| Virus Name | Human immunodeficiency virus 2 |
| Virus Short Name | HIV2 |
| Order | Unassigned |
| Virus Family | Retroviridae |
| Virus Subfamily | Orthoretrovirinae |
| Genus | Lentivirus |
| Species | Human immunodeficiency virus 2 |
| Host | Vertebrates |
| Cell Tropism | CD4+ T cells, macrophages and dendritic cells |
| Associated Disease | Acquired immunodeficiency syndrome |
| Mode of Transmission | Sexual contact, blood, breast feeding |
| VIPR DB link | N.A. |
| ICTV DB link | https://talk.ictvonline.org/ictv-reports/ictv_9th_report/reverse-transcribing-dna-and-rna-viruses-2011/w/rt_viruses/161/retroviridae |
| Virus Host DB link | http://www.genome.jp/virushostdb/view/?virus_lineage=Retroviridae |
| Paper Title | CCR5-Restricted HIV Type 2 Variants from Long-Term Aviremic Individuals Are Less Sensitive to Inhibition by -Chemokines Than Low Pathogenic HIV Type 1 Variants |
| Author's Name | HETTY BLAAK, PATRICK H.M. BOERS, MARCHINA E. VAN DER ENDE, HANNEKE SCHUITEMAKER, and ALBERT D.M.E. OSTERHAUS |
| Journal Name | AIDS Research and Human Retroviruses |
| Pubmed ID | 18327978 |
| Abstract | Many HIV-2-infected individuals maintain low, often undetectable, viral loads for prolonged periods. Virus and/or host factors that contribute to this high level of virus control are largely unknown. Previously we demonstrated that HIV-2 variants from long-term aviremic individuals have relatively low replication kinetics in vitro in comparison to HIV-1 variants. We hypothesized that the relatively low replication rates of HIV-2 in vitro as well as the high level of virus control in vivo might be explained by HIV-2 replication being more sensitive to inhibitory host factors like beta-chemokines or other CD8+ T cell-derived factors than HIV-1 replication. To test this we determined the effect of exogenously added beta-chemokines and healthy donor CD8+ T cells on the in vitro virus production of HIV-2 and HIV-1 variants from long-term nonprogressors (LTNPs). Contrary to expectations, HIV-2 replication was inhibited less efficiently by RANTES and MIP-1alpha than HIV-1 replication. CD8+ T cells from 8 of 12 healthy donors reduced HIV replication minimally 2-fold. Interestingly, cells from five of these donors inhibited HIV-1 but hardly affected HIV-2 replication, while the reverse was observed for cells from one donor. For HIV-1, but not HIV-2, the magnitude of the antiviral effect of CD8+ T cells correlated with their effect on RANTES levels in culture supernatants. Our findings indicate that RANTES is a more important factor of CD8+ T cell-associated anti-HIV-1 activity than it is of HIV-2 activity and that the benign clinical course of HIV-2 infection is not due to enhanced beta-chemokine sensitivity of HIV-2 variants. |
| Used Model | CD8 T cells |
| DOI | 10.1089/aid.2007.0001 |
