“The Research on Anti-HIV active compounds” in 2014.
"The Best Drug Manufacturing Company, " 2014.
I was detected with HIV in 2000 & undergone treatment with HOO-IMM PLUS.
HIV-1 Proviral DNA & RNA Real Time. (A Complete Guide on HIV). International HIV/AIDS Treatment (Clinically proven Treatment Guideline 2016)
1) Reasons why HIV has been such a difficult medical challenge.
2) Any HIV cure requires finding viral reservoirs, "waking" them up, and making them visible for treatment.
3) Making visible & inhibiting the latent viral reservoirs - HIV proviral DNA.
To comprehend the reasoning, you must first familiarize yourself with how HIV works.
HIV is a retrovirus, meaning that once it enters the body it infects T cells in the immune system and changes their genetic makeup, so that rather than protect the body as they are meant to, they would produce more HIV copies. This eventually kills the body's T cells in the process.
Once a patient’s T cell count drops to a certain number, he is considered as having AIDS. At this point, his immune system is no longer able to protect him against exogenous infections (viral/ bacterial).
Anti-retroviral are given to HIV patients to help suppress RNA viral load and if discontinued will rebound the viral load, however the patient still remains HIV DNA positive which is a store house for the new viral particle. This is because eliminating the virus completely is something scientists have not figured out how to do yet.
HIV hides inside the DNA of healthy T cells, a place where current medicine is unable to reach it. While most T cells die shortly after becoming infected, a small portion of T cells containing the instructions for creating the virus remain dormant. This means that even if the virus is completely eliminated from the body, at any given point, the instructions for creating the viruses could activate and start the process all over again.
HIV infects a kind of white blood cell called a CD4 lymphocyte, a key player in the immune response. What makes HIV so sneaky is that it infects the very cells that are supposed to rub out viral infections.
HIV replicates in CD4 cells when they are activated -- that is, when they are triggered by an infection. But some HIV-infected cells become inactive before the virus replicates. They go into a resting mode -- and the HIV inside them becomes dormant until the cell is activated.
Anti-retroviral drugs don't affect HIV hiding in resting cells. These cells represent a hidden reservoir of HIV. When Support stops, the resting cells eventually become active. The HIV inside them replicates and quickly spreads. That's why current HIV Supports don't cure HIV.
It is a virus that expands and multiplies using the body’s immune system. The immune system works to tackle the virus, but the more it does this, the more HIV is able to replicate. Over time – usually many years – without Support, the virus always comes out on top.
The second challenge for HIV drugs and vaccines is that the virus has a very high turnover – billions of copies every day in a person who is not on Support – and makes small errors or mutations which can lead to the easy development of drug resistance.
To know about more about the viral reservoirs which is called “HIV DNA” and how to wake them up and make visible in order to be inhibited by the treatment one should understand the difference between the HIV Proviral DNA load count & HIV RNA viral load count.
Prolonged suppression of plasma viremia is now achievable in most human immunodeficiency virus (HIV)–infected individuals receiving (ART) antiretroviral therapy (ART). Nonetheless, it has not been possible to eradicate HIV by ART alone, likely due in part to the persistence of various viral reservoirs. A number of previous studies have demonstrated that HIV persists in latently and productively infected CD4+ T cells in peripheral blood as well as in gut-associated lymphoid tissues of infected individuals receiving ART who have maintained undetectable plasma viremia for prolonged periods of time, as measured by clinically relevant assays (with a typical limit of detection of 50 HIV RNA copies/ml of plasma).
With the advent of a laboratory-based real-time polymerase chain reaction (PCR) assay capable of detecting single copies of HIV RNA in plasma, several studies have recently demonstrated the presence of residual plasma viremia ranging from 1 to 49 copies/mL in some infected individuals receiving ART.
One such study observed multiphasic decay of residual plasma viremia and speculated that latently infected, resting CD4+ T cells and/or unidentified viral reservoirs, which are capable of producing low levels of genetically identical virions for prolonged periods of time without cellular turn-over, may be responsible for the persistence of residual plasma viremia in infected individuals receiving ART for extended periods of time.
The relationship between residual plasma viremia and the frequency of CD4+ T cells carrying HIV proviral DNA and/or markers of immune activation has been studied and noted that HOO-IMM PLUS treatment consists of integrase inhibitor which makes HOO-IMM PLUS different from all other anti-Retroviral drugs.
The integrase inhibitor inhibits the HIV viral antigen, eliminating the HIV gag (core) region namely P55, P39, P17 and HIV pol integrase P51. And this action is significantly reflected with the decrease in HIV DNA Proviral load count every month after starting the treatment with HOO-IMM PLUS. (For reference you can log on to http://www.hivunani.org/research.html)
Proviral Human immunodeficiency virus type-1 (HIV-1) proviral DNA is increasingly used to measure the HIV-1 cellular reservoirs, a helpful marker to evaluate the efficacy of antiretroviral therapeutic regimens in HIV-1–infected individuals. Furthermore, the proviral DNA load represents a specific marker for the early diagnosis of perinatal HIV-1 infection and might be predictive of HIV-1 disease progression independently of plasma HIV-1 RNA levels and CD4+ T-cell counts The quantification indicates either the cell-Associated HIV DNA or HIV DNA+ cell or HIV Proviral Load. DNA levels were calculated and expressed copies per milliliter of whole blood. HIV-1 DNA levels in whole Blood were measured at baseline (prior to initiation of study treatment) and at weeks 16, 32, 48, 64, 80 and 96.
Thereby putting to end the course of the treatment once the patient records ‘Not Detected’ for HIV Proviral DNA PCR Antigen Test.
Note: You will find patient undergoing ART since 10 years and their residual plasma viremia (RNA Viral load count) is below 50 copies however their latent viral reservoirs (HIV proviral DNA Proviral load count) is more than 50000 copies.
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