Incoherent Noise and Quantum Information Processing

Incoherence in the controlled Hamiltonian is an important limitation on the precision of coherent control in quantum information processing. Incoherence can typically be modelled as a distribution of unitary processes arising from slowly varying experimental parameters. We show how it introduces artifacts in quantum process tomography and we explain how the resulting estimate of the superoperator may not be completely positive. We then go on to attack the inverse problem of extracting an effective distribution of unitaries that characterizes the incoherence via a perturbation theory analysis of the superoperator eigenvalue spectra.Comment: 15 pages, 5 figures, replaced with future JCP published versio

Quantum Process Tomography of the Quantum Fourier Transform

The results of quantum process tomography on a three-qubit nuclear magnetic resonance quantum information processor are presented, and shown to be consistent with a detailed model of the system-plus-apparatus used for the experiments. The quantum operation studied was the quantum Fourier transform, which is important in several quantum algorithms and poses a rigorous test for the precision of our recently-developed strongly modulating control fields. The results were analyzed in an attempt to decompose the implementation errors into coherent (overall systematic), incoherent (microscopically deterministic), and decoherent (microscopically random) components. This analysis yielded a superoperator consisting of a unitary part that was strongly correlated with the theoretically expected unitary superoperator of the quantum Fourier transform, an overall attenuation consistent with decoherence, and a residual portion that was not completely positive - although complete positivity is required for any quantum operation. By comparison with the results of computer simulations, the lack of complete positivity was shown to be largely a consequence of the incoherent errors during the quantum process tomography procedure. These simulations further showed that coherent, incoherent, and decoherent errors can often be identified by their distinctive effects on the spectrum of the overall superoperator. The gate fidelity of the experimentally determined superoperator was 0.64, while the correlation coefficient between experimentally determined superoperator and the simulated superoperator was 0.79; most of the discrepancies with the simulations could be explained by the cummulative effect of small errors in the single qubit gates.Comment: 26 pages, 17 figures, four tables; in press, Journal of Chemical Physic

Benchmarking quantum control methods on a 12-qubit system

In this letter, we present an experimental benchmark of operational control methods in quantum information processors extended up to 12 qubits. We implement universal control of this large Hilbert space using two complementary approaches and discuss their accuracy and scalability. Despite decoherence, we were able to reach a 12-coherence state (or 12-qubits pseudo-pure cat state), and decode it into an 11 qubit plus one qutrit labeled observable pseudo-pure state using liquid state nuclear magnetic resonance quantum information processors.Comment: 11 pages, 4 figures, to be published in PR

Spintronics and Quantum Dots for Quantum Computing and Quantum Communication

Control over electron-spin states, such as coherent manipulation, filtering and measurement promises access to new technologies in conventional as well as in quantum computation and quantum communication. We review our proposal of using electron spins in quantum confined structures as qubits and discuss the requirements for implementing a quantum computer. We describe several realizations of one- and two-qubit gates and of the read-in and read-out tasks. We discuss recently proposed schemes for using a single quantum dot as spin-filter and spin-memory device. Considering electronic EPR pairs needed for quantum communication we show that their spin entanglement can be detected in mesoscopic transport measurements using metallic as well as superconducting leads attached to the dots.Comment: Prepared for Fortschritte der Physik special issue, Experimental Proposals for Quantum Computation. 15 pages, 5 figures; typos corrected, references adde

Bidirectional lipid droplet velocities are controlled by differential binding strengths of HCV Core DII protein

Host cell lipid droplets (LD) are essential in the hepatitis C virus (HCV) life cycle and are targeted by the viral capsid core protein. Core-coated LDs accumulate in the perinuclear region and facilitate viral particle assembly, but it is unclear how mobility of these LDs is directed by core. Herein we used two-photon fluorescence, differential interference contrast imaging, and coherent anti-Stokes Raman scattering microscopies, to reveal novel core-mediated changes to LD dynamics. Expression of core protein’s lipid binding domain II (DII-core) induced slower LD speeds, but did not affect directionality of movement on microtubules. Modulating the LD binding strength of DII-core further impacted LD mobility, revealing the temporal effects of LD-bound DII-core. These results for DII-core coated LDs support a model for core-mediated LD localization that involves core slowing down the rate of movement of LDs until localization at the perinuclear region is accomplished where LD movement ceases. The guided localization of LDs by HCV core protein not only is essential to the viral life cycle but also poses an interesting target for the development of antiviral strategies against HCV

