Abstract: The present invention relates to a new method for successfully inducing the mutation of cell chemokine receptor CCR5 gene into CCR5?32 deletion gene by using the CRISPR-Cas9 genome editing technique. CCR5 is an important co-receptor for entry of Human Immunodeficiency Virus (HIV) into human host cells. CCR5?32 deletion is a 32-bp deletion in CCR5 coding region, which results in change and premature termination in the sequence following the 185th amino acid. Biallelic homozygous deletion of CCR5?32 is naturally resistant to HIV infection, i.e., the people carrying this mutation can't be infected by HIV. The present invention uses both lentiviral packaging system and the CRISPR technique to induce CCR5?32 deletion. Due to the characteristics of a wide range of Lentivirus infection, the invention can be applied to cells such as bone marrow stem cells and CD4+ T cells and can be expected to be the therapeutic drug for HIV/AIDS infection or other diseases.

Abstract: The present invention relates to a new method for successfully inducing the mutation of cell chemokine receptor CCR5 gene into CCR5?32 deletion gene by using the CRISPR-Cas9 genome editing technique. CCR5 is an important co-receptor for entry of Human Immunodeficiency Virus (HIV) into human host cells. CCR5?32 deletion is a 32-bp deletion in CCR5 coding region, which results in change and premature termination in the sequence following the 185th amino acid. Biallelic homozygous deletion of CCR5?32 is naturally resistant to HIV infection, i.e., the people carrying this mutation can't be infected by HIV. The present invention uses both lentiviral packaging system and the CRISPR technique to induce CCR5?32 deletion. Due to the characteristics of a wide range of lentivirus infection, the invention can be applied to cells such as bone marrow stem cells and CD4+ T cells and can be expected to be the therapeutic drug for HIV/AIDS infection or other diseases.