Can HIV infection be eradicated through use of potent antiviral agents?
OBJECTIVE
This review focuses on recent advances in HIV research and therapy that seek to eradicate persistent HIV in patients on suppressive therapy.


RESULTS
The source of persistent HIV in patients on suppressive therapy is debated. Recent studies of treatment intensification have produced varied results: no reduction in low-level plasma viremia indicating the source of persistent viremia is long-lived HIV-infected cells that release HIV when activated and increase in episomal HIV DNA indicating active replication persists in some infected individuals on suppressive therapy. In addition, clonal HIV sequences found in plasma from patients on long-term suppressive therapy are rarely found in CD4+ memory T cells. These results indicate that persistent viremia may arise from several different sources. Recent studies emphasize the complexity of HIV latency. Current strategies for HIV eradication focus on compounds that activate viral transcription in memory CD4+ T cells by many routes, including inhibiting histone deacetylation and activating nuclear factor kappa B. Several compounds and combinations of these compounds appear to induce the expression of integrated HIV in different latency models.


CONCLUSIONS
The eradication of HIV requires the elimination of persistent HIV during suppressive therapy. Recent studies have focused on the source of persistent viremia, mechanisms of intracellular HIV latency, and reactivation of latent HIV. It remains to be seen whether alternative treatment strategies may be required to eradicate HIV.
Josefsson
Lina
L
Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Sweden.
Dahl
Viktor
V
Palmer
Sarah
S
D019380:Anti-HIV Agents / Q000494:pharmacology / Q000627:therapeutic use*; D023241:Antiretroviral Therapy, Highly Active / Q000379:methods; D015496:CD4-Positive T-Lymphocytes / Q000821:virology; D006678:HIV / Q000187:drug effects* / Q000235:genetics / Q000502:physiology; D015658:HIV Infections / Q000188:drug therapy* / Q000276:immunology / Q000821:virology; D006679:HIV Seropositivity / Q000188:drug therapy / Q000821:virology; D006801:Humans; D012367:RNA, Viral / Q000097:blood / Q000187:drug effects; D016176:T-Lymphocyte Subsets / Q000821:virology; D014766:Viremia / Q000188:drug therapy / Q000821:virology; D014775:Virus Activation; D017735:Virus Latency / Q000187:drug effects / Q000502:physiology; D014779:Virus Replication / Q000187:drug effects / Q000502:physiology
D019380:Anti-HIV Agents; D012367:RNA, Viral