HIV are treated with combination of
- protease inhibitor
- reverse transicptase inhibitor
- intregase inhibitor optionally
- CCR5 receptor anatgonsit
— is an enzyme in the virus that reads the viral rna that enter the host and trascribes the sequence into the complementary dna sequence.
revise transpitase
the entry of HIV ,
HIV attached to the surface of —-and binds to two receptors which are —– and —- which loops through the cell membrane of the T-cell — times ( CCR5 ) . the ligand in this case HIV needs to bind to — for an infection to occur. and after the attachment the —— and HIV viral rna and the contents will —— and HIV will make —-
- lymphocyte aka the t-cell
- primary receptor : CD4 and secondary which is the transmembrane receptor
- seven
- both receptors
- 2 membrane fuse
- empties into the host cell
- copies of itself
true or false:
reverse transpitstse makes no mistakes in reading viral rna sequence
false , it makes mistakes , not all viruses are alike. viruses from the same host cell may end up with difference in shape surface coat or enzyme
the dna is made by —- from the viral dna that is incorporated into the host or T cells dna.
reverse transpitase
— is an enzyme that helps insert the viral dna into the host
intregase
one the viral dna is part of the hosts dna it is called —
provirus
there are — genes in HIV RNA and these genes are have important codes to make ——-
- nine
- structural viral envelope and core proteins and enzymes as reverse transpitase , intregase and protease
—– is made into long polypeptide sequence which is made up of several individual protons. these sections must be cut from long polypeptide chains in order for the proteins ( aka enzymes ) to be —- .
the —- act as chemical scissors and cut the chains into the component
- translated viral rna
- functional
- viral protease
finally the viral rna proteins are made and are packaged and released from the —
the newly formed virus take a lot of the T cell membrane containing —– and these proteins bind to receptors on other immune chells
hosts T cells
viral surface proteins
Nucleoside Reverse Transcriptases inhibitors:
because they lack 3 Og of the cyclic sugar ,termination dna chain — occurs
- elongation
( check slide 11)
Non Nucleoside RT inhibitors:
—- is very active against wild type and resistant mutant of HIV-1 and it gives virus inhibition
efavirenz
Non Nucleoside RT inhibitors (NNRTI):
— binds directly into the rt and blocks the RNA and DNA dependent polymerase activities disrupting the enzyme active site .
these inhibitors bind in a pocket formed between —- away from the —– active site .
the internal surface of the pocket is —–
- nevirapine
- w beta sheeted of p66 palms
- polymerase
- predominantly hydrophobic and consist of leucine , valine , tryptophan , tyrosine residues
—- play also a pivotal role
In the assembly and release of viral particles.
HIV protease
—- is an enzyme that is responsible for the post translational
modification of core proteins
HIV protease
—- group of drugs represent a major breakthrough in HIV
treatment when used in combination with RT inhibitors
HIV protease inhibitors as:SAQUINAVIR, RITONAVIR, INDINAVIR
are competitive antagonists of the natural substrate peptide.
how does the protease inhibitor works?
- it reassembles the protein chain the protease cut
- in binds to the site that normally binds to the protein chain
- once the inhibitor binds , the protease can’t bind the protein to be cleaved and cant be functional
— are reposible for inhibiting the integration of viral dna in the cells genome
intregase inhibitor
( Compounds of this class contain a b-ketoester or b-ketoamide )
intrgase inhibitors enter in the — and coordinates 2 essential — cations involved in catalytic cycle
- enzyme
-mg+2
CCR5 Antagonists: Maraviroc
they selectively bind to human —- which is present on the cell membrane
this binding prevents the interaction of — with — which leads to inhibition of the virus from entering the cell
- chemokine receptor CCR5
- HIV-1 with CCR5-tropic HIV-1
