the epidemiology underlying the 2012 Bundibugyo virus disease outbreak in the Democratic Republic of the Congo has been challenging. Hulseberg et al. acquire additional genomic and phylodynamic data indicating that multiple Bundibugyo virus spillover events, some of which occurred much earlier than previously known, contributed to the outbreak.

Ebola virus (EBOV) causes severe acute human disease with high lethality. Viremia is typical during the acute disease phase. However, EBOV RNA can remain detectable in immune-privileged tissues for prolonged periods of time after clearance from the blood, suggesting EBOV may persist during convalescence and thereafter. Eliminating persistent EBOV is important to ensure full recovery of survivors and decrease the risk of outbreak re-ignition caused by EBOV spread from apparently healthy survivors to naive contacts. Here, we review prior evidence of EBOV persistence and explore the tools needed for the development of model systems to understand persistence.

Ebolaviruses are emerging pathogens that cause severe and often fatal viral hemorrhagic fevers. Four distinct ebolaviruses are known to cause Ebola virus disease in humans. The ebolavirus envelope glycoprotein (GP1,2) is heavily glycosylated, but the precise glycosylation patterns of ebolaviruses are largely unknown. Here we demonstrate that approximately 50 different N-glycan structures are present in GP1,2 derived from the four pathogenic ebolaviruses, including high mannose, hybrid, and bi-, tri-, and tetra-antennary complex glycans with and without fucose and sialic acid. The overall N-glycan composition is similar between the different ebolavirus GP1,2s. In contrast, the amount and type of O-glycan structures varies widely between ebolavirus GP1,2s. Notably, this O-glycan dissimilarity is also present between two variants of Ebola virus, the original Yambuku variant and the Makona variant responsible for the most recent Western African epidemic. The data presented here should serve as the foundation for future ebolaviral entry and immunogenicity studies.

We discuss the progress in the calculation of the high-order electroweak radiative corrections to high-energy processes.

Several mammarenaviruses, chiefly Lassa virus (LASV) in Western Africa and Junin virus (JUNV) in the Argentine Pampas, cause severe disease in humans and pose important public health problems in their endemic regions. Moreover, mounting evidence indicates that the worldwide-distributed mammarenavirus lymphocytic choriomeningitis virus (LCMV) is a neglected human pathogen of clinical significance. The lack of licensed mammarenavirus vaccines and partial efficacy of current anti-mammarenavirus therapy limited to an off-label use of the nucleoside analog ribavirin underscore an unmet need for novel therapeutics to combat human pathogenic mammarenavirus infections. This task can be facilitated by the implementation of “drug repurposing” strategies to reduce the time and resources required to advance identified antiviral drug candidates into the clinic. We screened a drug repurposing library of 11,968 compounds (Repurposing, Focused Rescue and Accelerated Medchem [ReFRAME]) and identified several potent inhibitors of LCMV multiplication that had also strong anti-viral activity against LASV and JUNV. Our findings indicate that enzymes of the rate-limiting steps of pyrimidine and purine biosynthesis, the pro-viral MCL1 apoptosis regulator, BCL2 family member protein and the mitochondrial electron transport complex III, play critical roles in the completion of the mammarenavirus life cycle, suggesting they represent potential druggable targets to counter human pathogenic mammarenavirus infections.

The early events in Crimean–Congo hemorrhagic fever virus (CCHFV) have not been completely characterized. Earlier work indicated that CCHFV likely enters cells by clathrin-mediated endocytosis (CME). Here we provide confirmatory evidence for CME entry by showing that CCHFV infection is inhibited in cells treated with Pitstop 2, a drug that specifically and reversibly interferes with the dynamics of clathrin-coated pits. Additionally, we show that CCHFV infection is inhibited by siRNA depletion of the clathrin pit associated protein AP-2. Following CME entry, we show that CCHFV has a pH-dependent entry step, with virus inactivation occurring at pH 6.0 and below. To more precisely define the endosomal trafficking of CCHFV, we show for the first time that overexpression of the dominant negative forms of Rab5 protein but not Rab7 protein inhibits CCHFV infection. These results indicate that CCHFV likely enters cells through the early endosomal compartment.

