The human immunodeficiency virus

Introduction

The Human Immunodeficiency Virus ( HIV ) is classed as a Lentivirus. Such viruses are good known to exhibit long incubation periods and to do chronic diseases to host. During the class of this paper, a changing figure of subjects will be discussed in relation to this virus and the disease that is caused.

An estimated 77,400 people were populating with HIV in the UK at the terminal of 2007, of whom over a one-fourth ( 28 % ) were incognizant of their infection. — HPA

The HIV virion is known to be in two signifiers, these are HIV-1 and HIV-2 ( **1** ) . The virus type HIV-1 is referred to as being more infective than HIV-2. Due to the reduced pathogenicity, the spread of HIV-2 is confined largely to western Africa where as HIV-1 is found globally ( **1** ) . Due to this fact, much of the information provided in this paper will be directed towards the description and reading of HIV type 1.

Structure of the HIV Virion

The HIV virion is between 100nm to 120nm in diameter and consists of 3 membranous constructions. The most outer of these constructions is the spherical lipid bi-layer envelope, the 2nd most interior construction is the spherical viral P17/18 matrix ( **4** ) and the concluding most interior construction is the cone like viral P24/25 joke mirid bug ( **4** ) . Implanted and squeeze outing from the surface of the virion is complex of 3 proteins, 2 of which are GP120 and GP41 ( **4** ) , the importance of these bulges will be explained subsequently in this paper.

Within the gag mirid bug two individual stranded RNA strands. These are normally but non ever indistinguishable to one another and these are accompanied by the cardinal enzyme, rearward RNA polymerase every bit good as other enzymes needed for reproduction in the early portion of the virus ‘s lifecycle.

Transmission

The transmittal of any virus/ being is dependent upon the belongingss of that being, the physiological province of the host and the environment in which the two come into contact.

When the transmittal of HIV is investigated, three chief tracts can be identified:

• Transmission through infected blood/ blood merchandises – within the blood of an septic person, high Numberss of HIV infective virions can be detected, up to 10 billion. Due to this, any events affecting exchange of blood or blood merchandises can ensue in disease transmittal. Such events include: transition of contaminated blood in to host blood watercourse, sharing hyperdermic acerate leafs and having a blood transfusion, hemophiliac receiving contaminated coagulating factors.
• Transmission through infected fluid from the genitalias – HIV infective virions can besides be found in venereal fluids, although it should be noted that this is significantly reduced in female vaginal fluid ( but non male seminal fluid ) . Due to this fact the opportunity of transmittal is lower than that of blood merchandise exchange if the host is a male holding intercourse with an septic adult females. The same can non be said in the opposite status of a female host. Male homosexual intercourse besides carries high hazard while female homosexual Acts of the Apostless are markably lower. Other factors which affect transmittal rate vary between persons but include facets such as: presence of other venereal diseases, CD4 and CD8 lymph cell count, prophylactic usage and any medicines being taken by the host
• Transmission from an septic female parent to her unborn kid – the concluding manner of transmittal, although much less common, still does happen. Transmission of the HIV virus from female parent to child occurs normally during birth. Increased incidence is associated with low T-cell count and or high viral tonss in the female parent. Increased HIV infected vaginal cells besides play a key. It is of import to detect that increased Numberss of human serum glycoproteins really show a lessening in transmittal rate possible due to these proteins assailing or suppressing the virus.

Symptoms

Diagnosis

Resultatant Disease

Once a patient has been diagnosed as holding a HIV infection, until extremist progresss are made in medical research, the patient will necessarily hold a premature decease. Current promotions assistance in giving the patient a prolonger life span but as of yet, there is no remedy for HIV. HIV its ego is characterised as a viral disease that infects host immune cells and causes subsequent devastation of these cells through a assortment of mechanisms that shall be discussed subsequently in this paper.

Most patients with HIV will develop Acquired Immune Deficiency Syndrome ( AIDS ) within around 10 old ages of the initial HIV diagnosing **** . Without intervention, the patient can anticipate to decease within one twelvemonth of their AIDS diagnosing, nevertheless, with intervention the patient may populate to around 5 old ages past the HIV diagnosis**** . Again in the instance of AIDS, merely support intervention is available.

