Abstract
Failure of highly active antiretroviral therapy to eradicate the human immunodeficiency virus (HIV), even in patients who suppress the virus to undetectable levels for many years, underscores the problems associated with fighting this infection. The existence of persistent infection in certain cellular and anatomical reservoirs appears to be the major hurdle in HIV eradication. The development of therapeutic interventions that eliminate or limit the latent viral pools or prevent the reemergence of the viruses from producing cells will therefore be required to enhance the effectiveness of current antiretroviral strategies. To achieve this goal, there is a pressing need to understand HIV latency at the molecular level to design novel and improved therapies to either eradicate HIV or find a functional cure in which patients could maintain a manageable viral pool without AIDS in the absence of antiretroviral therapy. The integrated proviral genome remains transcriptionally silent for a long period in certain subsets of T cells. This ability to infect cells latently helps HIV to establish a persistent infection despite strong humoral and cellular immune responses against the viral proteins. The main purpose of this report is to provide a general overview of the HIV latency. We will describe the hurdles being faced in eradicating latent HIV proviruses. We will also briefly discuss the ongoing strategies aimed toward curing HIV infection.
Highlights
The human immunodeficiency virus (HIV) was first discovered in 1981, and in the last 30 years, >30 million people have died from HIV infection and progression to acquired immunodeficiency syndrome (AIDS)
AIDS is the ultimate consequence of unchecked HIV infection, where the virus kills a sufficient amount of CD4+ T cells
The Karn group demonstrated the role of EZH2, a histone methylase and a component of polycomb group corepressor (PcG) complexes, in inducing repressive chromatin structures during HIV latency [87]. To further extend these studies, we found that Cpromoter binding factor 1 (CBF-1) is responsible for the recruitment of EZH2 and other chromatin-modifying enzymes of PcG complex to HIV long terminal repeat (LTR) (M Tyagi, manuscript in preparation)
Summary
The human immunodeficiency virus (HIV) was first discovered in 1981, and in the last 30 years, >30 million people have died from HIV infection and progression to acquired immunodeficiency syndrome (AIDS). Since 2004, great strides have been achieved primarily by increasing the access to anti-HIV drugs, improving the awareness regarding HIV and introducing various preventive measures These efforts produced clear results in the form of a reduced number of AIDS-related deaths and a proportional decrease in new infections in many parts of the world (World Health Organization report 2010 [5]). Despite global anti-HIV efforts and better availability of HAART, new HIV infections are outnumbering the patients initiating HAART [32,33,34] It remains an important priority of HIV research to precisely define the molecular mechanisms that allow the establishment of latency in T cells and subsequently design therapies to achieve either complete HIV eradication or some kind of functional cure, which will allow the immune system to maintain the upper hand and keep HIV replication below threshold levels in the absence of anti-HIV drugs/therapy
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