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Nothing made the world highly concerned about the immune system, what are its components? How does it work?, better than the emergence of HIV in the 80s. It’s a disaster, but made us know more about the immune system. Anatomy of AIDS virus

HIV’s target is CD4 receptors, which are present mostly on T-helper cells. It has glycoprotein 120 (Why do they call it 120 any way?! Is it the UV absorption again?! Or maybe it has 120 amino acids?!) It’s on its envelope. By recognition & binding to the CD4 receptors, it kills the T-helper which result in suppression of the whole cell-mediated immunity mechanism. It’s like cutting the snack’s head off. T-helper cells are responsible for giving signals (Interleukins) to other members of the IS so they can kill the viruses. By the whole suppression idea, the IS is turned off, the human body will be opened like your friend’s heart to you, to all possible invaders of m.o.

When we talked about HIV, the professor told us:” You wanna fight HIV, young docs full of enthusiasm, block its binding site, so it can’t bind to CD4 anymore.” I remembered the wise man’s words when I surveyed this article “Antibodies to the CD4-binding site of HIV-1 gp120 suppress gp120-specific CD4 T cell response while enhancing antibody response” about studying the effect of monoclonal anti-bodies against only the highly conserved part of the gp 120 (The binding site). We know that after exposure to HIV, the IS produces Ab against gp 120 to neutralize it, but the HIV tends to change the gp 120, so it can’t fit with the neutralizing Ab, moving on to more destruction. With those highly specific binders, I thought it’ll be the ultimate success.

Unfortunately, the research group made in vivo (in mice) & in vitro studies using the normal virus & another recombinant one with no CD4bs. They called it CD4bs+ Env & CD4bs- Env (Like with or without cheese). They found that the Anti-CD4bs mAb have high neutralizing activity, they raised the Ab titer (mainly IgG but not IgM). But they hinder the ability of the proteolytic enzymes/ the degrading mechanisms of phagocytes/ T-helper response to the envelope Ag/ the ability of Antigen presenting cells & MHC II to present the Ag. Let’s think about it…. They can only present the virus’s Ag, not the gp120/anti-CD4bs complexes. This is too long in writing, how about presenting? Just kidding, It’s about that the Ag is already covered, so it’s useless to be presented.

This is so awful, even the last approach to bind HIV didn’t work. What are the researchers gonna do? What’s the next move? We’ll find out soon.

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Anatomy of AIDS virus:

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Nature, mother nature & the famous journal, taught us that every organism has its own defense mechanisms against various predators. For example, the famous antifungal agent (cyclohexamide) is obtained from the bacteria Streptomyces, on the other hand (Penicillin), the antibiotic, comes from the fungus Penicillium.

We all know phages, the nick name of Bacteriophages, the virus-like agents that infect bacteria making it sick.. Well not sick, but only degrade it like any other virus on the planet. As a matter of fact, Bacteria have to develop defense mechanisms against these phages:

1)They can cut their genome with restriction enzymes (endonucleases)

2)They can also undergo changes in their receptors, so the phage goes blind & never find it

3)They can act on the phage itself by making DNA modifications or even repression of their gene expression.

But now we’ll talk about a different defense mechanism (they love to call it: Special Forces). To know it, you’ve to meet CRISPR sequences (clustered, regularly interspaced, short, palindromic repeats). Not crispy, it’s CRISPR. Actually when I first read it, I was totally lost. I knew the meaning of every word separated from the very next. So I checked more & got this from the amazing blog of Tim “Phage Hunter“.

As you’ve read before, they are sequences found in almost 40% of sequenced bacteria & 90% of sequenced archaea. There are already identical repeats which form RNA stem-loops. Between those repeats, researchers found DNA which is similar to that of phages. That means that the bacteria use the RNA interference mechanism (an inhibitory gene expression mechanism).
CRISPR sequences are first transcribed, and then spliced to form small interfering RNA (siRNA), which are complementary to the target mRNA (the phage’s). Once binding achieved, no translation occurs, because they simply cleave it into little pieces.

Bacterial CRISPR is modeled to work as iRNA in eukaryotes

So the array of these sequences is highly useful in determining the bacterial resistance to different phages. Y. pestis (aka Black death) has three CRISPR sequences in its genome. It’s something like acquired immunity, bacteria develop it after the infection of the phage, the survivors of course.

For people On The Run: Bacteria have a complementary sequence of their phages, to capture their RNA, stop the translation process.

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Figure shows the role of siRNA in degradation of phage nucleic acids:

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