title: Tactics used by HIV-1 to evade host innate, adaptive, and intrinsic immunities.
abstract: OBJECTIVE
  To review the mechanisms by which HIV evades different components of the host immune system.
  
  
  METHODS
  This review is based on data obtained from published articles from 1991 to 2012. To perform the PubMed literature search, the following key words were input: HIV and immune evasion.
  
  
  METHODS
  Articles containing information related to HIV immune evasion were selected.
  
  
  RESULTS
  Although HIV is able to induce vigorous antiviral immune responses, viral replication cannot be fully controlled, and neither pre-existing infected cells nor latent HIV infection can be completely eradicated. Like many other enveloped viruses, HIV can escape recognition by the innate and adaptive immune systems. Recent findings have demonstrated that HIV can also successfully evade host restriction factors, the components of intrinsic immune system, such as APOBEC3G (apolipoprotein B mRNA-editing enzyme, catalytic polypeptide-like 3G), TRIM5α (tripartite motif 5-α), tetherin, and SAMHD1 (SAM-domain HD-domain containing protein).
  
  
  CONCLUSIONS
  HIV immune evasion plays an important role in HIV pathogenesis. Fully understanding the tactics deployed by HIV to evade various components of the host immune systems will allow for the development of novel strategies aimed toward the prevention and cure of HIV/AIDS.
authors.affiliation: Key Laboratory of Medical Molecular Virology of Ministries of Education and Health, Shanghai Medical College and Institute of Medical Microbiology, Fudan University, Shanghai 200032, China.
authors.forename: Lu
authors.initials: L
authors.lastname: Lu
authors.forename: Fei
authors.initials: F
authors.lastname: Yu
authors.forename: Lan-Ying
authors.initials: LY
authors.lastname: DU
authors.forename: Wei
authors.initials: W
authors.lastname: Xu
authors.forename: Shi-Bo
authors.initials: SB
authors.lastname: Jiang
mesh_terms: D000071480:APOBEC-3G Deaminase; D056704:Adaptive Immunity; D057134:Antibodies, Neutralizing / Q000276:immunology; D015703:Antigens, CD / Q000502:physiology; D000090103:Antiviral Restriction Factors; D002352:Carrier Proteins / Q000502:physiology; D003165:Complement System Proteins / Q000276:immunology; D003564:Cytidine Deaminase / Q000502:physiology; D058851:GPI-Linked Proteins / Q000502:physiology; D015497:HIV-1 / Q000276:immunology*; D006801:Humans; D057131:Immune Evasion; D007694:Killer Cells, Natural / Q000276:immunology; D020559:Monomeric GTP-Binding Proteins / Q000502:physiology; D000076106:SAM Domain and HD Domain-Containing Protein 1; D000070584:Tripartite Motif Proteins; D044767:Ubiquitin-Protein Ligases; D000074010:Bone Marrow Stromal Antigen 2
chemical_list: D000071480:APOBEC-3G Deaminase; D057134:Antibodies, Neutralizing; D015703:Antigens, CD; D000090103:Antiviral Restriction Factors; D002352:Carrier Proteins; D003165:Complement System Proteins; D003564:Cytidine Deaminase; D058851:GPI-Linked Proteins; D020559:Monomeric GTP-Binding Proteins; D000076106:SAM Domain and HD Domain-Containing Protein 1; D000070584:Tripartite Motif Proteins; D044767:Ubiquitin-Protein Ligases; C094572:BST2 protein, human; D000074010:Bone Marrow Stromal Antigen 2; C477346:TRIM5 protein, human; C484280:SAMHD1 protein, human; C464924:APOBEC3G protein, human