Pros And Cons Of Antiretroviral Therapy

(2011) was a multi-continent, randomized, controlled trial to evaluate the effectiveness of antiretroviral therapy on the speed of the disease process among HIV-1 infected and HIV-1 uninfected partners. In the study, 1,763 HIV mixed status couples were grouped into either early antiretroviral and delayed therapy groups. Inclusion criteria consisted of the HIV-1 infected participant having a CD4 count between 350 and 550 with no previous antiretroviral therapy usage, except to prevent mother-baby transmission. Participants attended three monthly sessions and then quarterly sessions until ill or requiring an additional amount of antiretroviral drugs (Cohen et al, 2011). The uninfected partners were tested each quarter for seroconversion, the period in time in which antibodies become detectable. The research study concluded that early antiretroviral therapy initiation had a greater effect on CD4 count than delayed antiretroviral therapy. The average CD4 count in the early therapy group originated at 400 and increased to 603 after 12 months of ART. A decline of CD4 cells were noted in the delayed group (Cohen et al, 2011). The authors concluded that a higher incidence of HIV transmission was noted in African countries and adverse effects were more likely to occur in the early therapy group. Early therapy had a positive effect on the HIV-1 uninfected and HIV-1 infected

The fact is that the medications stop new infections by killing the HIV virus before taking control in the body. This conclusion was obtained while investigating the way in which the virus develops

Cytokine therapy has been a crucial advance in the treatment of HIV because this disease is highly affiliated with cytokine production. Cytokines are inserted in tumor cells as immune stimulatory genes (5). Following insertion, the patient is injected with a cytokine based vaccine which is used as a therapeutic measure for cancer prevention in patients that have HPV. Activation of cytokines (IL-2, IL-12, GM-CSF) have been theorized to inhibit the growth on tumors. HIV is linked to a decline of the host’s immune system response and decrease of CD4 T cells, therefore cytokine therapy enables the production of these cells by treating patients with IL-2 (5). HPV has been associated with cancer and there is no cure for HPV, however, there are preventative and therapeutic medications (2,6). In the case of HPV vaccination, natural killer cells are activated which induce an immune response. Immune modulators have suppressive and stimulatory effects on macrophages. Stimulation allows for the secretion of cytokines which allows the immune system to produce antibodies due to the high antigen presentation in dendritic cells.

HIV is a quite detrimental virus that has caused much disruption during the 1980’s when it came to life. HIV is “one of the fastest evolving of all organisms” (Rambaut A. ET. Al. 2004) HIV has found ways in which to resist drugs and shows evolutionary mechanisms. The HIV virus has also

Introduction: Human Immunodeficiency Virus (HIV) has become a global issue that has infected an estimated 35 million people living today1. The strain HIV-1 has been of experimental concern for years in hopes of a cure. This retrovirus directly infects the immune system by binding helper T-cells via the CD4 receptor. This allows for integration of the viral RNA into the T-cells, and causes the immune system to weaken by killing these immune cells. Advancements in research led to the use of highly active anti-retroviral therapy (HAART) for treatment, however this does not cure the patient of HIV but it suppresses the viral replication of HIV-1 to very low levels2.

Human immunodeficiency virus is most commonly known as HIV.18 It debilitates a person’s immune system by destroying important cells that fight disease and infection. It can spread through certain body fluids that assault the body’s immune system, specifically the CD4 cells often called T cells.1 These essential cells help the immune system fight off infections.1 Untreated, HIV reduces the number of CD4 cells in the body.1 The damage brought on by HIV to the immune system makes it extremely difficult for the body to fight off infections and diseases. Eager infections or cancers take advantage of a very weak immune system and signal that the person has AIDS. No effective cure exists for HIV. Scientists identified a type of chimpanzee in

Currently, 1.2 million people in the United States have been diagnosed with HIV, or human immunodeficiency virus, with the number of new HIV diagnoses declining by 19% from 2005 to 2014 (aids.gov). This decrease in diagnoses is due to the new medical advancements and scientific findings, specifically the discovery of nonprogessers, broadly neutralizing antibodies (bNAbs), and how these bNAbs can offer a new insight on HIV treatment and prevention.

