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Cure for AIDS

About microscopic forms of life, including Bacteria, Archea, protozoans, algae and fungi. Topics relating to viruses, viroids and prions also belong here.

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Postby vinaya » Thu Jan 19, 2006 1:37 pm

sure doc 8) :wink:
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Postby victor » Thu Jan 19, 2006 2:06 pm

Dr.Stein wrote:HIV is a very smart virus that is capable to change its surface protein, just like its old friend influenza virus but HIV is much smarter and so naughty (We call both as "Masters of Mutation" hehe), by changing the active gene expression. A random change in a gene, a mutation, and the genes of HIV mutate extremely frequently, more often than any other virus known to science. When a gene encoding one of the virus surface proteins is the one that mutates, the shape of that protein is often altered, and as a result the immune system memory no longer recognizes it.


we know that Orthomyxovirus type can change it's surface protein like Lentivirus type do...but do both of them bear the same mechanism? what I know is, Orthomyxoviridae use two mechanisms in changing it's surface protein which is by Antigenic driff and antigenic shift..
what about Lentiviridae?
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Postby victor » Thu Jan 19, 2006 2:11 pm

ahh...got it..now read this... :lol:

Human immunodeficiency virus (HIV) is the causative agent for AIDS. The most common type is known as HIV-1 and is the infectious agent that has led to the worldwide AIDS epidemic. There is also an HIV-2 that is much less common and less virulent, but eventually produces clinical findings similar to HIV-1. The HIV-1 type itself has a number of subtypes (A through H and O) which have differing geographic distributions but all produce AIDS similarly. HIV is a retrovirus that contains only RNA.

HIV is a sexually transmitted disease. Infection is aided by Langerhans cells in mucosal epithelial surfaces which can become infected. Infection is also aided by the presence of other sexually transmitted diseases that can produce mucosal ulceration and inflammation. The CD4+ T-lymphocytes have surface receptors to which HIV can attach to promote entry into the cell. The infection extends to lymphoid tissues which contain follicular dendritic cells that can become infected and provide a reservoir for continuing infection of CD4+ T-lymphocytes. HIV can also be spread via blood or blood products, most commonly with shared contaminated needles used by persons engaging in intravenous drug use. Mothers who are HIV infected can pass the virus on to their fetuses in utero or to infants via breast milk.

When HIV infects a cell, it must use its reverse transcriptase enzyme to transcribe its RNA to host cell proviral DNA. It is this proviral DNA that directs the cell to produce additional HIV virions which are released.

The genome of HIV contains only three major genes: env, gag, and pol. These genes direct the formation of the basic components of HIV. The env gene directs production of an envelope precursor protein gp160 which undergoes proteolytic cleavage to the outer envelope glycoprotein gp120, which is responsible for tropism to CD4+ receptors, and transmembrane glycoprotein gp41, which catalyzes fusion of HIV to the target cell's membrane. The gag gene directs formation of the proteins of the matrix p17, the "core" capsid p24, and the nucleocapsid p7. The pol gene directs synthesis of important enzymes including reverse transcriptase p51 and p66, integrase p32, and protease p11.

In addition to the CD4 receptor, a coreceptor known as a chemokine is needed for HIV infection. Chemokines are cell surface fusion-mediating molecules. Such coreceptors include CXCR4 and CCR5. Their presence on cells can aid binding of the HIV envelope glycoprotein gp120, promoting infection. Initial binding of HIV to the CD4 receptor is mediated by conformational changes in the gp120 subunit, but such conformational changes are not sufficient of fusion. The chemokine receptors produce a conformational change in the gp41 subunit which allows fusion of HIV. The differences in chemokine coreceptors that are present on a cell also explains how different strains of HIV may infect cells selectively. There are strains of HIV known as T-tropic strains which selectively interact with the CXCR4 chemokine coreceptor to infect lymphocytes. The M-tropic strains of HIV interact with the CCR5 chemokine coreceptor to infect macrophages. Dual tropic HIV stains have been identified. The presence of a CCR5 mutation may explain the phenomenon of resistance to HIV infection in some cases. Over time, mutations in HIV may increase the ability of the virus to infect cells via these routes. Infection with cytomegalovirus may serve to enhance HIV infection via this mechanism, because CMV encodes a chemokine receptor similar to human chemokine receptors.
Here's some nice picture of my pet for you...:lol:
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and this,
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Guess it...typed by my own hand?? or somebody else's hand?? :lol:
I think after this, mods have to move this thread into microbiology topic..:mrgreen:
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Postby MrMistery » Thu Jan 19, 2006 7:23 pm

