Details, Explanation and Meaning About HIV

HIV Guide, Meaning , Facts, Information and Description

The Human immunodeficiency virus (HIV) is a frequently mutating retrovirus that attacks the human immune system and which has been shown to cause acquired immune deficiency syndrome (AIDS).

Table of contents
1 History
2 Signs and symptoms
3 The virus
4 Pathogenesis
5 Treatment
6 Immunity
7 Common myths regarding HIV
8 Life Cycle of HIV
9 External links
10 Topics to be covered
11 Reference
12 See also
13 External links

History

HIV was discovered and identified as the agent for AIDS by Luc Montagnier of France and Robert Gallo of the United States.

A very small minority of scientists continue to question the connection between HIV and AIDS and even the very existence of HIV (see AIDS reappraisal).

As of 27 November 2003, there were an estimated 54,862,417 worldwide HIV infections, 30% of which were in Southern Africa.

For a person with the HIV in the United States to knowingly infect a person with the virus is a crime in every state of the union.

Signs and symptoms

This section deals with seroconversion syndrome. This is not identical to AIDS.

Acute infection with HIV is a very aspecific syndrome, which is easily missed due to its likeness to infectious mononucleosis and other viral infections. Fever, fatigue and rash are the most common symptoms, and many develop lymphadenopathy (swollen lymph nodes). Pharyngitis, myalgia and several other symptoms also occur (Kahn & Walker, 1998).

The virus

HIV has three major genes coding for structural proteins. These are gag, pol, and env. The gag-derived proteins make up the viral capsid (p24, i.e. a 24 Kilodalton protein) the nucleocapsid protein (p17) and a matrix protein. The Pol gene codes for the virus enzymatically active proteins. Most important is the so-called reverse transcriptase which performs the unique reverse transcription of the viral RNA into double-stranded DNA. The latter is integrated into the genome of the host, which means into a chromosome of an infected cell of an HIV-positive person by the pol-encode integrase. Also, pol encodes a specific viral protease. This enzyme cleaves gag- and gag-pol-derived proteins into functional pieces. The third structural gene, env, stands for "envelope". The proteins derived from env are a surface (gp120) and a transmembrane protein (gp41). They are located at the outer part of the virus particle and enable the virus to attach to and to fuse with the target cells to initiate the infectious cycle.

Pathogenesis

HIV causes disease by infecting the CD4+
T cells. These are a subset of leukocytes (white blood cells) that normally coordinate the immune response to infection. By using CD4+ T cells to replicate itself, HIV spreads throughout the body and at the same time depletes the very cells that the body needs to fight the virus. Once an HIV-positive individual's CD4+ T cell count has decreased to a certain threshold, they are prone to a range of diseases that the body can normally control. These opportunistic infections are usually the cause of death.

There are several reasons why HIV is so hard to fight. First, the virus is an RNA virus, using the reverse transcriptase enzyme to convert its RNA into DNA. This additional process results in a greater chance of mutation than in DNA viruses. Therefore, the virus becomes quickly resistant to therapy. Second, the common notion that HIV is a killer feasting on T cells is not true. If HIV were a killer virus, it would have died out soon because there would be too little time for new infections. In reality, HIV stays in the body for years, infecting people through unsafe sex, blood transfusions and breastfeeding of infants by mothers oblivious to their infection. HIV can survive even when drugs eliminate all detectable virons in the blood (viremia). It integrates itself into the DNA of the host cell and can stay there for years, lying dormant, immune to all kinds of therapy because it is just DNA. When the cell divides and the DNA is copied, the virus is copied too. After years, the virus can become active again, seize the cell's machinery and replicate.

In recent years, the notion that the CD4+ T cells decrease because of direct HIV infection has become doubted as well. The HIV coating protein readily detaches from virus particles. The blood becomes filled with these proteins, which can stick to the CD4+ T cells, gluing them together. In addition, they are recognized by the immune system, causing the immune cells to attack their own CD4+ cells. Metaphorically, HIV is guerrilla terrorist of the viral world, keeping low and seeking shelter when threatened, but always ready to hit where it hurts.

Treatment

. AZT, a reverse transcriptase inhibitor, was the first treament for HIV]]

Patients today are given a complex regimen of drugs that attack HIV at various stages in its life cycle. These are known as antiretroviral drugs. They include:

  • Protease inhibitors (PIs) inhibit activity of protease, an enzyme used directly by HIV to cleave nascent viral proteins, and so prevent final assembly of HIV virions.
  • Reverse transcriptase inhibitors (RTIs) inhibit the activity of reverse transcriptase, an enzyme HIV needs to complete infection of a cell. Lack of this enzyme prevents HIV from building pro-viral DNA based on its RNA. They come in three forms:
    • Nonnucleoside reverse transcriptase inhibitors (NNRTIs)
    • Nucleoside analog reverse transcriptase inhibitors (NARTIs or NRTIs)
    • Nucleotide analog reverse transcriptase inhibitors (NtARTIs or NtRTIs)
  • Entry inhibitors inhibit the viral entry into the cell interacting directly with the viral receptor and avoiding the fusion of the viral membrane with the target cell membrane.

Many problems are involved in establishing a course of treatment for HIV. Each effective drug comes with side effects, often serious and sometimes life-threatening in themselves. Common side effects include extreme nausea and diarrhea, liver damage and failure, and jaundice. Any treatment requires regular blood tests to determine continued efficacy (in terms of T-cell count and viral load) and liver function.

Immunity

About 10% of all Europeans carry a polymorphism of CCR5, a cell surface receptor that plays a role in HIV-1 infection (particularily the R5 strain). People with this mutation have a decreased risk of infection with HIV-1.

Common myths regarding HIV

Life Cycle of HIV

HIV enters a CD4+ helper T-cell by bonding with either CXCR4 or both CXCR4 and CCR5 depending on what stage the HIV infection is in. During the early phases of an HIV infection typically both CCR5 and CXCR4 are bound while late stage infection often involve HIV mutations that only bond to CXCR4.

Once HIV has bound to the CD4+ T-cell a viral structure known as GP41 penetrates the cell membrane and the HIV RNA and various enzymes including but not limited to reverse transcriptase, integrase and protease are injected into the cell.

Since the host T-cell does not process RNA into proteins the next step is to generate DNA from the HIV RNA using the reverse transcriptase enzyme to perform reverse transcription. If this succeeds the pro-viral DNA must then be integrated into the host cell DNA using the integrase enzyme. If the pro-viral DNA becomes integrated into the host cell's DNA the cell is now fully infected but not actively producing HIV proteins. This is the latent stage of HIV an infection during which the infected cell can be an "unexploded bomb" for potentially a long time.

Once the host cell starts to produce proteins from the pro-viral DNA the HIV-supplied protease enzyme must cleave the nascent HIV proteins in order for them to be assembled into HIV virons. The virons leave the cell by budding through cholesterol rafts on the host cell surface.

External links

Topics to be covered

To be written:
  • shape
  • enzymes
  • structure proteins

Reference

See also

External links


This is an Article on HIV. Page Contains Information, Facts Details or Explanation Guide About HIV


Google
 
Web www.E-paranoids.com

Search Anything