Abstract
Toll-like receptors (TLRs) recognize pathogen-associated molecular patterns and are essential components of the host’s innate immune response. The aim of this study was to determine the TLR9 genotype frequency and investigate the association between TLR9 polymorphisms and cytomegalovirus (CMV) DNAemia in human immunodeficiency virus (HIV)/CMV co-infected patients. A total of 205 HIV/CMV co-infected adults were screened for the presence of the four TLR9 polymorphisms (−1237T/C, −1486T/C, 1174G/A, and 2848C/T) by using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Mutation presented in at least one allele of the TLR9 2848C/T single nucleotide polymorphism (SNP) was associated with the occurrence of CMV DNAemia among HIV-infected patients with CMV co-infection (p = 0.004). The level of CMV DNA was higher in patients who were homozygous recessive or heterozygous for the 2848C/T polymorphism compared with those who had a wild-type genotype for this polymorphism (p = 0.005). Mutation detected in at least one allele of this SNP was also associated with a lower interferon type β (IFN-β) concentration (p = 0.048), while no relationships between TLR9 −1237T/C, −1486T/C, and 1174G/A SNPs and CMV DNAemia were observed. Our findings suggest that the mutation present in at least one allele of the TLR9 2848C/T SNP may be associated with the active CMV infection in HIV/CMV co-infected subjects.
Highlights
Human cytomegalovirus (CMV) is a member of the Herpesviridae family and is a leading cause of morbidity and mortality in immunocompromised hosts, including patients with AIDS, organ transplant recipients, and neonates [1,2,3]
The TLR9 −1237T/C, −1486T/C, 1174G/A, and 2848C/T single nucleotide polymorphism (SNP) were genotyped in 205 human immunodeficiency virus (HIV)/CMV co-infected patients
For the TLR9 2848C/T SNP, the genotype distribution was significantly different between the HIV/CMV co-infected patients with CMV DNAemia and in co-infected subjects without CMV DNA in blood samples
Summary
Human cytomegalovirus (CMV) is a member of the Herpesviridae family and is a leading cause of morbidity and mortality in immunocompromised hosts, including patients with AIDS, organ transplant recipients, and neonates [1,2,3]. CMV infection in immunocompromised patients may lead to various clinical manifestations, such as pneumonia, nephritis, hepatitis, gastroenteritis, or central nervous system disease of severe or even fatal course [4,5]. The identification of host molecular determinants of the innate immune response to viruses is critical to understanding the pathogenesis of HIV/CMV co-infection and developing novel therapeutic strategies. Toll-like receptors (TLRs) are a family of transmembrane proteins, which are essential components of the innate immune response to various bacterial, parasitic, and viral pathogens. TLR9 recognizes cytosinephosphate-guanosine (CpG) motifs in viral DNA and activates interferon regulatory factor
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