First of all, to develop a vaccine for this virus, scientists took multiple approaches. One of these approaches is to find a way to prevent new HIV infections from happening in the first place. An example of this is the concept of evaluating the bivalent Env (gp120) protein by targeting T-cell responses. This was by introducing strong CTL responses. Although this study, which is called VAX004/VAX004, had some failures and was suspected to increase acquisition among the participants in their study. However, this was of the first studies to induce HIV-specific T cell responses. Although the solution didn’t reduce HIV acquisition among the 75% who received it, the vaccine did in fact impact the virus strains. The final result was that

First: HIV: The Human Immunodeficiency Virus is a lentivirus. It’s subgroup of retrovirus that causes the acquired immunodeficiency syndrome AIDS. A condition in humans that progressively lead to failure of the immune system. Without proper treatment, an average survival time after infection with The Human Immunodeficiency Virus is estimated to be around 9 to 11 years. We’ve learnt that infection with HIV occurs by the transfer of blood, semen, vaginal fluid, pre-ejaculate, or breast milk. HIV infects our T cells, macrophages, and dendritic cells. With infection present, viral killing of infected cells demonstrate low counts of

The introduction to antiretroviral treatment has proven to significantly reduce the mortality secondary to infections in HIV patients by restoring patients’ immune system (Chan and Brew). These studies and antiretroviral

HIV-1 establishes a reservoir in lymphoid tissue during acute infection that is the site of virus production from infected cells, storage in immune complexes on the surface of the follicular dendritic cell (FDC) network, and persistence in a pool of latently infected resting memory CD4+ T cells 1-8. While combinations of antiretroviral drugs can suppress viral replication and reduce viral RNA to undetectable levels in plasma, virus production from this reservoir of latently infected cells rekindles HIV-1 infection if drug treatment is stopped 9. The elimination or inactivation of latently infected cells in reservoirs that give the virus safe haven from antiretroviral drugs or immune attack is key to bring about a cure.

Human Immunodeficiency Virus (HIV) is a retro virus that causes AIDs by infecting the T Helper cells of the body’s immune system. The AIDS virus is the final stages of the HIV virus. HIV is a lentivirus genus, which is a subgroup of the retrovirus that causes the AIDS virus. Even with proper treatment, an infected person has a life expectancy of less than ten years.As the virus weakens the human immune systems, this effectleaves the patient compromised and at risk to opportunistic infections that the body would have once had the ability to fight, such as the flu, colds, and pneumonia. HIV attacks the cells in our immune system such as the helper T cells and is directly related to the CD4*T cells, macrophages, and dendritic cells. The HIV infection diminishes the levels of CD4*T cells. When the CD4*T cells drop to a critical low level, the body then becomes progressively more susceptible to opportunistic infections. Two types of HIV have been characterized: HIV-1 and HIV-2. HIV-1 is the virus that was initially discovered and termed both LAV and HTLV-III. It is a more virulent strain, more infective, and is the cause of the majority of HIV infections globally. The lower infectivity of the HIV-2 strain compared to HIV-1 implies that fewer of those exposed to HIV-2 will be infected per exposure. Because of its relatively poor capacity for transmission, HIV-2 is largely confined to West Africa. (Wikipedia, 2014)

AIDS is an extraordinarily serious disease and scientists have failed, thus far, to find a cure. AIDS, or acquired immune deficiency syndrome, develops from the human immunodeficiency virus, HIV (“What is AIDS” par 3). HIV is not the same thing as AIDS; HIV merely turns in to AIDS after a certain amount of time (“What is AIDS” par 4). HIV is also not a curable disease. HIV is a special type of pathogen, known as a retrovirus. This virus has to attach to a host cell in order to live and spread. What makes AIDS so deadly is that it targets the body’s lymphocytes, the cells that normally fight off infection (Nolen 4). Lymphocytes have CCR5 and CD4 molecules on their surface, when HIV enters the body, it attaches itself to these molecules. (Nolen 4). Once the virus has attached to the

Despite of the irrevocable efficacy of cART, therapy is not a cure for HIV-AIDS, as interruption of treatment inevitably lead to viral rebound in most individuals (Davey et al., 1999). HIV/SIV persistence in the form of latently infected cells that decayed very slowly was demonstrated using the PBMCs isolated from patients (Finzi et al., 1997, Finzi et al., 1999, Siliciano et al., 2003). Subsequent characterization of HIV-1 latent infection and testing of latency reversing agents utilize both molecular and cellular methods (Spina et al., 2013, Mbonye and Karn, 2014). Molecular biology is also instrumental in discovering clonal expansion of infected cell as another mechanism for HIV-1 persistence (Maldarelli et al., 2014, Wagner et al.,

HIV becomes drug resistance when the ARV treatments’ are not adhered to. Once the patient has taken their antiretroviral (ARVs) medication then stops the HIV is able to replicate and will do so at a rapid rate. As a result mutations are very common (Jen Gorgan and Ruth Suter;2009)