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We use an alternative interpretation of quantum mechanics, based on the Bohmian trajectory approach, and show that the quantum effects can be included in the classical equation of motion via a conformal transformation on the background metric. We apply this method to the Robertson-Walker metric to derive a modified version of Friedmann's equations for a Universe consisting of scalar, spin-zero, massive particles. These modified equations include additional terms that result from the non-local nature of matter and appear as an acceleration in the expansion of the Universe. We see that the same effect may also be present in the case of an inhomogeneous expansion., Comment: Accepted for publication in ApJ

We use an alternative interpretation of quantum mechanics, based on the Bohmian trajectory approach, and show that the quantum effects can be included in the classical equation of motion via a conformal transformation on the background metric. We apply this method to the Robertson-Walker metric to derive a modified version of Friedmann's equations for a Universe consisting of scalar, spin-zero, massive particles. These modified equations include additional terms that result from the non-local nature of matter and appear as an acceleration in the expansion of the Universe. We see that the same effect may also be present in the case of an inhomogeneous expansion., Comment: Accepted for publication in ApJ

We use an alternative interpretation of quantum mechanics, based on the Bohmian trajectory approach, and show that the quantum effects can be included in the classical equation of motion via a conformal transformation on the background metric. We apply this method to the Robertson-Walker metric to derive a modified version of Friedmann's equations for a Universe consisting of scalar, spin-zero, massive particles. These modified equations include additional terms that result from the non-local nature of matter and appear as an acceleration in the expansion of the Universe. We see that the same effect may also be present in the case of an inhomogeneous expansion., Comment: Accepted for publication in ApJ

We use an alternative interpretation of quantum mechanics, based on the Bohmian trajectory approach, and show that the quantum effects can be included in the classical equation of motion via a conformal transformation on the background metric. We apply this method to the Robertson-Walker metric to derive a modified version of Friedmann's equations for a Universe consisting of scalar, spin-zero, massive particles. These modified equations include additional terms that result from the non-local nature of matter and appear as an acceleration in the expansion of the Universe. We see that the same effect may also be present in the case of an inhomogeneous expansion., Comment: Accepted for publication in ApJ

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(DLPS) 5571095.0156.026, http://name.umdl.umich.edu/5571095.0156.026, http://quod.lib.umich.edu/t/text/accesspolicy.html, Where applicable, subject to copyright. Other restrictions on distribution may apply. Please go to http://www.umdl.umich.edu/ for more information.

We have found a close correlation between viral stavudine (d4T) resistance and resistance to d4T-triphosphate at the human immunodeficiency virus type 1 reverse transcriptase (RT) level. RT from site-directed mutants with 69S-XX codon insertions and/or conventional zidovudine resistance mutations seems to be involved in an ATP-dependent resistance mechanism analogous to pyrophosphorolysis, whereas the mechanism for RT with the Q151M or V75T mutation appears to be independent of added ATP for reducing binding to d4T-triphosphate.

Using a large panel of human immunodeficiency virus type 1 site-directed mutants, we have observed a higher correlation than has previously been demonstrated between zidovudine (AZT)-triphosphate resistance data at the reverse transcriptase (RT) level and corresponding viral AZT resistance. This enhanced-resistance effect at the RT level was seen with ATP and to a lesser extent with PP(i) when ATP was added at physiological concentrations. The ATP-dependent mechanism (analogous to pyrophosphorolysis) appears to be dominant in the mutants bearing the D67N and K70R or 69 insertion mutations, whereas the Q151M mutation seems independent of ATP for decreased binding to AZT-triphosphate.

Objective: To assess the relationship between viral susceptibility at baseline and virological response in human immunodeficiency virus (HIV)-infected patients treated with multi-drug salvage regimens after multiple previous treatment failures. Design: Retrospective analysis of 50 patients from the Frankfurt HIV cohort who had received treatment with a minimum of six drugs, and for whom a sample for baseline viral phenotyping was available. Methods: Viral drug susceptibility was measured retrospectively from stored samples using the Antivirogram, a recombinant virus assay based method. Virological response was defined as a viral load of <400 copies/ml at week 24. For analysis of treatment response, drop-outs were dealt with in two ways, either as failures (DAF) or censored (DAC). Several logistical regression models were applied to identify predictors of response, including baseline virus load, number of new drugs and phenotypic sensitivity scores. Results: At baseline, drug resistance was extensive: 96% of patients had viruses resistant to at least one drug class and 32% had viruses resistant to all three drug classes. In the DAF analysis, 39 patients experienced virological failure. In the DAC analysis, eight were censored and 31 patients experienced virological failure. In multivariate models that adjust for baseline viral load, the number of new drugs and total phenotypic sensitivity scores, the baseline viral load and phenotypic sensitivity score remained significantly associated with virological outcome, whereas in those adjusted for baseline viral load, the number of new drugs, NRTI phenotypic sensitivity score and PI phenotypic sensitivity score, only the latter remained significantly associated with virological outcome. Both the DAF and DAC analyses produced similar results. In all models used, virological failure was shown to be significantly associated with baseline viral load and phenotypic sensitivity score. Conclusions: In this retrospective analysis b

The causative agent of AIDS the human immunodeficiency virus (HIV) encodes as part of its pol gene a reverse transcriptase (RT) which has a key role in the replication of the virus and thus constitutes an ideal target for antiviral chemotherapy. The purified HIV RT from virus particles consists of two related polypeptides of 66 and 51 kd mol. wt and similar polypeptides are found on expression of the complete HIV pol gene using prokaryotic systems. Here we describe the expression of the 66-kd protein in Escherichia coli and demonstrate that this polypeptide alone has authentic RT activity. Thus, a central HIV pol gene segment encodes and is sufficient for high levels of RT activity. The RT has been purified from E. coli extracts using a purification procedure involving two chromotography steps resulting in an enzyme preparation near homogeneity. Deletion of the C-terminal region of the RT thought to encode the RNase H domain resulted in loss of polymerase activity.