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Scientists Find Potential Method to Deplete HIV Reservoirs
Human immunodeficiency virus (HIV) is the causative agent of acquired immunodeficiency syndrome (AIDS). HIV infects cells that are part of the immune system. The virus binds to CD4, a protein found on the surface of macrophages and helper T cells. Macrophages assist the immune system by ingesting foreign invaders and presenting antigen to the adaptive immune system. When a macrophage takes up an HIV particle, it can become infected, and pass the virus along to CD4+ T cells. Once HIV has infected a cell, its RNA genome is reverse transcribed into DNA. The DNA is then inserted into the host cell’s genome. This means that every time the host cell replicates, the viral genome is also replicated. While integrated in the host cell’s genome, the viral DNA is also transcribed into messenger RNA (mRNA) and translated into protein. This is how new viral particles are produced. The newly made viruses are then released from the host cell, without killing it, to infect new cells.

Antiretroviral is able to decrease HIV to undetectable levels in the bloodstream. However, once antiretroviral therapy is stopped, many patients experience a resurgence of viral load. Because the viral genome is integrated into the host cell’s DNA, it becomes a permanent part of the cell, unless some factor causes it to leave the genome. This means that even if viral RNA is not detectable in a patient’s blood, the patient is likely still infected. The viral genome integrated in the host cell DNA acts as a hidden reservoir for the virus. If the cell is not producing HIV proteins, it will not be targeted by the immune system for destruction, allowing the virus to live on indefinitely in the host. In addition, because antiretroviral therapies block replication of the actual virus, they will not be able to remove the integrated viral genome form cellular DNA.

Scientists had previously discovered a protein found in cells called SAMHD-1 that is able to prevent HIV replication. Strangely, though, the protein did not seem to function in macrophages, which can act as a reservoir for HIV. Researchers from the University of Rochester School of Medicine and Dentistry in Rochester, New York, recently used mass spectrometry to determine if different variations existed of the SAMHD-1 protein. Indeed, they found that SAMHD-1 can either be phosphorylated or unphosphorylated. The phosphorylated version of SAMHD-1 is present when the immune cell is replicating. This state also permits HIV replication, as would be expected. Actively replicating immune cells allow more efficient replication of HIV particles. The unphosphorylated form of SAMHD-1 is present in non-replicating immune cells. This state of SAMHD-1 seems to block HIV replication.

The researchers propose that preventing phosphorylation of SAMHD-1 would prevent HIV replication, and prevent viral reservoirs from being reactivated and repopulating the patient. If therapy preventing SAMHD-1 phosphorylation was administered early during infection for a short time, it might be able to prevent HIV from forming reservoirs in macrophages. This would be a method to prevent the patient from developing chronic HIV infection. However, long term blockade of SAMHD-1 may be problematic for HIV patients. If SAMHD-1 is indeed involved in allowing immune cells to replicate, then preventing the protein from functioning would also prevent strong immune responses from developing. This would leave the patient in an immunocompromised state, which is the end result of HIV infection.

The balance of immune activation during HIV infection has indeed been problematic for researchers trying to develop treatments and vaccines for HIV. It has long been known that active, replicating CD4+ T cells are more efficient at promoting replication of HIV. Many studies have shown that immune activation, particularly during the early stages of HIV infection in humans or SIV infection in monkeys, can cause extremely high viral loads and more severe disease. However, preventing an immune response during HIV infection may also result in increased viral loads. A strong T cell immune response is necessary to control viral levels. CD8+ T cells, which are able to directly kill HIV-infected CD4+ T cells, are an important factor in HIV immunity. In order to be properly activated, CD8+ T cells require antigen from HIV to be presented by macrophages, which are a target of HIV infection. Preventing the establishment of HIV infection, and curing chronic HIV infection, is therefore a delicate balancing act of the immune system that scientists still do not fully understand.

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He was 19 years old when first detected to have HIV in his blood. Kai Brothers, from San Francisco is just starting to show symptoms (HIV was detected in his blood in 1989!), having fought the disease without the need for any medication for nearly 30 long years! So is there anything special in the genes/blood of Kai that keeps/kept him safe from life threatening AIDS till date?

Quote:According to the tests conducted by Jay Levy, a leading AIDS researcher from University of California, Kai's WBCs secrete an "unidentified protein" that's suspected/hoped to control the damaging aspects of the deadly HIV virus.

It's hoped that the reproduction of this protein could pave the way for treatment of HIV!

I found this story at, a website for Kai brothers.
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Scientists Find Potential Method to Deplete HIV Reservoirs00