The analytic result for the singlet part of the Adler function of the vector current in a general gauge theory is presented in five-loop approximation. Comparing this result with the corresponding singlet part of the Gross-Llewellyn Smith sum rule (Baikov et al., 2010 [1] ), we successfully demonstrate the validity of the generalized Crewther relation for the singlet part. This provides a non-trivial test of both our calculations and the generalized Crewther relation. Combining the result with the already available non-singlet part of the Adler function (Baikov et al., 2008 [2] , Baikov et al., 2010 [3] ) we arrive at the complete O ( α s 4 ) expression for the Adler function and, as a direct consequence, at the complete O ( α s 4 ) correction to the e + e − annihilation into hadrons in a general gauge theory.

Reverse-genetics systems are powerful tools enabling researchers to study the replication cycle of RNA viruses, including filoviruses and other hemorrhagic fever viruses, as well as to discover new antivirals. They include full-length clone systems as well as a number of life cycle modeling systems. Full-length clone systems allow for the generation of infectious, recombinant viruses, and thus are an important tool for studying the virus replication cycle in its entirety. In contrast, life cycle modeling systems such as minigenome and transcription and replication competent virus-like particle systems can be used to simulate and dissect parts of the virus life cycle outside of containment facilities. Minigenome systems are used to model viral genome replication and transcription, whereas transcription and replication competent virus-like particle systems also model morphogenesis and budding as well as infection of target cells. As such, these modeling systems have tremendous potential to further the discovery and screening of new antivirals targeting hemorrhagic fever viruses. This review provides an overview of currently established reverse genetics systems for hemorrhagic fever-causing negative-sense RNA viruses, with a particular emphasis on filoviruses, and the potential application of these systems for antiviral research.

Crimean-Congo hemorrhagic fever (CCHF) is a tick-borne disease caused by CCHF virus (CCHFV), a nairovirus in the family Bunyaviridae. CCHF occurs sporadically in a number of countries in Asia, the Middle East, southeastern Europe and Africa. Patients may develop subclinical to severe hemorrhagic disease, with fatal outcomes in a substantial percentage of cases. Transmission usually occurs through contact with viremic livestock or patients or bites by infected ticks. The number of reported cases has increased in recent years, possibly due to global climatic change and human perturbations of biocenoses that may have led to the migration of tick vectors. There is currently no FDA-approved vaccine or specific antiviral therapy for CCHF. The classification of CCHFV as a WHO Risk Group IV pathogen and the lack of suitable animal models has caused progress in developing new prophylactic and therapeutic measures to be slow. Ribavirin is active against CCHFV in vitro, but its efficacy for human therapy has not been definitively demonstrated by clinical studies. CCHF-immunoglobulin is also in use, but without clear evidence of efficacy. In this article, we review the development of prophylaxis and therapy for CCHF and discuss future prospects for vaccine and drug development.

Summary Sexual transmission of filoviruses was first reported in 1968 after an outbreak of Marburg virus (MARV) disease and recently caused flare-ups of Ebola virus disease in the 2013–2016 outbreak. How filoviruses establish testicular persistence and are shed in semen remain unknown. We discovered that persistent MARV infection of seminiferous tubules, an immune-privileged site that harbors sperm production, is a relatively common event in crab-eating macaques that survived infection after antiviral treatment. Persistence triggers severe testicular damage, including spermatogenic cell depletion and inflammatory cell invasion. MARV mainly persists in Sertoli cells, leading to breakdown of the blood-testis barrier formed by inter-Sertoli cell tight junctions. This disruption is accompanied by local infiltration of immunosuppressive CD4+Foxp3+ regulatory T cells. Our study elucidates cellular events associated with testicular persistence that may promote sexual transmission of filoviruses and suggests that targeting immunosuppression may be warranted to clear filovirus persistence in damaged immune-privileged sites.

