Publications by authors named "V Thiers"
Viruses have evolved countless mechanisms to subvert and impair the host innate immune response. Measles virus (MeV), an enveloped, non-segmented, negative-strand RNA virus, alters the interferon response through different mechanisms, yet no viral protein has been described as directly targeting mitochondria. Among the crucial mitochondrial enzymes, 5'-aminolevulinate synthase (ALAS) is an enzyme that catalyzes the first step in heme biosynthesis, generating 5'-aminolevulinate from glycine and succinyl-CoA.
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- A specific genetic variation in the APOBEC3C enzyme, affecting a single amino acid (serine to isoleucine at position 188), is found in around 10% of African populations and significantly boosts the enzyme's ability to fight off HIV-1 and SIV.
- The study observed that this variant, APOBEC3CS188I, can edit the hepatitis B virus (HBV) both in lab cultures and in infected individuals.
- Utilizing next-generation sequencing, researchers discovered that this edited variant enhances activity in a specific DNA editing context (5'TpCpA to 5'TpTpA), marking a new understanding of the enzyme's function and potential implications for HBV and nuclear DNA.
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- APOBEC3 enzymes, particularly A3A and A3B, are significantly upregulated in patients with Systemic Lupus Erythematosus (SLE), especially during disease flares and with high levels of interferon-α (IFN-α).
- This upregulation, observed in a study of 57 SLE patients, was found in 14.9% of patients with a specific genetic polymorphism that enhances A3A, and it correlates with cellular DNA damage and low lymphocyte counts.
- The findings suggest that high levels of A3A and A3B may promote cell death and inflammation in SLE, indicating that targeting these enzymes might help alleviate symptoms and reduce the formation
Background: APOBEC1 (A1) enzymes are cytidine deaminases involved in RNA editing. In addition to this activity, a few A1 enzymes have been shown to be active on single stranded DNA. As two human ssDNA cytidine deaminases APOBEC3A (A3A), APOBEC3B (A3B) and related enzymes across the spectrum of placental mammals have been shown to introduce somatic mutations into nuclear DNA of cancer genomes, we explored the mutagenic threat of A1 cytidine deaminases to chromosomal DNA.
View Article and Find Full Text PDFNumerous human APOBEC3 cytidine deaminases have proven to be, inter alia, host cell restriction factors for retroviruses and hepadnaviruses. Although they can bind to genomic RNA and become encapsidated, they are only catalytically active on single-stranded DNA. As there are many cellular deoxyribonucleases (DNases), we hypothesized that a parallel could be struck between APOBEC3 and DNases.
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