The biological reason(s) behind persistent mother-to-child transmission (MTCT) of HIV (albeit at reduced rate compared to the preantiretroviral therapy era) in spite of the successful implementation of advanced control measures in many African countries remains a priority concern to many HIV/AIDS control programs. This may be partly due to differences in host immunogenetic factors in highly polymorphic regions of the human genome such as those encoding the killer-cell immunoglobulin-like receptor (KIR) molecules which modulate the activities of natural killer cells. The primary aim of this study was to determine the variants of KIR genes that may have a role to play in MTCT in a cohort of infants born to HIV-infected mothers in Yaoundé, Cameroon. We designed a cross-sectional study to molecularly determine the frequencies of 15 KIR genes in 14 HIV-exposed infected (HEI), 39 HIV-exposed/uninfected (HEU), and 27 HIV-unexposed/uninfected (HUU) infants using the sequence specific primer polymerase chain reaction (PCR-SSP) method. We found that all 15 KIR genes were present in our cohort. The frequency of KIR2DL1 was significantly higher in the unexposed (control) group than in the HIV-exposed group ( OR = 0.22 , P = 0.006 ). Stratifying analysis by infection status but focusing only on exposed infants revealed that KIR2DL5, KIR2DS1, and KIR2DS5 were significantly overrepresented among the HIV-exposed/uninfected compared to infected infants ( OR = 0.20 , P = 0.006 ). Similarly, the frequencies of KIR2DS1, KIR2DS5, and KIR2DL5 were significantly different between infants perinatally infected with HIV (HIV+ by 6 months of age) and HIV-negative infants. Our study demonstrates that KIR genes may have differential effects with regard to MTCT of HIV-1.
The Human Leucocyte Antigens (HLA) work in concert with other immune factors to modulate immunity to viral infections. Extensive variation has been reported in the genetic sequences and functions of classical HLA class I genes in many (mostly Western) populations, and several HLA associations with infectious disease outcomes have been reported. Little is known about their role in the susceptibility or resistance to hepatitis viruses in Central African populations. The aim of this study was to determine variants of two HLA class I genes (HLA-A and -C) in adults infected with hepatitis B (HBV)- or -C (HCV) virus in Cameroon. In this case-control study, a total of 169 unrelated adults comprising 68 HCV-infected, 38 HBV-infected and 63 uninfected (controls) individuals participated. Each consented participant was screened for HBV, HCV, and HIV infections and willingly donated a single blood sample for genomic DNA isolation and some clinical laboratory tests. HLA-A and HLA-C were genotyped using previously described sequence-based techniques (SBT). A total of 54 HLA alleles were identified in the study population (27 HLA-A and 27 HLA-C). HLA-A∗23:01 and HLA-C∗07:01 were the most common alleles with genotype frequencies of 31.4% and 29.3%, respectively. Hepatitis individuals were six times more likely to be HLA-A∗30:01 carriers than uninfected controls (OR = 6.30, p = 0.020 (HBV); OR = 6.21, p = 0.010 (HCV), respectively). Similarly, carriers of HLA-C∗17:01 were over-represented in the HBV-infected compared to the uninfected control group (21.9% vs. 6.4%, respectively) suggesting that this allele could play a role in the susceptibility to HBV infection. These findings demonstrate that carriers of HLA-A∗30:01 were over-represented in the hepatitis group compared to uninfected controls while HLA-C∗17:01 was completely absent in the HCV + group.
Background: HIV-exposed uninfected infants (HEU) experience appear more vulnerable to infections compared to their HIV-unexposed uninfected (HUU) peers, generally attributed to poor passive immunity acquired from the mother. This may be due to some genetic factors that could alter the immune system. We thus sought to determine the distribution of Killer Cells Immunoglobulin-Like Receptor (KIR) genes in HEU versus HUU, and study the association between KIR profiling and occurrence of infection-related hospitalization. Methods: A cohortstudy was conducted from May 2019 to April 2020 among HEU and HUU, followed-up at birth, week 6, 12, 24 and 48, in reference pediatric centers in Yaounde, Cameroon. Infant HIV status was determined, types of infections were analyzed, and 15 KIR genes were investigated using the sequence specific primer polymerase chain reaction (PCR-SSP) method. Rate of KIR genes and infection-related hospitalizations were compared in HEU versus HUU, with p<0.05 considered statistically significant. Results: In this cohort, a total of 19 infection-related hospitalizations occurred in 66 infants (14.81%, 04/27 HUU and 38.46%, 15/39 HEU, p=0.037), the majority occurring during the first 24 weeks of life: 10 (25.64%) HEU and 03 (11.11%) HUU, p=0.14. At week 48 (39 HEU and 27 HUU), the relative risk (RR) for infectionrelated hospitalizations was 2.42 (95% CI: 1.028 to 5.823) for HEU versus HUU, with aOR 3.59(95% CI: 1.037 to 12.448). Incidence of hospitalization was 3.2 (95% CI: 1.63 to 7.14) per 1002 infant-months among HEU versus 1.2 (95% CI: 0.57 to 3.60) in HUU, and RR was 2.22 (95% CI: 0.50 to 9.39). KIR2DL1 gene was significantly higher in HUU versus HEU (OR= 0.183, 95%CI: 0.053 to 0.629; p=0.003), and the absence of KIR2DL1 was significantly associated with infection-related hospitalization (p<0.001; OR=0.063; 95%CI: 0.017 to 0.229). Conclusion: Compared to HUU, the vulnerability of HEU is driving by KIR2DL1, indicating the protective role of this KIR against infection and hospitalizations.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.