The current status of the Adler function and two closely related Deep Inelastic Scattering (DIS) sum rules, namely, the Bjorken sum rule for polarized DIS and the Gross-Llewellyn Smith sum rule are briefly reviewed. A new result is presented: an analytical calculation of the coefficient function of the latter sum rule in a generic gauge theory in order O(alpha_s^4). It is demonstrated that the corresponding Crewther relation allows to fix two of three colour structures in the O(alpha_s^4) contribution to the singlet part of the Adler function., Comment: Talk presented at 10-th DESY Workshop on Elementary Particle Theory: Loops and Legs in Quantum Field Theory, W\"orlitz, Germany, 25-30 April 2010

We report on some technical aspects of our calculation of α s 4 corrections to R ( s ) and the semi-leptonic τ decay width [P.A. Baikov, K.G. Chetyrkin and J.H. Kuhn, Phys. Rev. Lett. 101 (2008) 012002, 0801.1821 ; P.A. Baikov, K.G. Chetyrkin and J.H. Kuhn, PoS RADCOR2007 (2007) 023, 0810.4048 ; P.A. Baikov, K.G. Chetyrkin and J.H. Kuhn, Nucl. Phys. Proc. Suppl. 135 (2004) 243]. We discuss the inner structure of the result as well as the issue of its correctness. We demonstrate recently appeared independent evidence positively testing one of two components of our full result.

Objective. Deep brain stimulation (DBS) increasingly attracts attention as a potential treatment of mental disorders. Beside depression and obsessive–compulsive disorders, DBS has already been shown to be beneficial for Tourette syndrome (TS). Clinical Presentation/Method. The authors report on the outcome of a patient with treatment-resistant TS who underwent bilateral DBS of the nucleus accumbens and the internal capsule. Results. Within the 10-month follow-up, a substantial reduction of tics has been observed. Yet, as a side-effect of DBS, the patient developed a transient manic-like episode when primarily stimulated by the most proximally contact in the internal capsule. Conclusions. This case supports the hypothesis that DBS of the nucleus accumbens and the internal capsule represents an effective therapeutic alternative for otherwise treatment-resistant TS. Yet, future controlled studies are needed to determine optimal stimulation parameters and to reduce negative side-effects such as transient hypomanic episodes.

A partial-wave analysis of the reaction π − p → η η π − p at 18 GeV/c has been performed on a data sample of approximately 4000 events obtained by Brookhaven experiment E852. The J P C = 0 − + π ( 1800 ) state is observed in the a 0 ( 980 ) η and f 0 ( 1500 ) π decay modes. It has a mass of 1876 ± 18 ± 16 MeV / c 2 and a width of 221 ± 26 ± 38 MeV / c 2 . The J P C = 2 − + π 2 ( 1880 ) meson is observed decaying through a 2 ( 1320 ) η . It has a mass of 1929 ± 24 ± 18 MeV / c 2 and a width of 323 ± 87 ± 43 MeV / c 2 . Both states are potential candidates for non-exotic hybrid mesons.

The exclusive reaction π − p → η π 0 n , η → π + π − π 0 at 18 GeV / c has been studied with a partial wave analysis on a sample of 23 492 η π 0 n events from BNL experiment E852. A mass-dependent fit is consistent with a resonant hypothesis for the P + wave, thus providing evidence for a neutral exotic meson with J P C = 1 − + , a mass of 1257 ± 20 ± 25 MeV / c 2 , and a width of 354 ± 64 ± 60 MeV / c 2 . New interpretations of the meson exotics in neutral η π 0 system observed in E852 and Crystal Barrel experiments are discussed.

