Confused-different life cycle of HIV infection of cells and meds to stop this

[friskyguy]

Hi everyone,

I have read the lessons which explain the life cycle of HIV and its infection of cells and how the different classes of meds work at different ways to stop the further replication of HIV.......but still a little confused......not sure if anyone out there can help?

Entry inhibitors meds such as 'maraviroc ' prevent HIV from entering healthy CD4 cells (T-cells) in the body. If entry inhibitors are successful, HIV is unable to bind to the surface of CD4 cells and gain entry into the cells in the first instance.

They work differently than many of the approved anti-HIV drugs—ie the protease inhibitors (PIs), the nucleoside reverse transcriptase inhibitors (NRTIs), and the non-nucleoside reverse transcriptase inhibitors (NNRTIs)—which are active against HIV AFTER it has infected a CD4 cell or macrophage.

So wouldn't the entry inhibitors meds be the best meds to take cause they prevent HIV from entering and infecting the cells in the first place?

Having cells infected with HIV (although not able to replicate due to other meds like the NRTIs and NNRTIs etc) would be second best option due to the fact that the cells, ie CD4 and macrophages have actually still been infected by HIV and because of this would cause potentially other issues, maybe larger viral reservoirs of cells and/or in tissues etc? 

I know the question is quite complicated but it has always mystified me why we all would not want to strive to take meds that stop HIV from infecting cells at the very beginning of its infection life cycle.

Surely that would be best or doesn't it really matter or not enough research has been conducted as yet?

Any scientific minds out there willing to have a go?




 

[spacebarsux]

Friskyguy, I don’t know if mine is a scientific mind but I’ll have a go from whatever I understand on the subject, which I should admit is very limited. Perhaps someone better informed can fill in the gaps.

I might be a bit off-base but as I understand it (and as I was edified by someone knowledgeable) HIV is a highly variable virus that mutates readily and easily. Once a person is infected with a strain of HIV, the virus rapidly mutates into different sub-strains within your body (yes, even within the body of a single person). Though each of us was infected with a particular viral strain, post infection, this strain quickly mutates into several sub-strains, which are all coursing through our blood stream.

What’s more, post-seroconversion, HIV is already present in your body at different stages of its life-cycle. There’s HIV provirus that is just waiting to infect the CD4 cells, and this could well be targeted by entry inhibitors, but then there's also the HIV that has already penetrated the membrane of CD4 cells, and this has to be tackled by the PI’s and NNRTI’s.

So, in short, HIV is a bug that needs to be squashed from all angles and in different ways. 

[friskyguy]

Thank you spacebarsux for taking the time to answer.....ur explanation makes perfect sense.......HIV is already present in the body in many different stages of its lifecycle hence the need for a cocktail of drugs that work in different ways to squash it.....got it!

thanks again