Effects Of Hiv-1 Pathogenesis

Dr. N.A.S states that one of the antiretrovirals blocks translation of RNA into the proteins required to make new viruses. Some of the current antiretrovirals include reverse transcriptase, fusion and entry, protease, and integrase inhibitors;6,10 however there is not an inhibitor that blocks translation of rna into proteins on the market. Targeting inhibitors specific to HIV has made ARVs increasingly effective and less harmful to humans.

As have been described above, HIV can have a potential effect on immunological cells, which are important to protect the body from additional infections such as Tuberculosis (TB), Cytomegalovirus (CMV) and other viral or bacterial infections. An effective treatment is needed to reconstruct what HIV has damaged. Antiretroviral therapy (ART) is a common treatment to stop the viral replication and decrease the disease progression, which may lead to a vast decline of the morbidity and mortality. The standard treatment involves a combination of at least three drugs; often known as a highly active antiretroviral therapy (HAART) where the most common types are Nucleoside reverse transcriptase

Since the arrival of triple therapy, the challenge of sustained and complete viral suppression has been solved for the majority of patients [1]. The major limiting factors for improving the long-term success of ART are tolerability and convenient pill burden [2]. The latest class of the antiretroviral drug developed are Integrase inhibitors (INI). Dolutegravir (DTG) is an Integrase inhibitor, particularly focused on maintaining a favorable safety profile and a high efficiency rate, within a single-tablet regime (STR), it improves resistance barrier and allowing co-formulation with an NRTI backbone. Dolutegravir has been compared against both other classes of HIV anti-retrovirals as well as other integrase nuclear strand inhibitors. In August 2013, DTG was approved by FDA for its use in both patients who have never taken ART (ART-naïve) and patients who have taken ART (ART-experienced) [3]. It is predicted that very soon a STR containing Dolutegravir (DTG), abacavir (ABC) and lamivudine (3TC) will become

When the HIV virus was identified in the 1980’s, many companies began to search for an antiviral drug but Burroughs Wellcome led the research effort. There were three drugs being tested by other companies as well including, AZT by Burroughs Wellcome, DDI by Bristol Myers and DDC by Hoffman-LaRoche. These drugs inhibit reproduction of HIV and slow the damage it causes.

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]

Our chosen article is titled “HIV and AIDS News and Updates: New Strain of HIV Found in Cuba Which Can Develop Into a Full-Blown AIDS in a Span of Only 3 Years” written by Steff Lyn Smetham. It was published on November 5th, 2015 on the Crossmap online website. The article was written to inform the readers on a newly discovered strain of HIV, which develops faster than the average known types of HIV. This article mentioned many recently studied concepts including, the rate of disease progression, CRF19’s involvement in the AID’s rapid progression (AID’s-RP), the adverse effects of RANTES defense molecules, and proper HIV treatment. The general consensus is that the average rate of disease progression takes approximately 5 to 10 years to progress into AIDS, however, it is quite complicated to pinpoint the rate due to many factors. Based on many clinical studies done with a diverse group of patients in Cuba, CRF19 has shown to be one of the main recombinant subtype responsible for AIDs-RP. In addition, CCL5 and CCL2 of the RANTES family, have proven to be two specific chemokines that display the adverse effects . Finally, regardless of CD4+ count, treatment should be started immediately preferably with the common therapies Isoniazid preventive therapy (IPT) and Co-trimoxazole preventive therapy (CPT). The authors have used information through studies being done at the University of Leuven located in Belgium, and Professor Anne-Mieke Vandamme and a team

Nancy R. Calles, MSN, RN, PNP, ACRN, MPH Desiree Evans, MD, MPH DeLouis Terlonge, MD

Human immunodeficiency virus type 1 (HIV-1) is a retrovirus infecting approximately 35.3 million people worldwide that leads to the development of acquired immunodeficiency syndrome (AIDS). HIV-1 selectively infects certain host immune cells, including CD4+ T cells, macrophages, and dendritic cells, resulting in the continual depletion of the host immune system (Global Report, 2013). More specifically, HIV-1 prevalence is concentrated in sub-Saharan Africa and other developing countries worldwide. In recent years, there has been much effort devoted to developing an effective vaccine against HIV-1. The vaccine clinical trials are typically held in these developing countries where HIV-1 prevalence is highest. The dilemma that continues

