That Target The Gene Codes For A Protein Found On The Surface Of White Blood Cells

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

In the episode of “Secretes of the Dead III: Mystery of the Black Death”, Dr. Stephen O’Brien, a geneticist, discovers an explanation as to why some individuals succeeded to survive the Black death while others just seemed to die. With this being said, the film is clearly devoted to convincing us that the C-C chemokine receptor type 5, also known as CCR5-delta 32, mutation is the ultimate reason to the survival of certain individuals during the bubonic plaque in the city of Eyam, England. Furthermore, this same CCR5 mutation can confer immunity to the current human immunodeficiency virus (HIV) and thus prevent AIDS. Although the evidence such as the DNA testing of the living ancestors and that of HIV-negative individuals proving immune resistance

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

One of the first approved therapies for the treatment of HIV was a modified DNA base pair of thymidine that replaced the terminal hydroxyl (-OH) group with an azido (-N3).

After reviewing the study of the effects of chimeric antigen receptor-modified T cells (CAR T-cells) on acute lymphocytic leukemia, it appears that this type of treatment shows promise for the treatment of this and many other difficult-to-kill cancers. This technique was pioneered and developed by Dr. Carl June. He began his research on T cells in the late 1980s to early 1990s while in the Navy. The research he would do and the other researchers he would meet at this time would pave the way for what could be considered to be groundbreaking cancer research today. What started as the study of T cells and their relationship with the HIV virus specifically, would turn into the

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

This paper will discuss the current efforts at an HIV vaccine including different approaches to solving the vaccine problem and how close scientists are. Scientists have been struggling with a HIV vaccine for a while. One solution is a drug that has enhanced and extended the lives of people with HIV/Aids. Other scientists have similar methods to solving the Vaccine problem with clinical trials and patients. However the solutions suggested in my literature review also say that they have difficulties with following through.

They include an extensive range of undifferentiated cells that provide vital functions to treat infected patients. These undifferentiated cells can give rise to many cell lineages; these lineages can be later reprogrammed to become HIV resistance or used help introduce a gene of interest that produces helper T-cells to fight off foreign pathogens and build a patient’s immune system. Many drugs that are used to treat HIV today, may not treat HIV in an effective way; a donor may not always be a match. These stem cells are the ideal therapy for these types of diseases, and provide a patient-specific treatment that unlike drugs, do not. These stem cells, embryonic, hematopoietic, mesenchymal, and induced pluripotent, have transformed the field of research and medicine, providing new applications to the world of biotechnology and science to

Researchers have moved one step closer to developing a cure for AIDS, the killer which claimed 39 million lives since its discovery in the 1980s. Using the relatively new CRISPR/Cas9 technology, scientists at the Lewis Katz School of Medicine at Temple University have eliminated HIV-1 genomes from human T-cells. CRISPR/Cas9 is a powerful biological tool used for genome editing and altering gene expressions. Applications of CRISPR/Cas9 range widely from modifying yeast to produce biofuels, to inactivating genes in human cell lines. Kaminski et al. (2016) believe that CRISPR/Cas9 is the key to curing AIDS because it holds more potential compared to the current method, antiretroviral therapy (ART). ART uses multiple medications to combat against

The goal of this experiment is to prevent HIV through vaccination using ex vivo gene therapy.

Another recent study involved transplanting these modified T cells into mice using the CRISPR/cas9 to see if the engineered cells would transfer resistance to HIV. After transplanting the T cells and exposing the mice to HIV, the mice tested resistant to the virus (Zu, 2017).

Documentation shows that CD4+ T-lymphocytes are essential in the origination and development of acquired immunodeficiency syndrome (AIDS) (39). The advancing immunosuppressive feature of AIDS and its predisposition to tumors and infectious organisms (Toxoplasma, Haemophilius influenza, Mycobacterium tuberculosis, and Pneumocystis carinii is attributable to a gradual reduction in CD4+ T-lymphocytes (40). Investigators suggest that the process through which CD4+ cells are destroyed may be linked to apoptosis, autoimmunity, and replication of human immunodeficiency virus (HIV) infection (39-42).

Many HIV+ patients develop HIV nephropathy and require kidney transplantation (2). HIV binds to the surface proteins that bind antigens on host cells. HIV protein gp120 binds a combination of CD4 and CXCR4 on T-cells. Cells are killed by direct cytopathic effect, which is an anti-viral response or by transformation of host cells via oncogene expression (3). HIV effects immune system and may interfere with interpreting correct results or placing compatible organs (2). Crossmatching an HIV+ patient with potential donors poses serious challenges due to HIV induced B- cell deregulation and presence of auto-antibodies. HIV+ patients may have false positive test results that may be difficult to interpret or find compatible organs. HIV+ cases can create confusion, therefore supplementary testing is needed to better assess suitability of the organ or graft tolerance (2, 3). New tests have been developed that target a different route of antibody activity. This is a great opportunity to discover how C1q testing may benefit those special cases of HIV+ patients (4).

These drugs are effective against a wide range of wild-type and drug resistance HIV, including the strains that use CCR5 or CXCR4 coreceptors for entry into the host cell.