期刊
JOURNAL OF GENERAL VIROLOGY
卷 87, 期 -, 页码 2055-2065出版社
MICROBIOLOGY SOC
DOI: 10.1099/vir.0.81709-0
关键词
-
资金
- NICHD NIH HHS [R01 HD042402, R01 HD042402-03, R01 HD042402-02, R01 HD042402-05, R01 HD042402-04, R01 HD042402-01A1, HD 36177, HD 42402] Funding Source: Medline
- Wellcome Trust [076352] Funding Source: Medline
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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据