Core Viewpoint - The article discusses the discovery and significance of the CCR5delta32 gene mutation, which provides resistance to HIV-1, and its evolutionary history, implications for gene editing, and potential medical applications [2][4][6]. Group 1: Discovery and Significance of CCR5delta32 - CCR5 was identified as a receptor for HIV-1, and the CCR5delta32 mutation provides natural resistance to the virus, found in about 1% of Caucasians [2][3]. - Timothy Ray Brown, known as the "Berlin Patient," was cured of HIV-1 through a bone marrow transplant from a donor with the CCR5delta32 mutation, highlighting the mutation's therapeutic potential [3][6]. - The mutation's presence in European populations but absence in African and East Asian populations raises questions about its evolutionary origins [4][6]. Group 2: Evolutionary History - Research indicates that the CCR5delta32 mutation originated over 6,700 years ago among nomadic groups in the Siberian steppe, with evidence found in ancient remains [4][8]. - The mutation underwent strong positive selection between 8,000 and 2,000 years ago, coinciding with significant population movements and the spread of pathogens [11][13]. - The study challenges traditional views that linked the mutation's prevalence to historical pandemics, suggesting a more complex evolutionary narrative [6][11]. Group 3: Implications for Gene Editing and Medicine - The CCR5delta32 mutation is associated with various diseases, including Alzheimer's and diabetes, raising concerns about the implications of gene editing targeting this mutation [13]. - The research emphasizes the need for caution in gene editing, as it may disrupt other genetic elements and the complex interactions within the human genome [13]. - Ancient DNA technology offers new avenues for understanding the genetic basis of complex diseases, potentially informing treatments beyond HIV-1 [13].