The cellular receptor for human coronavirus NL63 (HCoV-NL63), a group I coronavirus, is angiotensin-converting enzyme2 (ACE2). ACE2 is also the receptor for the SARS coronavirus (SARS-CoV), a group II coronavirus. Here we describe the ability of HCoV-NL63 to utilize a number of ACE2 variants previously characterized as SARS-CoV receptors. Several ACE2 variants that reduced SARS-CoV S-protein association similarly reduced that of HCoV-NL63, whereas alteration of a number of solvent-exposed ACE2 residues did not interfere with binding by either S protein. One notable exception is ACE2 residue 354, at the boundary of the SARS-CoV binding site, whose alteration markedly inhibited utilization by the HCoV-NL63 but not SARS-CoV S proteins. In addition, the SARS-CoV S-protein receptor-binding domain inhibited entry mediated by the HCoV-NL63 S protein. These studies indicate that HCoV-NL63, like SARS-CoV, associates region of human ACE2 that includes a key loop formed by β-strands 4 and 5.

We report results for the virtual photon asymmetry A{sub 1} on the nucleon from new Jefferson Lab measurements. The experiment, which used the CEBAF Large Acceptance Spectrometer and longitudinally polarized proton ({sup 15}NH{sub 3}) and deuteron ({sup 15}ND{sub 3}) targets, collected data with a longitudinally polarized electron beam at energies between 1.6 GeV and 5.7 GeV. In the present paper, we concentrate on our results for A{sub 1}(x,Q{sup 2}) and the related ratio g{sub 1}/F{sub 1}(x,Q{sup 2}) in the resonance and the deep inelastic regions for our lowest and highest beam energies, covering a range in momentum transfer Q{sup 2} from 0.05 to 5.0 GeV{sup 2} and in final-state invariant mass W up to about 3 GeV. Our data show detailed structure in the resonance region, which leads to a strong Q{sup 2}--dependence of A{sub 1}(x,Q{sup 2}) for W below 2 GeV. At higher W, a smooth approach to the scaling limit, established by earlier experiments, can be seen, but A{sub 1}(x,Q{sup 2}) is not strictly Q{sup 2}--independent. We add significantly to the world data set at high x, up to x = 0.6. Our data exceed the SU(6)-symmetric quark model expectation for both the proton and the deuteron whilemore » being consistent with a negative d-quark polarization up to our highest x. This data set should improve next-to-leading order (NLO) pQCD fits of the parton polarization distributions.« less

We report the results of the first complete QCD five-loop calculation, viz. analytical contribution of order m q 2 α s 4 , to the (absorptive part of) the vacuum polarization function. The contribution directly leads to the knowledge of the the full O ( α s 4 m q 2 / s ) correction to the total cross-section of e+e− annihilation into hadrons. We compare our results with predictions following from various optimization schemes.

We give a short presentation of the first genuine QCD five-loop calculations, viz. analytical contributions of order αs4nf2 and mq2αs4nf2 to the vacuum polarization function of vector currents. These corrections form an important gauge-invariant subset of the full O(αs4) correction to e+e− annihilation into hadrons.

New measurements of peripheral meson production are presented. The data confirm the existence of exotic mesons at 1.4 and 1.6 GeV/c2. The latter state dominates the eta'pi- decay spectrum. The data on eta pi+pi-pi- decay show large strength in several exotic (Jpc = 1- +) waves as well.

The total cross section for the production of massive quarks in electron–positron annihilation can be predicted in perturbative QCD. After expansion in m 2 /s the quartic terms, i.e., those proportional to m 4 /s 2 , are calculated up to order α s 3 for vector and axial current induced rates. Predictions relevant for charm, bottom and top quarks production are presented. The α s 3 corrections are shown to be comparable to terms of order α s and α s 2 . As a consequence, the predictions exhibit a sizeable dependence on the renormalization scale. The stability of the prediction is improved and, at the same time, the relative size of the large order terms decreases by replacing the running mass m (μ) with the scheme independent invariant one m . By combining these results with the prediction for massless case and the quadratic mass terms the cross section for massive quark production at electron–positron colliders is put under control in order α s 3 from the high energy region down to fairly low energies.

