The Use Of Highly Active Anti Retroviral Therapy

CD4 is a glycoprotein found on the surface of immune cells such as T helper cells, monocytes, macrophages, and dendritic cells. HIV infects cells of the immune system called T lymphocytes (T cells) and macrophages. HIV has an envelope and contains two copies of single-stranded RNA as the genome. Within the viral capsid are important viral enzymes called reverse transcriptase, integrase, and protease. The HIV virus has a spike protein that is called gp120, and the host cell receptor is CD4+. HIV belongs to a class of viruses called retroviruses. Retroviruses are RNA viruses, and to replicate or reproduce, they must make a DNA copy of their RNA through transcription and translation. It is the DNA genes that allow the

Recent studies suggested that CD4 domain specific monoclonal antibody such as mAb (15A7) and Ibalizumab have a great revolution in HIV-1 treatment area. The majority of previous mentioned treatments constitute to either restore the immune response or decline the plasma vireamia, however, this type of treatment is more likely to interfere with the HIV-1 structure. Before explaining how this category of drugs works, it is necessary to clarify the reaction between HIV-1 glycoproteins and CD4. Once the virus enters the body, HIV-1 envelope glycoprotein (gp120) attaches to a cellular CD4 receptor. As CD4/gp120 is formed, it allows gp120 to attache to chemokine receptor-5 (CCR5) or CX chemokine receptor-4 (CXCR4) allowing gp41, another viral envelope molecule, to insert into the target cell membrane leading to fusion the viral envelope and cellular membrane (Christopher et al., 2010). Ibalizumab is CD4 domain-2 monoclonal antibody using as an effective treatment to enhance the CD4 counts. In a study which set out to determine the antiviral efficacy of Ibalizumab on HIV-1 positive patients not on (ART), (Christopher et al., 2010) found that the CD4 counts increase after one day of drug initiation even before the viral load decline. This suggested that the rise of CD4 counts is possibly due to redistribution of CD4 cells from lymphoid tissues rather than regeneration of these cells. Notably, niegher

The University of Pennsylvania19 performed a phase 1 clinical trial to test the safety in humans of CCR5-modified cells and how “zinc finger” modified T cells affect HIV. They took 12 participants and isolated large numbers of their T-cells. A viral vector was then used to insert the ZFN into the cells to knock out the CCR5 protein. The cells were then re-infused back into the patient and the patient was followed up with every three months for four years to check if the ZFN modified CD4+T cells were still found in the blood. They were able to allelic disrupt 11-28% of the modified autologous CD4-enriched T-cells that was infused into each person. The decline in circulating CCR5-modified cells was significantly less than the decline in un-modified cells with a p-value of 0.02. In most patients overall the blood level of the HIV DNA was decreased. The results of this study found that within the limits of this study CCR5-modified autologous CD4 T-cells infusion were safe.15 Sangamo Biosciences and colleagues17, 18 has performed two phase 1 clinical trials and one phase 2 clinical trial to test autologous T-cells that were genetically modified at the CCR5 gene. The purpose of these clinical studies was to determine if “zinc finger” modified CD4+ T-cells were safe to give to humans and how it affected HIV. They took 54 participants

infected cells, have opened new avenues for strategies for HIV vaccine design” (39). These antibodies

Treatment development focused on limiting the virus' ability to transcribe and replicate copies of itself within the host cell. Reverse transcriptase is an enzyme coded by the virus RNA. Reverse transcriptase (RT) allows the RNA to make a functioning DNA copy that is inserted into the host cell DNA and begin manufacturing copies of new viral RNA identical to the strands in the initial viron. RT is found only in retroviruses and focus on AIDS treatment has been on inhibiting the function of RT in HIV action within a host cell( Furman, P. A. Fyfe, J. A. St.Clair, M. H.; Wenhold, J. Rideout, J. L., Broder, S., Mitsuya, H.; Barry, D. W. 1985).

