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  • In comparison to the standard HPLC assay

    2022-05-27

    In comparison to the standard HPLC assay to detect LPV above or below 1,000 ng mL-1, the accuracy of the PIs-IC strip was 97.8 %, the sensitivity was 100% and the specificity was 97.1 %. This suggests that the PIs-IC strip test has the potential accurately to semi-quantify PI concentrations in plasma samples from HIV-infected patients. Adherence to ART can improve health and prolong the life of HIV-infected patients. However, non-adherence to antiretroviral drugs may lead individuals to be susceptible to opportunistic infections and to develop HIV drug-resistance strains. Due to its relative simplicity and ability to be used for high-throughput screening, the PIs-IC strip represents an attractive, alternative assay that could be applied to assess drug adherence and determine if specific interventions to improve adherence are needed. Also, the screening for the presence of PIs concentrations in plasma samples before and after assessing antiretroviral drug resistance may be useful to help determine the utility of performing the test and/or interpretation of drug resistance results. Studies have reported that PI-based ART treatment failure is associated with the presence of protease mutations [38,39]. For example, the V32I mutation results in relatively high-level darunavir (DRV) resistance [40]. Therefore, in terms of a further clinical application, this novel PIs-IC strip test may be useful for drug discovering of new PIs active against drug resistance strains by cloning of mutant strains derived from patients and screening for effective therapeutic PIs.
    Conclusion
    Acknowledgments
    Introduction Human Immunodeficiency virus type 1 (HIV-1) takes advantage of many host factors for its replication. Because of this intimate virus-host relationship, severing host functions essential for virus replication has become an attractive strategy for therapeutic intervention [1]. The advent of advanced Pepstatin A techniques like RNA interference (RNAi)-based [[2], [3], [4]] or CRISPR-based [5] genome-wide screens have resulted in the identification and/or characterization of over 800 host factors potentially required for HIV-1 replication with only a few confirming the specific requirement of these host factors by reconstitution experiments. Nonetheless, there are host proteins that restrict HIV-1 replication for which the virus ought to overcome, and precedents exist for the identification of such restrictive factors along with protein fragments that have strong HIV-1 restrictive activity [[6], [7], [8]]. The POZ/BTB and AT-hook-containing Zinc finger protein 1 (PATZ1) gene codes for four protein isoforms and belongs to the POZ and Zinc Finger (POK) family of transcriptional factors, involved in many biological processes like embryogenesis [9], senescence [10], T-cell development [11] and cancer [12]. Some members of the POK proteins including PATZ1 have been shown to be deeply involved in p53-dependent cellular processes and regulate p53-dependent genes [10,[13], [14], [15]]. Several reports [16,17] show that p53 itself plays different roles in HIV-1 infection including modulating viral cDNA synthesis [18]. Here, a carboxy-terminally truncated human PATZ1 was identified by cDNA expression cloning as a potent inhibitor of HIV-1 infection. Using RNAi-mediated knockdown and CRISPR-mediated knockout of PATZ1 gene we report for the first time that HIV-1 replication requires two isoforms of PATZ1 after viral entry and before the completion of viral cDNA synthesis and that this role of PATZ1 in HIV-1 infection is independent of p53 status.
    Materials and methods
    Results
    Discussion HIV-1 depends on many host factors in order to replicate. Here, we have demonstrated and validated the dependency of HIV-1 on cellular PATZ1 by first studying a mutant of PATZ1 that was isolated by our cDNA expression cloning, thus, making cDNA expression cloning not only suitable for finding restriction factors [6] but also host proteins required for HIV-1 infection. The finding that PATZ1 functions in HIV-1 infection after entry and before completion of viral cDNA synthesis for both HIV-1 (Fig. 2) and VSVG-pseudotyped HIV-1 vector (Fig. 3) resonates well with our VSVG-pseudotyped HIV-1 selection virus.