@article{mbs:/content/journal/jgv/10.1099/vir.0.81709-0, author = "Meddows-Taylor, Stephen and Donninger, Samantha L. and Paximadis, Maria and Schramm, Diana B. and Anthony, Fiona S. and Gray, Glenda E. and Kuhn, Louise and Tiemessen, Caroline T.", title = "Reduced ability of newborns to produce CCL3 is associated with increased susceptibility to perinatal human immunodeficiency virus 1 transmission", journal= "Journal of General Virology", year = "2006", volume = "87", number = "7", pages = "2055-2065", doi = "https://doi.org/10.1099/vir.0.81709-0", url = "https://www.microbiologyresearch.org/content/journal/jgv/10.1099/vir.0.81709-0", publisher = "Microbiology Society", issn = "1465-2099", type = "Journal Article", abstract = "The role of CC chemokines in protection against mother-to-child human immunodeficiency virus type 1 (HIV-1) transmission is not well understood. It was observed that mitogen-induced production of CCL3 and CCL4 by cord-blood mononuclear cells was increased among infants born to HIV-positive compared with HIV-negative mothers, and that a deficiency in production of CCL3 was associated with increased susceptibility to intrapartum HIV-1 infection. CCL3-L1 gene copy number was associated with CCL3 production and with vertical transmission. However, at equivalent CCL3-L1 gene copy numbers, infants who acquired HIV-1 infection relative to their exposed but uninfected counterparts had lower production of CCL3, suggesting that they may harbour some non-functional copies of this gene. Nucleotide changes that may influence CCL3 production were evident in the CCL3 and CCL3-L1 genes upstream of exon 2. Our findings suggest that infants who display a deficient-production phenotype of CCL3 are at increased risk of acquiring HIV-1, indicating that this chemokine in particular plays an essential role in protective immunity.", }