Yes sir. Understood sir. Topic moved, sir. Anything else, sir?
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Postby Dr.Stein » Fri Jan 20, 2006 4:38 am

victor wrote:Guess it...typed by my own hand?? or somebody else's hand?? :lol:
I think I know the secret ;) :lol:

I like students who can answer their own questions :) Hail! :D
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Postby victor » Fri Jan 20, 2006 12:34 pm

Yeah, as you see...I'm a species whose has a close link to Lazyus sleeperius, so I think you'll know the answer... :lol:
By the way Dr.Stein, I'll (once again) answer my own question and share it with others here...(now it's truly typed by my own hands) :lol:

I think I've got the point why the RNA of Lentiviridae vary from one to another....the mechanism is like this, Lentiviridae is a family (subfamily) under Retrovoridae who're well famous with their Reverse Transcriptase enzyme which act like DDRRT (DNA Dependent RNA Reverse Transcriptase)...(I create the abbreviation by my own.. :lol:

When entering the host cell, (Macrophage and T-cell) they use that enzyme and oftenly this enzyme doesn't reverse-transcripted the whole RNA to DNA succesfully (I mean there're some mutation in the DNA reverse-transcripted here, there and everywhere)...
that means the genetic mutation occur in DNA and continue to the stuctural protein (I think it's called gp120 or gp70, I forgot about that)...
that's what I read according to my JMAMMB.. :lol:

question of the day: what is JMAMMB? :lol:
Last edited by victor on Sat Jan 21, 2006 1:28 pm, edited 2 times in total.
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AIDS

Postby Jennifer » Fri Jan 20, 2006 9:33 pm

Did anyone hear about the guy who supposedly was cured from AIDS just by taking vitamins alone?
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Postby victor » Sat Jan 21, 2006 11:53 am

Now I'll ask you? what is the definition of "cure from AIDS"?
Let me show you the case:
the association (I don't know the name) has determined that one is positive AIDS (not positive HIV) if the T-lymphocyte level is <200 units/µL.
Treatment can be done with giving AZT (Zidovudine) and 3CT (Lamivudine) and Indinavir (Protease inhibitor)..After a few weeks later, the T-lymphocyte level is up till 250 units/µL.
In this case, the patient is "cured" from AIDS (because t-cell level is above the minimum limit) but he/she is not free from the HIV itself..
so, do you got what I mean?? :wink:

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Victor, Eathybus anythingus
Last edited by victor on Sun Jan 22, 2006 12:19 pm, edited 1 time in total.
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AIDS Revealed

Postby pankaaj » Sat Jan 21, 2006 2:17 pm

I have read that ' Dahi '(curd) is cure for AIDS.
Does anybody want to make a reaserch in this? :roll:
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Postby victor » Sun Jan 22, 2006 12:33 pm

See my previous post..it seems you don't get my point..
getting infected by HIV doesn't mean that you get AIDS directly (HIV is a laten virus and it's progeny need at least 7 years to become AIDS).

Someone can be said having AIDS IF if his/her T-cell amount is <200 cell/µL.
If someone who get AIDS is treated carefully with HAART (Highly Active Anti-Retroviral Treatment) then, his/her T-cell level can be raised up till 250 cell/µL. Now, he/she doesn't have AIDS anymore....but still having HIV.

that's the common thing happen...so, if you ever heard that someone get cured from AIDS, maybe the thing which actually happen is like the thing above...but if it's really cured (HIV inside body is totally vanished), maybe it's a miracle...
I can say like this because HIV is the virus that cause death nearly 100%...it's a deadly weapon which runs from the nature's biology warbase..
Hope you got my point. :wink:
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Postby 2810712 » Sun Jan 22, 2006 3:31 pm

Oh those harmyMOMs [ harmful MAsters Of Mutations]!!!
But the discussion was rreally good one.

Journal of Microbio And Medical MicroBio?
Jourmal of Medicine And Medical Microbiology?


Inheritance + only vitamins maybe = cured AIDS

Curd? really absurd?

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Postby victor » Mon Jan 23, 2006 12:40 pm

haha..I try to give the best to topics related to Virology..
JMAMMB = Jawetz, Melnick & Adelberg's Medical Microbiology..:lol: it's my reference book, but it's more medical than biology..

Well, it's still a mystery and need further research..wait till I become virologist..:lol:
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