Essay on Congenital Neonatal Infections in Vertical HIV

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

The virus fuses with the cell’s plasma membrane. The capsid proteins are removed, releasing the viral proteins and RNA. Reverse transcriptase catalyzes the synthesis of a DNA strand complementary to the viral RNA. Reverse transcriptase catalyzes the synthesis of a second DNA strand complementary to the first. The double-stranded DNA is incorporated as a provirus into the cell’s DNA. Proviral genes are transcribed into RNA molecules, which serve as genomes for the next viral generation and as mRNAs for translation into viral proteins. The viral proteins include capsid proteins and reverse transcriptase (made in the cytosol) and envelope glycoproteins (made in the ER). Vesicles transport the glycoproteins from the ER to the cell’s plasma membrane. Capsids are assembled around viral genomes and reverse transcriptase molecules. New viruses bud off from the host cell.

On encountering a host cell, the retrovirus attaches itself to receptors on the surface of the host cell’s membrane. Once inside the cell, the capsid opens, releasing RNA and reverse transcriptase into the cell’s cytoplasm.

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.

Riviere, L., Darlix, J., & Cimarelli, A. (2009). Analysis Of The Viral Elements Required In The Nuclear Import Of HIV-1 DNA. Journal of Virology, 729-739. Retrieved October 4, 2014.

CCR5 gene encodes a receptor protein on the white blood cells that is involved in the entry of many forms of HIV virus into the cell. As of today, an estimated 10-20% of the Caucasian population possesses a mutated copy of CCR5 gene, which is also called CCR5-∆32. This mutated CCR5 gene contains a 32-base pair deletion. If an individual has

Viruses, after entering a host cell, integrates its genome with the host cell’s DNA using the enzyme reverse transcriptase. During normal DNA replication, the virus’ genome will be replicated to produce more viral particles. During this process, host cell genes can be triggered by viral genes

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]

A retrovirus infects a cell by connecting itself and then fusing with the host cell. Once it is connected and fused, a retrovirus can transform its RNA into DNA supporting the reproduction of it, also known as reverse transcription (College, 2013). After reproduction happens, all the new mutated cells leave the host cell to start this process all over within other healthy cells in the body (College, 2013).

to 30%, which is estimated that there were as many as 2,000 HIV infected infants

During the past decade, the human immunodeficiency virus (HIV) has become a leading cause of mortality among women. This population is now accounting for the most rapid increase in cases of acquired immunodeficiency syndrome (AIDS) in recent years. As the numbers of cases of HIV infection have increased among women, particularly of childbearing age, increasing numbers of children have become infected as well. "Various studies conducted to date indicate that between 1/4 and 1/3 of infants born worldwide to women infected with HIV have become infected with the virus themselves" (HIV InSite, 1997). This is due to the route of transmission known as vertical transmission, from mother to infant.

This paper presents an ethical analysis of the mandatory newborn HIV testing law enacted in New York State. The law was passed as an effort to decrease maternal transmission of HIV, by treating infants born to HIV positive mothers immediately after birth with AZT. Newborn testing was promoted by the legislative and medical community following the overwhelmingly positive response from HIV infected pregnant women who were given AZT in the ACTG 076 clinical trials. Pregnant mothers who were given AZT had a markedly lower transmission rate than mothers who had not received it. This paper examines this newborn testing policy from a Utilitarian perspective to ascertain if the goals of the policy are feasible. The potential advantages, as

The HIV-1 virion is approximately 120 nm in diameter, roughly spherical, and is composed of two copies of a single stranded positive sense RNA enclosed by a capsid (24). The HIV-1 genome is less than 10 kb and encodes for more than nine different gene products. It encodes for 3 major structural protein genes: gag (group-specific antigen), pol (DNA polymerase), and env (Envelope), which code for major structural proteins and essential enzymes. Gag generates the mature Gag protein matrix (MA or p17), capsid (CA or p24), nucleocapsid (NC or p7), and p6, which encompass proteins for the basic infrastructure of the virus such as the inner core of the viral particle (25). Pol encodes for reverse transcriptase (RT), which enables the virus to reproduce, integrase (IN), which is necessary to integrate the viral double stranded DNA into the host genome, RNAse H, and HIV protease, which are all encapsulated in the core of the inner particle formed by the viral capsid protein p24 (25). Env encodes for glycoproteins of the outer membrane such as outer gp120 (which enables the virus to attach and fuse to cells of the host), and transmembrane gp41 that anchors the glycoprotein complex to the surface of the virion (25). Between the core and the envelope is the HIV matrix proteins which are composed of the viral protein p17 (23). HIV-1 also encodes for proteins with important regulatory elements (tat (Trans-Activator of Transcription) and rev

In today’s world HIV/AIDS has become an epidemic that has not only challenged the research of our medical professionals, but also the lives of several children born with this infectious disease. In order to understand this epidemic we have to travel the path in which it was discovered. In 1985, human immunodeficiency also known as HIV was discovered by scientist and that discovery alone brought up many questions with very little definite answers. Due to this discovery several people are in search of an understanding & cure for this disease, but the question still remains what is AIDS and how can we prevent the transmission from mother to fetus?

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).