Analysis of hepatitis C virus RNA dimerization and core–RNA interactions

The core protein of hepatitis C virus (HCV) has been shown previously to act as a potent nucleic acid chaperone in vitro, promoting the dimerization of the 3′-untranslated region (3′-UTR) of the HCV genomic RNA, a process probably mediated by a small, highly conserved palindromic RNA motif, named DLS (dimer linkage sequence) [G. Cristofari, R. Ivanyi-Nagy, C. Gabus, S. Boulant, J. P. Lavergne, F. Penin and J. L. Darlix (2004) Nucleic Acids Res., 32, 2623–2631]. To investigate in depth HCV RNA dimerization, we generated a series of point mutations in the DLS region. We find that both the plus-strand 3′-UTR and the complementary minus-strand RNA can dimerize in the presence of core protein, while mutations in the DLS (among them a single point mutation that abolished RNA replication in a HCV subgenomic replicon system) completely abrogate dimerization. Structural probing of plus- and minus-strand RNAs, in their monomeric and dimeric forms, indicate that the DLS is the major if not the sole determinant of UTR RNA dimerization. Furthermore, the N-terminal basic amino acid clusters of core protein were found to be sufficient to induce dimerization, suggesting that they retain full RNA chaperone activity. These findings may have important consequences for understanding the HCV replicative cycle and the genetic variability of the virus

Trafficking of Hepatitis C Virus Core Protein during Virus Particle Assembly

Hepatitis C virus (HCV) core protein is directed to the surface of lipid droplets (LD), a step that is essential for infectious virus production. However, the process by which core is recruited from LD into nascent virus particles is not well understood. To investigate the kinetics of core trafficking, we developed methods to image functional core protein in live, virus-producing cells. During the peak of virus assembly, core formed polarized caps on large, immotile LDs, adjacent to putative sites of assembly. In addition, LD-independent, motile puncta of core were found to traffic along microtubules. Importantly, core was recruited from LDs into these puncta, and interaction between the viral NS2 and NS3-4A proteins was essential for this recruitment process. These data reveal new aspects of core trafficking and identify a novel role for viral nonstructural proteins in virus particle assembly

Requirement of cellular DDX3 for hepatitis C virus replication is unrelated to its interaction with the viral core protein

The cellular DEAD-box protein DDX3 was recently shown to be essential for hepatitis C virus (HCV) replication. Prior to that, we had reported that HCV core binds to DDX3 in yeast-two hybrid and transient transfection assays. Here, we confirm by co-immunoprecipitation that this interaction occurs in cells replicating the JFH1 virus. Consistent with this result, immunofluorescence staining of infected cells revealed a dramatic redistribution of cytoplasmic DDX3 by core protein to the virus assembly sites around lipid droplets. Given this close association of DDX3 with core and lipid droplets, and its involvement in virus replication, we investigated the importance of this host factor in the virus life cycle. Mutagenesis studies located a single amino acid in the N-terminal domain of JFH1 core that when changed to alanine significantly abrogated this interaction. Surprisingly, this mutation did not alter infectious virus production and RNA replication, indicating that the core–DDX3 interaction is dispensable in the HCV life cycle. Consistent with previous studies, siRNA-led knockdown of DDX3 lowered virus production and RNA replication levels of both WT JFH1 and the mutant virus unable to bind DDX3. Thus, our study shows for the first time that the requirement of DDX3 for HCV replication is unrelated to its interaction with the viral core protein

Direct Binding of a Hepatitis C Virus Inhibitor to the Viral Capsid Protein

Over 130 million people are infected chronically with hepatitis C virus (HCV), which, together with HBV, is the leading cause of liver disease. Novel small molecule inhibitors of Hepatitis C virus (HCV) are needed to complement or replace current treatments based on pegylated interferon and ribavirin, which are only partially successful and plagued with side-effects. Assembly of the virion is initiated by the oligomerization of core, the capsid protein, followed by the interaction with NS5A and other HCV proteins. By screening for inhibitors of core dimerization, we previously discovered peptides and drug-like compounds that disrupt interactions between core and other HCV proteins, NS3 and NS5A, and block HCV production. Here we report that a biotinylated derivative of SL209, a prototype small molecule inhibitor of core dimerization (IC50 of 2.80 µM) that inhibits HCV production with an EC50 of 3.20 µM, is capable of penetrating HCV-infected cells and tracking with core. Interaction between the inhibitors, core and other viral proteins was demonstrated by SL209–mediated affinity-isolation of HCV proteins from lysates of infected cells, or of the corresponding recombinant HCV proteins. SL209-like inhibitors of HCV core may form the basis of novel treatments of Hepatitis C in combination with other target-specific HCV drugs such as inhibitors of the NS3 protease, the NS5B polymerase, or the NS5A regulatory protein. More generally, our work supports the hypothesis that inhibitors of viral capsid formation might constitute a new class of potent antiviral agents, as was recently also shown for HIV capsid inhibitors