SLC11A1 (rs3731865) polymorphism and susceptibility to visceral leishmaniasis in HIV-coinfected patients from Northeastern Brazil

• Published in: Parasitology research (1987) 2020-02, Vol.119 (2), p.491-499
• Main Authors: Barbosa Júnior, Walter Lins, Justo, Alda Maria, dos Santos, Ana Maria Aguiar, do Carmo, Rodrigo Feliciano, de Melo, Fábio Lopes, Vasconcelos, Luydson Richardson Silva, de Medeiros, Zulma Maria
• Format: Article
• Language: English
• Subjects: Acquired immune deficiency syndrome; Acquired Immunodeficiency Syndrome - epidemiology; Adult; AIDS; Analysis; Biomedical and Life Sciences; Biomedicine; Brazil - epidemiology; Cation Transport Proteins - genetics; CD4 antigen; CD4-Positive T-Lymphocytes - immunology; Cell number; Chemokine CCL1 - genetics; Chemokines; Chemokines, CC - genetics; Coinfection - epidemiology; Coinfection - genetics; Comorbidity; Disease susceptibility; Evolution; Female; Gene polymorphism; Genetic aspects; Genetic factors; Genetic markers; Genetic polymorphisms; Genetic Predisposition to Disease - genetics; Genetics; Genotype; Genotyping; HIV; HIV (Viruses); HIV patients; Human immunodeficiency virus; Humans; Immunology; Intercellular Signaling Peptides and Proteins - genetics; Interleukin 4; Interleukin-4 - genetics; Kala-azar; Leishmaniasis, Visceral - epidemiology; Lymphocytes T; Male; Medical Microbiology; Medical records; Medical research; Medicine, Experimental; Microbiology; Middle Aged; Nutritional status; Parasitic diseases; Patients; Peripheral blood; Phylogeny - Original Paper; Polymorphism; Polymorphism, Genetic - genetics; SLC11A1 gene; T cells; Therapeutic applications; Visceral leishmaniasis
• ISSN: 0932-0113; 1432-1955
• DOI: 10.1007/s00436-019-06596-0

Following the emergence of human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS), the number of visceral leishmaniasis-HIV (VL-HIV) coinfections has increased worldwide, mainly in Brazil. The development of clinical forms of VL can be influenced by nutritional status, age, and host genetic factors, which are important variables determining susceptibility to disease. There are no studies with a candidate gene approach assayed directly in the VL-HIV-coinfected population. Herein, we determined and analyzed the associations of SLC11A1 , LECT2 , CCL1 , CCL16 , and IL4 genetic polymorphisms with susceptibility to VL-HIV coinfection in Northeastern Brazil. We analyzed 309 DNA samples extracted from the peripheral blood of HIV patients, and clinical and hematological data were collected from medical records. The diagnosis of VL was confirmed in 110 out of 309 patients; genotyping was carried out by TaqMan assays afterwards. Our results confirmed the association between the SLC11A1 polymorphism (rs3731865) and VL-HIV coinfection ( p  = 0.0206, OR 1.8126, 95% CI 1.1050–2.9727). In addition, the SLC11A1 genotype GG ( p  = 0.0050, OR 3.0395, 95% CI 1.4065–6.5789) and CD4+ T lymphocyte count ( p  = 0.0030, OR 0.9980, 95% CI 0.9970–0.9990) were associated with VL-HIV coinfection in a multivariate model. The polymorphism of the SLC11A1 gene (rs3731865) was associated with VL-HIV coinfection, suggesting a possible genetic mechanism involved in the susceptibility to VL in HIV patients. This finding can suggest new therapeutic targets and genetic markers for the VL-HIV-coinfected population.