Both the mechanisms of the disease class and those of the current disease intervention will be discussed subsequently in this paper.

Mechanism of Infection

Upon the HIV virus being transmitted to a new host the following phase of HIV life rhythm is to get down procedures of self reproduction. Due to HIV being a virus, this end is achieved by integrating itself into the host cells and using host cell ‘machinery ‘ .

For viral intergration to happen, parts of the viral GP120 protein interact with CD4 receptors that are expressed on the cell membrane of CD4+ cells ( **7** ) . Authoritative illustrations of such cells are CD4+ T-lymphocytes. Although HIV association with CD4 receptor is indispensable, it is thought ( **7** ) that HIV virion association with CD209 is a cardinal portion to this procedure. CD209 is a binding receptor found upon the surface of macrophages and dendrite cells and is bound to by the virion via its external GP120 protein ( **7** ) . This binding holds the virion in topographic point and allows for better association with the CD4 receptor nowadays on CD4+ T-lymphocytes. Now, other GP120 molecules located at a different site on the virion can adhere to CD4 receptors on CD4+ cells. This binding causes a conformational alteration to the GP120-CD4 composite and this allows binding of the co-receptor.

One of two chemokine co-receptors ( CCR5 and CXCR4 ) are needed for the completion of the virion and host cell membrane merger. Binding of one of these receptors non merely completes the concluding phase in conformational transmutation needed, but it besides induces leukocyte chemotaxis to the country. This is good as a local addition of leucocytes increases possible figure of cells there are present to infect.

For membrane merger to happen, the extracellular subdivision of the GP41 protein which contains a hydrophobic terminal to its peptide concatenation. This inserts itself into the host cell membrane giving anchorage. Due to a figure of conformational rearrangements, another insertional peptide ( called the merger peptide ) inserts into the host membrane. As a consequence, the membranes now fuse and the intracellular constituents of the virion are combined with the intracellular matrix of the host cell.

Once inside the cell, the following phase is to transcribe its familial RNA into DNA and to so infix that into the host familial DNA. Transcription is carried out by contrary RNA polymerase which converts the viral RNA into DNA and this is so inserted in to the host Deoxyribonucleic acid in the karyon by the enzyme intergrase.

Now the familial information is inserted, the information now has to be replicated and the attendant proteins reassembled to organize new HIV virions. Protease enzyme plays a cardinal function in spliting big peptides into smaller 1s. This is indispensable for the formation of infective virions. Familial reproduction occurs in the presence of certain indispensable written text factors ( eg NF kappa B ) . One of import note to do here is that NF kappa B is over produced when T-cells are activly contending infection and so I shall be these peculiar immune cells that shall be most effected.

Once the new virion molecules are assembled with the mirid bug in topographic point, they move to the inner cell membrane surface and ‘pinch-out ‘ of the host cell via budding. This gives the mirid bug coated familial stuff a lipid bi-layer incorporating both host and viral proteins. The new virions are now released and free to infect other host cells.

Infects… causes lessening in…

Pathogen endurance schemes in the organic structure ( virulence factors ) ;

The HIV virus one time in the organic structure, has a half life of between 28 and 110mins ( **1** ) . This is non really advantageous to the being as without the correct environment, the virion may be destroyed before its had opportunity of reproduction. However, one infected cell can bring forth 200 to 1000 virions per twenty-four hours ( norm of 200 of which are infective atoms due to some virions being damaged or uncomplete ) ( **1** ) . Such a high production of virions ensures adequate

Upto 10 billion virus atoms in blood of a diagnostic platinum ( **1** )

Adhering sites on external GP120 — — page 11 of ( **1** )

HIV can adhere to different cell types and travel about host with these cells. As these cells go to trip their mark, HIV nowadays and so may infect the mark cell ( **1** ) page 32

Host defense mechanism mechanisms relevant to this disease

Viral infection of a host is some what more debatable for the host than that of a bacterial infection. Chiefly this is because, for most of the infective rhythm, the HIV virus is present intracellularly with the hosts own cells. This makes sensing and pathogen riddance much more hard. However, although it is more hard, the host still gives opposition to the virus.