Deletion of the APOBEC3B gene strongly impacts susceptibility to falciparum malaria

Jha, Pankaj; Sinha, Swapnil; Kanchan, Kanika; Qidwai, Tabish; Narang, Ankita; Kumar, Pankaj; Pati, Sudhanshu S.; Mohanty, Sanjib; Mishra, Saroj K.; Sharma, Surya K.; Awasthi, Sanjay; Venkatesh, Vimala; Jain, Sanjeev; Basu, Analabha; Xu, Shuhua; Mukerji, Mitali; Habib, Saman

doi:10.1016/j.meegid.2011.11.001

Cited by 31 publications

(34 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Also, a study by Jha et al depicts a strong association of deletion allele with susceptibility to falciparum malaria in endemic regions [32], which was in corroboration with our study.…”

Section: Resultssupporting

confidence: 93%

“…The APOBEC3B deletion, which results in the loss of at least one copy of the unique coding portion of APOBEC3B, ranges in frequency from 0 to 43% in Indian populations with the lowest deletion frequency seen in populations inhabiting in malaria endemic regions of India [32]. This is the only human APOBEC3 protein with intrinsic anti-HIV-1 activity that is resistant to HIV-1 Vif [16,20,27,34].…”

Section: Resultsmentioning

confidence: 99%

“…Genotyping for the APOBEC3B variants was carried out using polymerase chain reaction (PCR) followed by gel electrophoresis analysis. The primer sequences for APOBEC3B (A3B) were: A3B (Deletion) sense 5′-TAGGTGCCACCCCGAT-3′ and antisense 5′-TTGAGCATAATCTTACTCTTGTAC -3′ and A3B (Insertion) sense 5′-TTGGTGCTGCCCCCTC -3 and antisense 5′-TAGAGACTGAGGCC-CAT-3′ [32,33]. Finally, the Insertion and Deletion reactions were performed separately in 20 μl volume containing 10 μl 2X PCR master mix (Fermentas, Vilnius, Lithuania), 0.1 mM of each primer and 100 ng of extracted DNA.…”

Section: Genotyping Of Apobec3b (A3b) Polymorphismmentioning

confidence: 99%

See 2 more Smart Citations

Association between Apolipoprotein B mRNA-editing Enzyme Catalytic Polypeptide-Like 3B (APOBEC3B) Deletion with HIV-1 Acquisition and AIDS among North Indian Population

Kakkar¹,

Sharma²,

Rathore³

et al. 2017

J AIDS Clin Res

View full text Add to dashboard Cite

“…Also, a study by Jha et al depicts a strong association of deletion allele with susceptibility to falciparum malaria in endemic regions [32], which was in corroboration with our study.…”

Section: Resultssupporting

confidence: 93%

Section: Resultsmentioning

confidence: 99%

Section: Genotyping Of Apobec3b (A3b) Polymorphismmentioning

confidence: 99%

See 1 more Smart Citation

Association between Apolipoprotein B mRNA-editing Enzyme Catalytic Polypeptide-Like 3B (APOBEC3B) Deletion with HIV-1 Acquisition and AIDS among North Indian Population

Kakkar¹,

Sharma²,

Rathore³

et al. 2017

J AIDS Clin Res

View full text Add to dashboard Cite

“…Analysis of the frequency distribution of selected SNPs and haplotypes of the THBS1 gene was carried out in the existing Indian Genome Variation Consortium (IGVC) panel II [25]. This panel consisted of 552 samples from 24 ethnically and linguistically diverse populations representing tribal, caste, and religious groups from different geographical regions of India.…”

Section: Populations and Study Subjectsmentioning

confidence: 99%

“…The case-control panel comprised existing patient and control samples collected from a P. falciparum hyper-to mesoendemic region (Antagarh, Chhattisgarh and Sundargarh, Orissa) and a non-endemic region (Lucknow and surrounding areas of Uttar Pradesh) of India, as described previously [4,25,27]. The control panel comprised individuals ethnically matched with the patient group; these belonged to the Bhumij, Munda, Oraon, and Gond tribal populations in the endemic region and the Aggarwal, Brahmin, Kayastha, Pasi, Thakur, Yadav, Shia, and Sunni caste and religious groups in the nonendemic region.…”

Section: Populations and Study Subjectsmentioning

confidence: 99%

Polymorphisms in host genes encoding NOSII, C-reactive protein, and adhesion molecules thrombospondin and E-selectin are risk factors for Plasmodium falciparum malaria in India