Brookhaven Experiment E852 is an experiment in meson spectroscopy configured to detect final states interactions of π − p collisions in search for meson states incompatible with the constituent quark model. A description of the experimental apparatus and a general overview of the latest results is given.

We analyze sum rules for the $\Upsilon$ system with resummation of threshold effects on the basis of the nonrelativistic Coulomb approximation. We find for the pole mass of the bottom quark $m_b=4.75\pm 0.04 GeV$ and for the strong coupling constant $\al_s(M_Z)=0.118\pm 0.006$. The origin of the contradiction between two recent estimates obtained within the same formal framework is clarified.

In this paper the three-loop polarization functions \Pi(q^2) are calculated for the cases of an external vector, axial-vector, scalar or pseudo-scalar current. Results are presented for the imaginary part which directly leads to the cross section $\sigma(e^+e^- \to Z \to hadrons)$ and to the Higgs decay rates, respectively.

QCD corrections to the electron positron annihilation cross-section into hadrons and to the hadronic $Z$ boson decay rate are reviewed. Formal developments are introduced in a form particularly suited for practical applications. These include the operator product expansion, the heavy mass expansion, the decoupling of heavy quarks and matching conditions. Exact results for the quark mass depen- dence are presented whenever available, and formulae valid in the limit of small bottom mass ($m_{b}^2\ll s$) or of large top mass ($m_{t}^2\gg s$) are presen- ted. The differences between vector and axial vector induced rates as well the classification of singlet and nonsinglet rates are discussed. Handy formulae for all contributions are collected and their numerical relevance is investi- gated. Prescriptions for the separation of the total rate into partial rates are formulated. The applicability of the results in the low energy region, relevant for measurements around 10 GeV and below, is investigated and numerical predictions are collected for this energy region.

We present analytical calculation of the first seven moments of the heavy quark vacuum polarization function in the three-loop order. The obtained results are compared against the asymptotic formulas following from the threshold singularities. We also discuss the $\mu$ dependence of the moments within the BLM procedure.

Secondary radiation of hadrons from a tau pair produced in electron positron collisions may constitute an important obstacle for precision measurements of the production cross section and of branching ratios. The rate for real and virtual radiation is calculated and various distributions are presented. For Z decays a comprehensive analysis is performed which incorporates real and virtual radiation of leptons. The corresponding results are also given for primary electron and muon pairs. Compact analytical formulae are presented for entirely leptonic configurations. Measurements of $Z$ partial decay rates which eliminate all hadron and lepton radiation are about 0.3\% to 0.4\% lower than totally inclusive measurements, a consequence of the ${\cal O}(\alpha^2)$ negative virtual corrections which are enhanced by the third power of a large logarithm., Comment: 16 pages, LaTeX (18 uuencoded ps-figures included as an extra file) The complete paper, including figures, is also available via anonymous ftp at ftp://ttpux2.physik.uni-karlsruhe.de/ , or via www at http://ttpux2.physik.uni-karlsruhe.de/cgi-bin/preprints/

Electroweak radiative corrections for Γ(τ→ e ν e ν τ ) are calculated in the two Higgs doublet model. For a large ratio of vacuum expectation values and moderate mass splitting in the Higgs sector the ratio Γ(τ→ e ν e ν τ )m μ 5 /Γ μ m τ 5 is smaller than the result obtained in the minimal standard model by up to half a percent. The effect goes into the right direction, but is too small to explain the 2.5σ discrepancy between present experimental results for the τ lifetime and the predictions within the standard model. However, future experiments at a charm −τ or B meson factory may be sufficiently accurate to determine the τ lifetime to a precision of (2–3)%. This would allow to observe deviations from the predictions of the standard model induced by the two Higgs doublet model.

QCD corrections to the decay rate of the Z-boson are affected by the non-vanishing mass of the b-quark. Large logarithms of M 2 z m 2 b are absorbed through the use of the running b-quark mass. We analytically calculate the next-to-leading corrections to the axial part of the hadronic Z-decay rate in the order α 2 s m 2 b M 2 z . The corrections are found to be remarkably small.