The Distribution Of PI-Induced Mutational Changes In Gag And Protease Coding Region?

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.

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

recognize a protein that is present on the surface of all HIV strains and neutralize the effects of the

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]

Gp120 is exposed on the surface of the HIV envelope. GP120 is important for when the virus enter because they attach to certain cell surface receptors. These receptors are essential because they are the ones that bind to CD4 cells. The binding of these receptors start a change in the gp120 protein. Gp120 is coded by the HIV gene, so this means that gp120 plays a vital role in the ability of HIV to enter CD4 cells. Gp120 was among the first targets in finding and HIV vaccine.

The first Human Immunodeficiency Virus (HIV) showed up decades ago, as far as we know. However, there could have been many more infections over the years that were either recorded as unknown cases or got called with a different disease name. Nevertheless, humans have been trying to understand how this tricky virus work and what strategies they can use to prevent or cure the virus. Since it can mutate and adapts so quickly, finding a cure or an antivirus is a challenging task. Therefore, this paper will discuss some of the strategies that are being used to develop a vaccine against this virus, including: strategies that can be done before a person is infected, strategies for immediately after infection, and complete cures.

HIV-1 integrase is one of the key enzymes required for the successful replication of HIV-1 and is often a common therapeutic target to help treat HIV-1 infections. Integrase is a

HIV infects CD4 + T cells. The viral particles of HIV keep their genetic information stored as double-stranded RNA. They use a reverse transcriptase that converts their genome into double-stranded DNA (Edina, Misawa, Kanemura, Koyanagi, 2013). During this process the virus can mutate quickly because many errors occur in the HIV genome. “The DNA is inserted into the host cell genome by integrases which use LTR (long terminal repeat) sequences on the viral genome to integrate with the host DNA” (Ebina, Misawa, Kanemura, Koyanagi, 2013). This results in a provirus that can continuously produce new viruses that infect other immune cells.

In general, the two main types are classified as HIV-1 and HIV-2 [12], and while both types appear to have the same clinical manifestations, HIV-2 tends to have a lower transmission rate upon effective contact (direct contact between infectious and susceptible individuals) and a lower incubation period (the time period between infection and clinical symptoms) [13-15]. HIV-2 is rarely found outside of West Africa which prompts the public to imply HIV-1 when talking about HIV in public literature worldwide [16]. HIV-1 is further divided into groups based on their close phylogenetic association with the Simian immunodeficiency virus (SIV) which is also a retrovirus capable of infecting around 45 species of primates [17, 18]. HIV-1 subtypes include groups M, N, O, P, with Group M (which stands for Major) encompassing over 90% of HIV-1 infections worldwide and is believed to be closely related to the SIVcpz isolated from the common chimpanzee (Pan troglodytes) [10, 19]. Other groups of HIV-1 appear to be less prevalent and geographically limited centered in west-central Africa with groups O and P showing phylogenetic similarities with SIVgor isolated from the Western Gorilla (Gorilla gorilla) [20, 21]. Analysis of HIV-1 has led to further create subtypes within group M based on the geographic prevalence, with subtypes

CD4 cells are targets for contracting HIV as a transmembrane protein that is part of the virus has a high affinity for CD4 cells, this protein is gp41 (Coico, & Sunshine, 2009, P. 269). Dendritic cells, CD4+ T cells, and macrophages all contain CD4 and therefore, are targeted by HIV. Another glycoprotein that is introduced by HIV is gp120. Gp120 and gp41 are bound to each other and, once gp41 is bound to the CD4 molecule, gp120 binds to a second molecule, allowing HIV to invade the cell (Coico, & Sunshine, 2009, P. 269). The CD4+ cell that becomes the target of the gp120 is determined by the coreceptor on the gp120 molecule (Coico, & Sunshine, 2009, P. 269). After the CD4 cells has a gp120 bound to it, the cell membrane is then

We applied massively parallel sequencing to HIV-1 provirus populations in cells from blood and lymph nodes collected at three separate times (day 0, and after 3 months and 6 months of treatment) and virus particles in the blood (day 0) from three study subjects studied previously (Fig. 1; 12). Two subjects (1727 and 1679) were well-suppressed patients; and the third subject (1774) continued to have measureable amounts of viral RNA in plasma after 3 months, but not 6 months of treatment. Subjects 1727 and 1679 were each infected with HIV-1 for approximately 3 to 4 months and were antiretroviral drug naïve. Subject 1774 was infected with HIV-1 for approximately 17 years and was antiretroviral drug

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

Resistant viruses can recognize, bind to and utilize the maraviroc/CCR5 complex for entry. Amino acid mutations in gp120 alters the way the protein interacts with CCR5. These modifications cause resistant viruses to be heavily reliant on the CCR5 N-terminus for entry (Roche et al 2015). There are two mutations on maraviroc resistant R5 HIV. These mutations replace Ala316 and Ile323 with Thr316 and Val323 on the V3 loop of the wild type HIV-1 CCR5 tropic strain. The Val323 mutation in the V3 loop of gp120 changes the secondary structure of the V3 loop making the loop less rigid and permits altered interactions with the N-terminus that allows for HIV-1 entry. A loss of beta sheets in the stem of the V3 loop occurs with the presence of the Val323 mutation. In addition, the smaller valine side chain may reduce steric interference and permit closer interaction with the residues on the N-terminus of CCR5. Thus, the Val323 mutation makes the V3 loop more fluid, allowing for closer interactions with the N-terminal of CCR5. In the presence of Maraviroc, HIV-1 resistant strains become considerably dependent on the interaction with N-terminal residues Try3, Tyr10, Tyr13, Tyr14, Tyr15, Glu 18, and Asp11.

Phenotypes are more expensive than genotypes but have more limited availability and also a problem of interpretation exists, the values (or “cutoffs”) that define resistance phenotypically have been based on the technical variability of the assay or, more recently, the biologic variability of wild type strains. Two companies have developed standardized assays amenable to high-throughput performance (Virco, Mechelen, Belgium and ViroLogic, South San Francisco, CA, USA) (Hertogs et al., 1998; Petropoulos et al., 2000). Both assays amplify the entire PR, much of RT and some of gag from HIV-1 RNA extracted from patient plasma.