Kanchan

Pati

Mohanty

et al. 2015

Eur J Clin Microbiol Infect Dis

View full text Add to dashboard Cite

Cytoadherence of Plasmodium falciparum-infected red blood cells (RBCs) in host microvasculature and complex regulation of the immune response are important contributors to the clinical outcome of disease. We tested the association of 23 single nucleotide polymorphisms (SNPs) and a microsatellite repeat in adhesion molecule genes THBS1 and ESEL, and immune regulatory molecule genes NOSII, CRP, and MBL2 with falciparum malaria in populations residing in a malaria-endemic and a non-endemic region of India. The THBS1 haplotype CCCCA (rs1478604, rs7170682, rs2664141, rs12912082, rs3743125) was a risk factor in the endemic region (relative risk = 3.78) and an ESEL SNP (rs5368, His468Tyr) associated with cerebral malaria (CM) [CM vs. non-cerebral malaria (NCM), odds ratio (OR) = 2.23, p = 0.03]. In the non-endemic region, an ESEL 3'UTR SNP (rs5359) associated with enhanced risk of disease (OR = 3.62, p = 1 × 10(-4)) and the CT genotype of the CRP promoter SNP (C/T/A) strongly associated with protection (severe vs. control, OR = 0.29, p = 6 × 10(-5)). Long repeat alleles of the NOSII promoter microsatellite (CCTTT)n exhibited strong association with protection and the NOSII ATG haplotype (rs3729508, rs2297520, rs9282801) was strongly protective against severe malaria in both regions (endemic, severe vs. control, OR = 0.05, p = 0.0001; non-endemic, severe vs. control, OR = 0.3, p = 1 × 10(-5)). Our results suggest differential contribution of variants of the investigated genes in determining the outcome of malaria in Indian populations.

show abstract

Epstein–Barr virus and malaria upregulate AID and APOBEC3 enzymes, but only AID seems to play a major mutagenic role in Burkitt lymphoma

et al. 2022

View full text Add to dashboard Cite

Endemic Burkitt lymphoma (eBL) is characterized by an oncogenic IGH/c-MYC translocation and Epstein-Barr virus (EBV) positivity, and is epidemiologically linked to Plasmodium falciparum malaria. Both EBV and malaria are thought to contribute to eBL by inducing the expression of activation-induced cytidine deaminase (AID), an enzyme involved in the IGH/c-MYC translocation. AID/apolipoprotein B mRNA editing catalytic polypeptidelike (AID/APOBEC) family enzymes have recently emerged as potent mutagenic sources in a variety of cancers, but apart from AID, their involvement in eBL and their regulation by EBV and P. falciparum is unknown. Here, we show that upon inoculation with EBV, human B cells strongly upregulate the expression of enzymatically active APOBEC3B and APOBEC3G. In addition, we found significantly increased levels of APOBEC3A in B cells of malaria patients, which correlated with parasite load. Interestingly, despite the fact that APOBEC3A, APOBEC3B, and APOBEC3G caused c-MYC mutations when overexpressed in HEK293T cells, a mutational enrichment in eBL tumors was only detected in AID motifs. This suggests that even though the EBV-and P. falciparum-directed immune response triggers the expression and activity of several AID/APOBEC members, only the upregulation of AID has oncogenic consequences, while the induction of the APOBEC3 subfamily may primarily have immunoprotective functions.

show abstract

Deletion of the APOBEC3B gene strongly impacts susceptibility to falciparum malaria

Cited by 31 publications

References 35 publications

Association between Apolipoprotein B mRNA-editing Enzyme Catalytic Polypeptide-Like 3B (APOBEC3B) Deletion with HIV-1 Acquisition and AIDS among North Indian Population

Association between Apolipoprotein B mRNA-editing Enzyme Catalytic Polypeptide-Like 3B (APOBEC3B) Deletion with HIV-1 Acquisition and AIDS among North Indian Population

Polymorphisms in host genes encoding NOSII, C-reactive protein, and adhesion molecules thrombospondin and E-selectin are risk factors for Plasmodium falciparum malaria in India

Epstein–Barr virus and malaria upregulate AID and APOBEC3 enzymes, but only AID seems to play a major mutagenic role in Burkitt lymphoma

Contact Info

Product

Resources

About