The mutation of Transportin 3 gene that causes limb girdle muscular dystrophy 1F induces protection against HIV-1 infection.
Sara Rodríguez-MoraFlore De WitJavier García-PerezMercedes BermejoMaría Rosa López-HuertasElena MateosPilar MartíSusana RochaLorena VigónFrauke ChristZeger DebyserJuan Jesus VilchezMayte CoirasJosé AlcamíPublished in: PLoS pathogens (2019)
The causative mutation responsible for limb girdle muscular dystrophy 1F (LGMD1F) is one heterozygous single nucleotide deletion in the stop codon of the nuclear import factor Transportin 3 gene (TNPO3). This mutation causes a carboxy-terminal extension of 15 amino acids, producing a protein of unknown function (TNPO3_mut) that is co-expressed with wild-type TNPO3 (TNPO3_wt). TNPO3 has been involved in the nuclear transport of serine/arginine-rich proteins such as splicing factors and also in HIV-1 infection through interaction with the viral integrase and capsid. We analyzed the effect of TNPO3_mut on HIV-1 infection using PBMCs from patients with LGMD1F infected ex vivo. HIV-1 infection was drastically impaired in these cells and viral integration was reduced 16-fold. No significant effects on viral reverse transcription and episomal 2-LTR circles were observed suggesting that the integration of HIV-1 genome was restricted. This is the second genetic defect described after CCR5Δ32 that shows strong resistance against HIV-1 infection.
Keyphrases
- muscular dystrophy
- antiretroviral therapy
- hiv infected
- human immunodeficiency virus
- hiv positive
- duchenne muscular dystrophy
- genome wide
- sars cov
- amino acid
- hiv aids
- copy number
- wild type
- induced apoptosis
- nitric oxide
- hepatitis c virus
- early onset
- transcription factor
- cell proliferation
- oxidative stress
- dna methylation
- small molecule
- regulatory t cells
- hiv testing
- protein protein
- protein kinase
- endoplasmic reticulum stress