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There is a lot of hope for the treatment of the most dangerous virus, HIV. Millions of people could be stabilized by Anti-retroviral therapy (ART) in the future, it is just an access issue. On the contrary, there is little success in the ‘cure’ effort as of yet. We are committed to studying HIV reservoirs for a decade and some societies like the IAS have recently also focused on the topic.
With nearly 7000 new infections daily, the Human Immunodeficiency Virus (HIV) has been the main public health issue. Anti-retroviral Therapy has scarcely reduced the plasma viremia but there is only one report of an HIV infected individual who has been treated and cured.
As the virus completely rebounds upon the interruption of treatment, thus the burden of lifelong ART in millions of patients across the world may not be sustainable.
For the past two decades, a lot of research has been done in this field. For example, vaccine development and designing of new anti-retrovirals to block HIV replication are the basic reasons for the research.
Persistent HIV
ART has been extremely effective with controlling viral replication in HIV infected individuals. Recent studies have demonstrated that intensified standard ART with an additional potent drug such as non-nucleoside reverse transcription inhibitors or lopinavir / ritonavir or atazananavir/ ritonavir, these do not reduce residual viremia. The activated CD4+ T cell are primarily infected by HIV and the infection of those cells quickly leads to cell death. The initial two phases of decay of viremia has long been assumed to originate first from activated CD4 cells, then from other cells such as macrophages. The final phase consists of a stable, low level of plasma viremia of 1-5 copies per ml with no measurable rate of decay.
Resting memory CD4 + T cell are relatively resistant to HIV infection due to the intrinsic resting phenotype of the cell. This results in lower efficiency of entry, that is (1 per millions contains a replication competent integrated genome) . However the reservoir is rapidly generated early in infection.
Nevertheless, patients who are stably suppressed on ART rarely develop resistance to anti-retroviral drugs. Plasma viremia stems from virus that has been released from an unidentified cell or clonal population of cell.
Mechanism of pro-viral latency
Numerous transcriptional and post- transcriptional blocks to HIV replication in resting CD4+ T cells has been identified. For instance, low –level of NFAT, sequestration of NF-KB p 50-65 or of the positive transcription elongation factor (p-TEFB). Furthermore, virus that integrates into euchromatin be subject to transcriptional.
In addition to processing numerous blocks to replication, resting CD4+ T cells contribute to the persistence of HIV due to their intrinsic stability and processes of antigen-driven and homeostatic proliferation.
The memory subset includes central memory (TCM) cells, transitional memory (TTM) cells, effective memory cells and terminally differentiated memory cells. A recent study that examined the prevalence of HIV proviral DNA within these sub-populations observed that TCM cells posses the highest rate of latent HIV in patients with high CD4 counts.
Until recently, the research has primarily made use of cell-line models, humanized mouse models.
Several strategies as described in this contribution but no approach have been practical or successful. Developing the ability to eradicate established HIV infection will require prolong scientific commitment.
HIV Reservoirs Workshop
Since 2003 we organize every 2-year the reference workshop on HIV reservoirs in Saint Martin. In July 2010, the International AIDS Society (IAS) organized the first edition of the ‘Towards a Cure’ workshop dealing also with HIV reservoirs and HIV persistence. The interest manifested by the IAS to this topic is recognition of our long-term investment. The next saint Martin HIV reservoirs workshop is scheduled in December 2010.
