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filingDate 2021-02-12-04:00^^<http://www.w3.org/2001/XMLSchema#date>
inventor http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_4365857e32fc58089f41a1dcf46a6896
http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_840beac426febb52a8e19c60d129c5cd
publicationDate 2021-08-19-04:00^^<http://www.w3.org/2001/XMLSchema#date>
publicationNumber WO-2021163515-A1
titleOfInvention Crispr-cas9 mediated disruption of alcam gene inhibits adhesion and trans-endothelial migration of myeloid cells
abstract Migration of HIV- 1 infected monocytes across the endothelial barrier plays an essential role in establishing and maintenance of viral reservoir in the brain and leads to neuroinflammation, neuronal damage, and subsequent HIV-induced central nervous system (CNS) dysfunction. These processes continue despite antiretroviral therapy (ART) due to limited pharmacological permeability of the blood-brain barrier, the presence of residual viral replication, and the reactivation of latent viruses. Compositions comprising Clustered Regularly Interspaced Short Palindromic Repeat (CRISPR)-associated endonucleases targeted to activated leukocytes cell adhesion molecule (ALC AM/CD 166), chemotactic recruitment (CCR2/5), adhesion to the endothelium (ALC AM) and junctional diapedesis (JAM-A) achieves maximum repression of leukocyte transmigration and block of the spread of the virus to different tissues and organs.
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