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Heterogeneous susceptibility of circulating SIV isolate capsids to HIV-interacting factors
- Source :
- Retrovirology, Retrovirology, BioMed Central, 2013, 10 (1), pp.77. ⟨10.1186/1742-4690-10-77⟩
- Publisher :
- Springer Nature
-
Abstract
- Background Many species of non-human primates in Africa are naturally infected by simian immunodeficiency viruses (SIV) and humans stand at the forefront of exposure to these viruses in Sub-Saharan Africa. Cross-species transmission and adaptation of SIV to humans have given rise to human immunodeficiency viruses (HIV-1 and HIV-2) on twelve accountable, independent occasions. However, the determinants contributing to a simian-to-human lasting transmission are not fully understood. Following entry, viral cores are released into the cytoplasm and become the principal target of host cellular factors. Here, we evaluated cellular factors likely to be involved in potential new SIV cross-species transmissions. We investigated the interactions of capsids from naturally circulating SIV isolates with both HIV-1 restricting (i.e. TRIM5 proteins) and facilitating (i.e. cyclophilin A and nucleopore-associated Nup358/RanBP2 and Nup153) factors in single-round infectivity assays that reproduce early stages of the viral life-cycle. Results We show that human TRIM5α is unlikely to prevent cross-species transmission of any SIV we tested and observed that the SIV CA-CypA interaction is a widespread but not a universal feature. Moreover, entry in the nucleus of different SIV appeared to follow pathways that do not necessarily recruit Nup358/RanBP2 or Nup153, and this regardless of their interaction with CypA. Nevertheless, we found that, like HIV-1, human-adapted HIV-2 infection was dependent on Nup358/RanBP2 and Nup153 interactions for optimal infection. Furthermore, we found that, unlike HIV CA, SIV CA did not require a direct interaction with the Cyp-like domain of Nup358/RanBP2 to carry out successful infection. Conclusions Circulating SIV present a variety of phenotypes with regard to CA-interacting restricting or facilitating factors. Altogether, we unveiled unidentified pathways for SIV CA, which could also be exploited by HIV in different cellular contexts, to drive entry into the nucleus. Our findings warrant a closer evaluation of other potential defenses against circulating SIV.
- Subjects :
- Lentiviral capsids
Pan troglodytes
Virus Integration
viruses
Cypa
Simian
Virus Replication
medicine.disease_cause
Cell Line
03 medical and health sciences
TRIM5α
Virology
medicine
Animals
Humans
[SDV.BBM]Life Sciences [q-bio]/Biochemistry, Molecular Biology
Nup153
Immunodeficiency
030304 developmental biology
Infectivity
0303 health sciences
biology
Research
030302 biochemistry & molecular biology
virus diseases
Simian immunodeficiency virus
biology.organism_classification
medicine.disease
Nup358/RanBP2
Phenotype
3. Good health
Infectious Diseases
SIV
Capsid
Viral replication
Host-Pathogen Interactions
HIV-2
Immunology
HIV-1
Capsid Proteins
Simian Immunodeficiency Virus
TRIMCyp
Subjects
Details
- Language :
- English
- ISSN :
- 17424690
- Volume :
- 10
- Issue :
- 1
- Database :
- OpenAIRE
- Journal :
- Retrovirology
- Accession number :
- edsair.doi.dedup.....b6e5bcaf5101b5e28ba86bd6339db323
- Full Text :
- https://doi.org/10.1186/1742-4690-10-77