However, this observation does not completely explain why some babies are infected with HIV and others are not. In a landmark study, Gonzalez and colleagues (2005) showed that segmental duplication occured in the gene CCL3L1-like chemokine. CCL3L1 as well as CCL3 are ligands for CCR5 and are associate with lower susceptibility to HIV. Moreover, a study of maternal-infant HIV transmission has shown that a phenotype of deficient mitogen-induced CCL3 production is associated with a greater risk of HIV infection during labor and delivery. Thus the maternal-infant model has demonstrated that the protein encoded for one or both of the functional genes (CCL3 or CCL3L1) is involved, suggesting that the abundance of this protein may be important in HIV-protective immunity. Functional capacity, not just gene copies (four or more in some cases) of these proteins, is important. This suggests that the “susceptibility phenotype” lives at the level of induction of gene expression of CCL3 and CCL3L1, resulting in qualitative differences in protein production.

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