HIV virus and how it works.
Simply about science.
This Article is an overview of the HIV virus in the simplest manner - so everyone can understand it.
HIV is retrovirus - Unlike the most mammalian cells, retrovirus genetic material flow in reverse direction Generally speaking, the virus hack into a cell host with help of reverse transcriptase enzyme that allows the viral RNA to be copied in to the hybrid DNA/RNA and incorporated into the cell genome.
NORMAL cell process :DNA -> RNA-> Protein -> function. HIV virus pathway: viral RNA -> back transcript -> DNA, stop , DNA viral -> RNA viral - viral proteins – as viruses released.
Structure of HIV is very simple but very deadly.
There are two layers or cores in the virus, the first one is a lipid bilayer (look pic 1) with protruding “spikes” (they composed of glycoprotein/peplomers). They serve as anchors because they help to attach to the host cell. The two essential glycoproteins gp41 and gp120 are key players in whole HIV initialization process. GP41 is an anchor that attaches the peplomer (glycoprotein gp120) to HIV lipid Envelope, while gp120 is an anchor that binds to the particular host cell binding site ( CD4 + in human) CD4 is present on surface of T helper cell ( subset of immune cell “ T lymphocyte” 70% of all lymphocytes in the body) and other immune response cells ( microphages).
Process is sneaky.
GP 120 binds to the CD4 cell receptor, the binding initialize gp40 and now whole virus penetrate the host cell wall (embedding) and get inside.
Second layer of HIV is a killer.
Inside of the host cell, virus outer core breaks down leaving the second (outer) core. This second core consist of : reverse transcriptase enzyme (RT), proteases (P’s) and RNA strands (viral information strands). First step belongs to RT, who overwrites or hacks into host cell replication machinery and try to incorporate itself into cell genome, later it will use mRNA to use the process of replication and create many viruses like itself. Those small viruses that were formed are immature and they need to be activated by proteases (P’s) to become fully infectious viruses. Then they leave infected cell and attach themselves to other CD4 cells and the process repeats.
(Photo Credit : Martin M. Zdanowicz) of Pathophysiology for Pharmacy
Consequences
Reduction in circulating lymphocytes and decrease in immune system ability to fight diseases.
Extras : Just to know about (*Reference )
Common diseases in AIDS.
Pneumocystis pneumoniae —A parasite that can cause a severe pulmonary infection
Histoplasmosis — Generalized fungalinfection
Toxoplasmosis — A parasite that primarily infects the brain
Tuberculosis — Bacteria that primarily infects the lungs
Candida — A fungus that can infect the oral cavity (oral “thrush”)
Cryptococcal infection — A fungus that primarily infects the brain
Cryptosporidium — A gastrointestinal parasite that can cause severe diarrhea
Cytomegalovirus — Herpes virus that can infect the eye, intestine,
esophagus, lungs
Treatment ( at least something)
Nucleoside reverse transcriptase inhibitors
Examples: zidovudine (AZT), didanosine
Competitive inhibitors of HIV reverse transcriptase enzyme
Cause termination of growing viral DNA chain.
Common side effects include rash, nausea, diarrhea and peripheral neuropathy
Non-nucleoside reverse transcriptase inhibitors
Examples: nevirapine, efavirenz
Bind directly to HIV reverse transcriptase to inhibit it
Side effects include severe skin rashes, nausea, diarrhea and central nervous
system effects
Protease inhibitors
Examples: saqiunavir, ritonavir
Inhibit HIV protease enzymes that are essential for enzymatic activation of newly
replicated HIV viruses
Adverse effects include abnormal fat distribution (“buffalo hump”),
hyperlipidemia, diarrhea, gastrointestinal disturbances and parasthesia.
Reference : * (Martin M. Zdanowicz) of Pathophysiology for Pharmacy
* (Lodish) Molecular Cell Biology, 5 edition
