Υπάρχει ζωή για τις βιβλιοθήκες μετά το Internet;

Περιέχει την περίληψηΜέσα στα πλαίσια της Κοινωνίας της Πληροφορίας οι βιβλιοθηκονόμοι διεκδικούν, άλλοτε πετυχημένα, άλλοτε όχι και τόσο, ένα πιο ενεργό και απαιτητικό ρόλο, προβάλλοντας το επιχείρημα πώς όσο μεγαλύτερη είναι η παραγωγή πληροφορίας και γνώσης και η παροχή πληροφόρησης τόσο mo απαιτητική είναι και η διαδικασία που αναγκάζεται να ακολουθήσει ο χρήστης ώστε να ικανοποιήσει τις ανάγκες του. Αλλά, η αναγκαιότητα του βιβλιοθηκονόμου (ως επιστήμονα της πληροφόρησης πλέον), του διαμεσολαβητή, δηλαδή, ανάμεσα στην πληροφορία και στον χρήστη, δικαιολογεί απαραιτήτως και την αναγκαιότητα για την ίδια τη Βιβλιοθήκη; Τεκμηριώνεται, δηλαδή, η ύπαρξη αυτού του οργανισμού ως μη κερδοσκοπικού, πολιτιστικού ιδρύματος που εξυπηρετεί όχι μόνο πληροφοριακές αλλά και ψυχαγωγικές, εκπαιδευτικές, κοινωνικοοικονομικές ανάγκες των επισκεπτών του; Και τότε, το έργο του βιβλιοθηκονόμου πώς προδιαγράφεται; Ποιο το περιεχόμενο και ο τρόπος της διαμεσολάβησης; Πρόκειται για σύνθεση ή μηχανιστική διάδοση της πληροφορίας; Αν η Πληροφορία διακινείται, στις μέρες μας κυρίως και πρωτίστως, με ηλεκτρονικά μέσα, τότε το αυτονόητο της ύπαρξης ενός απτού οικοδομήματος που στεγάζει την πληροφορία παύει να ισχύει και είτε πρέπει να καταλυθεί, είτε να εφευρεθεί από την αρχή, προσδίδοντας νέα επίκαιρα χαρακτηριστικά σε ένα αρχαιότατο κατασκεύασμα

Harnessing the CRISPR/Cas9 system to disrupt latent HIV-1 provirus.

Even though highly active anti-retroviral therapy is able to keep HIV-1 replication under control, the virus can lie in a dormant state within the host genome, known as a latent reservoir, and poses a threat to re-emerge at any time. However, novel technologies aimed at disrupting HIV-1 provirus may be capable of eradicating viral genomes from infected individuals. In this study, we showed the potential of the CRISPR/Cas9 system to edit the HIV-1 genome and block its expression. When LTR-targeting CRISPR/Cas9 components were transfected into HIV-1 LTR expression-dormant and -inducible T cells, a significant loss of LTR-driven expression was observed after stimulation. Sequence analysis confirmed that this CRISPR/Cas9 system efficiently cleaved and mutated LTR target sites. More importantly, this system was also able to remove internal viral genes from the host cell chromosome. Our results suggest that the CRISPR/Cas9 system may be a useful tool for curing HIV-1 infection

Identification of amino acids in the human tetherin transmembrane domain responsible for HIV-1 Vpu interaction and susceptibility.

Tetherin, also known as BST-2/CD317/HM1.24, is an antiviral cellular protein that inhibits the release of HIV-1 particles from infected cells. HIV-1 viral protein U (Vpu) is a specific antagonist of human tetherin that might contribute to the high virulence of HIV-1. In this study, we show that three amino acid residues (I34, L37, and L41) in the transmembrane (TM) domain of human tetherin are critical for the interaction with Vpu by using a live cell-based assay. We also found that the conservation of an additional amino acid at position 45 and two residues downstream of position 22, which are absent from monkey tetherins, are required for the antagonism by Vpu. Moreover, computer-assisted structural modeling and mutagenesis studies suggest that an alignment of these four amino acid residues (I34, L37, L41, and T45) on the same helical face in the TM domain is crucial for the Vpu-mediated antagonism of human tetherin. These results contribute to the molecular understanding of human tetherin-specific antagonism by HIV-1 Vpu

Protocol to isolate temperature-sensitive SARS-CoV-2 mutants and identify associated mutations

Summary: An inability to proliferate at high temperatures typically gives viruses an attenuated phenotype. Here, we present a protocol to obtain and isolate temperature-sensitive (TS) SARS-CoV-2 strains via 5-fluorouracile-induced mutagenesis. We describe steps for the induction of mutations in the wild-type virus and selection of TS clones. We then show how to identify the mutations associated with the TS phenotype, following forward and reverse genetics strategies.For complete details on the use and execution of this protocol, please refer to Yoshida et al. (2022).1 : Publisher’s note: Undertaking any experimental protocol requires adherence to local institutional guidelines for laboratory safety and ethics

Integrase-independent HIV-1 infection is augmented under conditions of DNA damage and produces a viral reservoir.

HIV-1 possesses a viral protein, integrase (IN), which is necessary for its efficient integration in target cells. However, it has been reported that an IN-defective HIV strain is still capable of integration. Here, we assessed the ability of wild type (WT) HIV-1 to establish infection in the presence of IN inhibitors. We observed a low, yet clear infection of inhibitor-incubated cells infected with WT HIV which was identical to cells infected with IN-deficient HIV, D64A. Furthermore, the IN-independent integration could be enhanced by the pretreatment of cells with DNA-damaging agents suggesting that integration is mediated by a DNA repair system. Moreover, significantly faster viral replication kinetics with augmented viral DNA integration was observed after infection in irradiated cells treated with IN inhibitor compared to nonirradiated cells. Altogether, our results suggest that HIV DNA has integration potential in the presence of an IN inhibitor and may serve as a virus reservoir

APOBEC1-Mediated Editing and Attenuation of Herpes Simplex Virus 1 DNA Indicate That Neurons Have an Antiviral Role during Herpes Simplex Encephalitis ▿ †

APOBEC1 (A1) is a cytidine deaminase involved in the regulation of lipids in the small intestine. Herpes simplex virus 1 (HSV-1) is a ubiquitous pathogen that is capable of infecting neurons in the brain, causing encephalitis. Here, we show that A1 is induced during encephalitis in neurons of rats infected with HSV-1. In cells stably expressing A1, HSV-1 infection resulted in significantly reduced virus replication compared to that in control cells. Infectivity could be restored to levels comparable to those observed for control cells if A1 expression was silenced by specific A1 short hairpin RNAs (shRNA). Moreover, cytidine deaminase activity appeared to be essential for this inhibition and led to an impaired accumulation of viral mRNA transcripts and DNA copy numbers. The sequencing of viral gene UL54 DNA, extracted from infected A1-expressing cells, revealed G-to-A and C-to-T transitions, indicating that A1 associates with HSV-1 DNA. Taken together, our results demonstrate a model in which A1 induction during encephalitis in neurons may aid in thwarting HSV-1 infection