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DOI 10.1089/aid.2019.0038

Медицинская библиотека · AIDS research and human retroviruses · 2019

Short Communication: The Association of WNT16 Polymorphisms with the CD4+ T Cell Count in the HIV-Infected Population.

Xie Li, Huang Yiyong, Zhong Jianing, Wei Huiping, Chen Siyuan, Jiang Kongmei, Li Shan, Qin Xue

СтатьяПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

WNT16 is one of the 19 members of the human Wnt gene family, and it plays a positive role in lymphocyte proliferation. We investigated the possible association of WNT16 rs3801385 and rs2707466 with the CD4+ T cell count among the HIV-infected population in Guangxi, China. A total of 93 HIV-1-infected patients aged 20-75 years were separated into a CD4+ T cell count ≥200/mm3 group (60 cases) and a <200/mm3 group (33 cases), and 76 healthy subjects were selected as the control group. All patients have not received any antiretroviral treatment. Direct sequencing was used to detect two functional WNT16 polymorphisms. After adjusting for age and gender, our results showed that rs2707466 A alleles and combined GA+AA genotypes were associated with a CD4+ T cell count maintained ≥200/mm3 in the context of HIV infections compared with the control group (odds ratio [OR] = 2.22, 95% confidence interval [CI]: 1.10-4.48, p = .026, and OR = 2.33, 95% CI: 1.03-5.29, p = .044, respectively). When stratified by viral load, this positive association was significantly strengthened in the viral load group of <20 copies/mL. In contrast, there was no significant difference in any genotype and allele of rs3801385 between the patients and healthy controls. In conclusion, the results suggest that the rs2707466 A allele may have a positive effect on maintaining the CD4+ T cell count in HIV-infected individuals.

Для цитирования: Xie Li, Huang Yiyong, Zhong Jianing, Wei Huiping, Chen Siyuan, Jiang Kongmei, Li Shan, Qin Xue. Short Communication: The Association of WNT16 Polymorphisms with the CD4+ T Cell Count in the HIV-Infected Population.. AIDS research and human retroviruses. 2019. DOI: 10.1089/aid.2019.0038.

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