What Is Highly Active Antiretroviral Therapy?

b. HIV is an incurable disease that relies on coreceptors to initiate host cell interaction and proliferates by utilizing the host cell’s own machinery to reproduce new virus. We will more deeply explore the mechanism in which HIV virions infiltrate and deceive our host cell. In addition, we will discuss current treatment and research that are in the process of finding a highly coveted cure.

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

Several viral components were found to contribute to the transport of HIV-1 through nuclear pores for mediation or for the gathering of the host’s protein. Although these viral components were found, none of them showed any purpose when on their own.

gp41 (envelope antigen), are highly immunogenic, the antibody responses vary according to the virus load and the immune competence of the host. The antigenicity of these various components provides a means for detection of antibody, the basis for most HIV testing.[35] Accessory genes carried by HIV include tat, rev, nef, vif, vpr, and vpu (for HIV-1) or vpx (for HIV-2). The rev gene encodes for a regulatory protein which switches the processing of viral RNA transcripts to a pattern that predominates with established infection, leading to production of viral structural and enzymatic proteins. The long terminal repeat (LTR) serves as a promoter of transcription.[22,30,32,33]

HIV is a retrovirus that that contains RNA and is a member of the subfamily of viruses called lentivirus, in this group infection develops slowly. It

HIV-1, responsible for most of the disease today, was first discovered to have originated from Chimpanzees in 1999. HIV-2, the second type of the virus, was discovered to be transmitted through monkeys most likely through the consumption of their meat. There are two different types of the illness: HIV-1 and HIV-2. HIV, Human Immunodeficiency Virus, essentially breaks down the body’s CD4 cells which help to assist fighting off infections in your body. Overtime, this will hindrance your body’s ability to fight off diseases which can be potentially life threatening. The last stage of HIV is linked to AIDS, Acquired Immunodeficiency Syndrome. AIDS is a specific group of diseases/conditions that are indicative of severe immunosuppression related to infection with HIV. This makes people infected with the disease more vulnerable to opportunistic infections which their body will be unable to fight off towards the later stages of the disease. Most people diagnosed with AIDS have an estimated three years to live, but people that do not get diagnosed have an estimated one year to survive.

There are three stages of Human Immunodeficiency Virus. The beginning stage of HIV is Acute Retroviral Syndrome, where symptoms may or may not first start occurring. At about one to four weeks after infection takes place, the infected person can start experiencing flu like symptoms. During this stage, the virus attacks CD4 cells using them to replicate and destroy already existing cells. The next stage is called Clinical Latency, or chronic HIV infection. At this time no symptoms will be experienced, but the virus will

On a molecular level HIV is unique in its structure relative to other viruses from the retrovirdire family. The virus itself has the basic structural components of virus in that it has a capsid, envelope, and genome. The genome maintains the nucleic acid and is surrounded by the capsid which is comprised of protein. The capsid is covered by a lipid layer called the envelope. The envelope is connected to the sheath which is anchored to the base of the

Human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS) is a global epidemic: 25 million people have died from it and 35 million people are currently infected1. While anti-retroviral therapies are available that control viral replication, those treatments are unable to purge the latent reservoir of virus resident in resting CD4+ memory T cells. Additionally, these treatments are extremely expensive and largely unavailable to those in developing countries where 90% of infected individuals reside1. Therefore, the best approach for controlling and preventing the transmission of HIV would be a prophylactic vaccine.

There have been two strains of HIV identified in the world, HIV 1 and HIV 2. Both strains of the virus produce the same effects, but are still very different. One of the ways in which the two strains differ is by where they

To investigate the distribution of PI-induced mutational changes in HIV-1 across Gag and protease regions, Codoner et al. sequenced the HIV-1 Gag-protease coding region from longitudinal plasma samples from four patients receiving PI treatment over a 9-year period. Sequence analysis confirmed that HIV-1, in response to PIs, demonstrates a stepwise accumulation of Gag cleavage site mutations (CSM) at the following positions: V128I in the p17/p24 junction; S373P and I376V at the p2/NC junction; A431V at the NC/p1 junction; K436R at the NC/p1 junction and P453A at the p1/p6 junction (Codoner et al, 2017). Of these Gag CSM, A431V and K436R have been previously associated with drug resistance mutations in the protease and V128I, A431V, K436R

According Canadian public health agency (2010), Human Immunodeficiency Virus (HIV) is a virus that affects the human immune system, leading to a chronic, progressive sickness that leaves people susceptible to opportunistic infections. When the body no longer can fight or resist infections, the condition is at this point referred to as AIDS, which means Acquired Immunodeficiency Syndrome. Averagely, it has been found to take more than ten years to develop from initial infection of HIV to AIDS. Though simple in description, HIV and AIDS is a dangerous disease that has by now killed more than 20 million people across the world. Basing on the report released by the Joint United Nations Programme on HIV and AIDS, no cure for AIDS has been established to date, and currently there is no vaccine against HIV and AIDS infection. This paper therefore discusses the biology of HIV and AIDS, Back ground, modes of infection, clinical consequences, current research, preventive and modes of transmission, and diagnostic procedures specifically in N.America.

HIV/AIDS is one of the greatest health concern faced by the world in the health care today. Currently, there is no cure available for HIV, also, the vaccines viable

Analyzing the three-dimensional distribution of coevolving Gag residues, Codoner et al found that the correlated residues in the matrix are clustered on the inner surface on the trimer. As these surfaces were previously associated with interactions between gp41, a subunit of HIV-1 envelope protein, and the matrix, Codoner et al. concluded that these mutated residues are representative of novel interprotein interactions that modifies matrix stability in order to affect viral fusogenicity. This is further supported by several coevolving p17 residues (residues 66, 69, and 98) were also previously shown to be contributed to matrix stabilization and the incorporation of viral envelope proteins into immature viral particles. Thus, Codoner et al hypothesized that coevolving residues in HIV-1 matrix may affect HIV-1 resistance to PIs by modifying particle maturation and viral fusogenicity (Codoner et al, 2017).

Acute Human Immunodeficiency Virus (HIV) infection is the small period of time after a person has been exposed to HIV and before they have seroconverted. Seroconversion is the process in which the body starts to create antibodies to fight the HIV virus (Pietrangelo, 2013). During this period of time, which is usually a few days, the virus replicates rapidly. The rapid replication results in extremely high amounts of HIV in the blood because the body has not had time to respond to the infection. As the viral load increases more CD4 white cells are destroyed. CD4 cells are a responsible in protecting the body from infection. When these cells are destroyed they no longer are able to adequately activate the body 's immune system. (AIDS.GOV).