HIV is an RNA virus that is part of the retrovirus family called Lentivirinae. These specific retroviruses cause chronic diseases that progress at a slow rate in the organism (Beck-Sague

Atazanavir sulfate is a HIV-1 aza-dipeptide protease inhibitor that has been approved and is indicated for co-administration as part of therapy for Human Immunodeficiency Virus-1 (HIV-1) infection.1,2 The therapy is available in 100 mg, 150 mg, 200 mg, and 300 mg capsules. Prescribed doses in adults are taken once daily and include either 300 mg in combination with 100 mg of ritonavir or a single therapy 400 mg dose. Pediatric dosages are determined by patient body weight. Atazanavir is sparingly soluble in water due to large hydrophobic projections from its structure but exhibits increasing solubility with decreasing pH.1

The infected cells, which contain viral RNA, are lined with envelope proteins that penetrate the lipid bilayer of the cell. Spikes protrude out from the envelop capsule. The spikes consist of gp141 stem and gp120 protein, which is located at the tip of the stem. The protein gp120 on the infected cells binds to the co-receptor CCR5 on the T cells. This allows the virus to become physically closer to the T cells. P24 is an antigen produced in response to HIV infection. Increased levels of P24 show increased levels of virus.

The human immunodeficiency virus (HIV) is a lentivirus (a subgroup of retrovirus) that causes HIV infection and acquired immunodeficiency syndrome (AIDS). AIDS is a condition in humans in which progressive failure of the immune system allows life-threatening opportunistic infections and cancers to thrive. Without treatment, average survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype. Infection with HIV occurs by the transfer of blood, semen, vaginal fluid, pre-ejaculate, or breast milk. Within these bodily fluids, HIV is present as both free virus particles and virus within infected immune cells.

HIV is a retrovirus and it differs from normal RNA viruses because they contain an enzyme known as reverse transcriptase. This enzyme transcribes an RNA template into DNA, opposite of what normally occurs in a replication cycle (Reece et al., 2014). There is viral DNA produced through this method; which then invades the nucleus of the cell and combines itself into the DNA of a chromosome. This differs from the typical process, as it is a multistep process; contrary to the single step mechanism of incorporating mRNA into host cells to produce viral proteins (MCRH). HIV is a retrovirus and has a much more complex viral replication, compared to the

Proteolytic processing of the Gag polyprotein results mature HIV-1 structural proteins: p17 matrix (MA), p24 capsid (CA), p7 nucleocapsid (NC), p6 domains, and two spacer peptides, SP1 and SP2. Each of these HIV-1 structural proteins play a crucial role in the HIV-1 retroviral replication cycle. MA is responsible for targeting Gag to the plasma membrane and promoting the incorporation of viral envelop glycoproteins into the forming virions; CA drives Gag multimerization during assembly to form the Gag lattice that encapsidates the viral RNA genome; NC recruits the viral RNA genome into the virions; and the p6 domain recruits the endosomal sorting complex required for transport (ESCRT) apparatus that catalyzes the membrane fission step responsible for the budding off of new virions from the infected cell (Freed, 2015). In HIV-1 pathogenesis, HIV-1 matrix protein p17 participates in several processes, including RNA targeting to the plasma membrane, incorporation of the envelope into virions, and particle assembly. Furthermore, p17, acting as a viral cytokine, can act on reactivated T-cells, promoting viral proliferation (Florentini et al, 2006).

HIV can currently be regulated by several successful treatments. The current rates of infection have been on the decline due to education, prevention, and getting people treatment according to UNAIDS1. However, a cure has not been found. With a rapidly changing virus, it will be hard to definitively create a cure anytime soon. However, there are a few new ways of treating the virus already infecting genomes of many people. These treatments will work with the current methods being used and will not be an alternative to them. The main treatments that will be discussed are the current Highly Active Antiretroviral Therapy (HAART), and the new CRISPR/CAS9 treatment.