A Brief Summery of the Evolution of Medical Therapy for HIV/AIDS

Medical therapy for HIV/AIDS has evolved staggeringly since HIV's first appearance in the 1930's when HIV is thought to have developed from SIV in primates. Reverse transcriptase inhibitors are an effective treatment, as reverse transcriptase (RT) (enzyme carried by the virus that makes DNA copies of HIV's RNA genes) blocks this process by impersonating a chemical RT needs to use. Additionally protease inhibitors can be used as agents to block the virus's enzyme that cuts other protein's in HIV that are needed to assemble more copies of its self.

In a previous blog I mentioned the CD4 receptors that HIV binds to for entry (using endocytosis) into the host cell. But there are other surface receptors that can inhibit HIV. The CD8 receptor secretes chemokines, and research suggests that HIV has to bind to another receptor (CCR5) to stop this secretion process. It is fascinating to know that people with a deficient ccr5 gene are resistant to the HIV-1 virus, and this excites scientists with hope of taking advantage of this pathway, for future therapies. All though it is unlikely that a cure will come from this past advance alone, any advance in terms of understanding in science is always a positive.

Thank you for reading.

 I will be posting blogs more regularly throughout the summer.



    

Comments and explanations for the BMJ's article on 'Discontinuation of aspirin for secondary prevention' (July 2011)

Aspirin, or acetylsalicylic acid is a commonly used drug for a wide range of conditions requiring prevention of clotting, analgesia and the reduction of inflammation. These effects are mainly due to aspirin's ability to inactivate irreversibly the COX (cylooxygenase) enzyme which is partly responsible for the production of thromboxanes.  Thromboxanes are a lipid and a vasoconstrictor, responsible for action in the clotting process. Thus by reducing this clotting agent aspirin can prevent such conditions as venous thromboembolism, colorectal cancer and  myocardial infarction (heart attack).

The BMJ article expressed concern and evidence to explain the negative effects of patients that do not take there medication. Evidence from Garcia Rodriguez's study showed that patients with non-fatal myocardial infarction that have had aspirin discontinued are have significantly increased risk of future myocardial infarction. Whereas there was no significant difference found when coronary heart disease patients stopped taking aspirin.

Conversely aspirin has the drawbacks of varying greatly from individual to individual, mainly because of the way the mechanism of aspirin that I outlined above works. Furthermore the use of aspirin is more difficult to medicate with patients with diabetes and some other subsets of conditions.

Conclusively  Rodriguez's research is so vital to patients, doctors and the general understanding of science: outlining that thrombotic  events can occur just 11-15 days after stopping the medication. Additionally from a drug design point of view aspirin is such a cheap, effective and safe drug to use that with the additional high risk to benefit ratio of the drug, making aspirin such a success in the pharma industry.

Simplified explanation of the cause of HIV/AIDS

It is estimated the 40 million people world wide are infected with HIV, this is a unimaginable amount of people who have no choice but to live with this Acquired Immunodeficiency. Simply because of the huge impact this virus has on the whole word, especially sub-Saharan African's, I have chosen to study and explain the cause in a simplified fashion:

HIV-1 is a lentivirus. A lentivirus is a slow acting virus meaning it has a long incubation period, and usually delivers a lot of genetic material into the DNA of the host cell. The HIV-1 virus consist of an RNA genome wrapped in a viral protein and a cellular membrane. HIV-1 along with other leniviruses, infects cells carrying the surface protein CD4 (using this CD4 molecule as a receptor). CD4 lymphocytes are part of the immune system that support other tasks, however CD4 receptors are found on a large range of cells, from the immune system to the brain. This is one example of the servility of HIV.

Once the virus is inside a cell with the CD4 receptor the virus then transcribes its genes from RNA to DNA, which is then slotted into the cell's genetic structure. The virus now has the power to make copies of its own genes, and order the cell it has infected to make proteins the virus needs. And that is how the lentivirus can reproduce its self.

In my next blog I will discuss relevant medical theories for HIV. Thank you for reading.