TY - JOUR
T1 - Elimination of infectious HIV DNA by CRISPR–Cas9
AU - Das, Atze T.
AU - Binda, Caroline S.
AU - Berkhout, Ben
N1 - Copyright © 2019. Published by Elsevier B.V.
PY - 2019/10
Y1 - 2019/10
N2 - Current antiretroviral drugs can efficiently block HIV replication and prevent transmission, but do not target the HIV provirus residing in cells that constitute the viral reservoir. Because drug therapy interruption will cause viral rebound from this reservoir, HIV-infected individuals face lifelong treatment. Therefore, novel therapeutic strategies are being investigated that aim to permanently inactivate the proviral DNA, which may lead to a cure. Multiple studies showed that CRISPR–Cas9 genome editing can be used to attack HIV DNA. Here, we will focus on not only how this endonuclease attack can trigger HIV provirus inactivation, but also how virus escape occurs and this can be prevented.
AB - Current antiretroviral drugs can efficiently block HIV replication and prevent transmission, but do not target the HIV provirus residing in cells that constitute the viral reservoir. Because drug therapy interruption will cause viral rebound from this reservoir, HIV-infected individuals face lifelong treatment. Therefore, novel therapeutic strategies are being investigated that aim to permanently inactivate the proviral DNA, which may lead to a cure. Multiple studies showed that CRISPR–Cas9 genome editing can be used to attack HIV DNA. Here, we will focus on not only how this endonuclease attack can trigger HIV provirus inactivation, but also how virus escape occurs and this can be prevented.
UR - https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85070945593&origin=inward
UR - https://www.ncbi.nlm.nih.gov/pubmed/31450074
U2 - https://doi.org/10.1016/j.coviro.2019.07.001
DO - https://doi.org/10.1016/j.coviro.2019.07.001
M3 - Review article
C2 - 31450074
SN - 1879-6257
VL - 38
SP - 81
EP - 88
JO - Current opinion in virology
JF - Current opinion in virology
ER -