Molecular epidemiologic data suggest that HIV type 1 (HIV-1), the most common subtype of HIV that infects humans, has been derived from the simian immunodeficiency virus, called SIVcpz, of the Pan troglodytes troglodytes subspecies of chimpanzee. The lentivirus strain SIVcpz is highly homologous with HIV-1, and another form of simian immunodeficiency virus found in sooty mangabeys (SIVsm) has similarities as

The Human Immune system is made up of a variety of chemical and cellular components that are classified as either innate or adaptive immunity. The cellular immune response to the bubonic plague is carried out through the innate response as the bacterium is able to avoid the adaptive response by infecting macrophages in the host’s body. Similarly, the immune response to HIV infection is not able to reach the adaptive response, as the virus infects the body and destroys vital CD4 cells which in turn damage the immune system itself. Furthermore, the immune system relies heavily on the action of B and T cells, which are antigen-specific cellular immune responses to battle the HIV virus. Though it is unable to completely rid the host of the virus,

While it is still largely unknown why the HIV vaccination was a complete failure, most believe that the it was unsuccessful mostly because of the researchers’ neglect to realize that they cannot only study certain components of the immune system without looking at the system as a whole. They assumed that by learning how one strand of the virus affected our system that they could produce a dead version to inject into the body so that it could begin to produce cytotoxic T-cells so that when it would come into contact with a live form of the virus, the body would already have immunity to it (Gilbert, 2012). The problem with this assumption is that for it to work the virus must maintain the same shape and the HIV virus changes shape. During clinical trials, the researchers tested the vaccine on humans who had high rates of preexisting immunity to adenovirus 5 (Aderem, 2011). These test subjects should have been even more likely to experience successful results with the experimental treatment, however adverse effects resulted from it. The people with predisposed immunity were found to be twice as likely to

The most fundamental question to ask about an HIV vaccine is: 'What evidence exists that protection against disease after exposure to HIV is possible?' The best evidence for successful protection against a virulent primate lentivirus such as HIV is that monkeys are almost always protected against challenge with pathogenic SiVmac after vaccination with an attenuated (ne/-deleted) SIVmac

Recently in Cuba a new and aggressive strain of HIV has been discovered and this strain causes an early development of AIDS in people within 3 years of being infected with HIV. Usually it takes five to ten years for a person with HIV to progress to AIDS but only if the person is not under anti-retroviral therapy treatment. Individuals who are HIV positive usually don’t feel or look sick immediately which is why they do not take ART treatment during the clinical latency stage of the infection. The new “recombinant” strain of HIV takes advantage of this situation by causing a rapid progression of HIV to AIDS and cutting short the time needed for HIV positive patients to exhibit early symptoms, which could help them be aware of their infection

HIV-1’s ability to mutate rapidly has hindered researchers to finding an effective vaccine. The characteristics of bNAbs show that it can target the surface of the virus to reduce the chance of an infection. A recent finding of calves being able to produce antibodies similar to bNAbs when exposed to the virus has provided a glimpse of hope, however further trials will still need to be carried out to initiate the same response in humans. Nonetheless, government funding has helped researchers to find a cure against HIV-1 by incorporating bNAbs into a vaccine.

HIV has been a life destroying disease since the early 1980s. Originally discovered in gay men, it was once thought to only effect homosexuals. Thankfully to great efforts on research and outbreaks in hemophiliacs, it is now associated with other social groups outside of the gay community. The risks of contracting this disease are still high among gay men, highly sexually active individuals (hetero-, homo-, and bi- sexual), intravenous drug users, and health care professionals. By understanding the biological make up of the disease researchers have been able to come up with many options to treating the disease, its progression into AIDs, and other infections that can occur

Human Immunodeficiency Virus (HIV) is a retrovirus responsible for the acquisition of HIV infection which leads to the development of acquired immunodeficiency syndrome (AIDS). HIV targets cells that are part of the human immune system such as CD4+ T cells, macrophages and dendritic cells which results in the levels of these cells falling dangerously low as they are exterminated via different mechanisms. Such mechanisms typically involve the induction of signaling cascades that result in 'self-killing' protocols being executed by the cell, as well as becoming targets for direct killing of other cytotoxic cells in the immune system. As HIV is a lentivirus it contains two single-stranded, positive sense, RNA molecules each coding nine viral

This recognition of HIV coreceptors and progress in understanding how HIV fuses with the cell has opened up new possibilities for antiviral drugs. A number of new agents are being designed to prevent infection by blocking fusion of HIV with its host cell. Following fusion of the virus with the host cell, HIV enters the cell. The genetic material of the virus, which is RNA, is released and undergoes reverse transcription into DNA.

HIV replicates at impeccable speeds creating billions of new HIV viruses to infect the body every day.18 The virus is able to mutate and evolve which makes it that much harder to defeat the virus.19 The CD4 cells and T cells are destroyed daily by HIV which eventually causes the immune system to regenerate or defeat infections.20 HIV is able to hide in the cytoplasm of the cell that it infects or makes its way into the cell’s chromosomes.21 The virus does this to hide from the immune system so it will not be destroyed.22 Some drugs have been found to