Study on HIV Replication cycle Prevention of individual protein release (HIV proteins) prevention of release of viral RNA and

proteins. Immobilization dissemination prevention of movement in cell surface. Analysis of immature virus examination for consistency cell division meiosis mitosis etc. experimentation and prevention of division. Prevention of new viral DNA to be used as genomic DNA. DNA and analysis of amino acids for the prevention of making viral proteins Analysis and movement the regression and the stoppage of viral DNA being transported across the nucleus sharing of the link that integrates it to host DNA. Prevention of coupling sequencing intervention Reverse transcription analysis and deconstruction the prevention of the formation of viral DNA Blockage of the host cell to HIV RNA reverse transcription integrase and other viral proteins. Prevention of fusion of the HIV cell to the host surface The viral core- structure of HIV P7 HIV Nucleocapsid Protien The reversal of the process of production three enzymes reverse transcriptase integrase and protease the production of these examined the protein P17 HIV Matrix protein that lies between the viral core and the viral envelope changing its use and productivity The ends of each strand of HIV contain an RNA sequence of LTR long terminal repeat to be switched off as proteins from HIV and host cell are configured to either support its non active switch or non existent so the switch isnt activated HIV has 6 regulatory cases TAT REV NEF VIF VER VPU NEF replication VPU release of new particles from infected cells VIF the protein encoded by VIF gene interacts with an antiviral protein in host cells APOCEL3G Causing inactivation of the antiviral effect and enhancing HIV replication NEF-reversal of meiosis mitosis etc. VEU- stoppage of virus control of metastisis VIF the counteracting of the protein or the process Viral protein P-24- 2000 copies in capsid reverse process of contents to single strands of HIV RNA each with a copy of the viruses genes 3 structural genes GAG POL and ENV the complete reversal of the processes of RNA with encoding the reversal process for viral RNA delivery Makes structural proteins from new virus particles

ENV-gp160->gp120gp41 broken down by a viral enzyme- counteract the enzyme and have usage for the opposite of gp120 and gp41 Spherical in shape or whatever shape is most useful the diameter will be evaluated HIV1/10,000 of a millimetre, outer coating antibody and opposite of viral envelope Lipids replaced by antiviral entities protiens from the host cell are replaced by proteins from the opposite of HIV 72 copies of ENV replaced by microscopic proteins that counteract the HIV process Envelope proteins<->antiviral processes HIV evades the immune system usage of holograms as diverse and varied as needed for productivity and analysis to adapt to the constantly changing HIV overall monitoring system to keep in check new and diverse strains. HIV devastates the immune system HIV prevention of destroying precursor cells perhaps with stem cell treatments and replacement therapies Management of development of precursor cells into mature immune cells Protection of the bone marrow and the thymus inducing regeneration in both Prevention of immune suppression Prevention of the HIV cells binding to the cell surface CD8 T cells controlled and only deployed when necessary Prevention (and proper inducement) of apoptosis- cells not infected with HIV-no apoptosis Cells infected-apoptosis with dissemination dissolving and disintegration Blood stream and lymph nodes controlling apoptosis CD$+T cells rid of infection of HIV prevention of the virus of infected cells form budding. Normal activities of the cell looked at /regulated. Other infections immune system CD4+T cells regeneration to fight infections HIV hides from the immune system Disinfection of the cytoplasm cleansing of the chromosomes Latent reservoirs looked at examined and determined to be rid of all infective materials Brain lymph nodes reticulo-endothelial system bone marrow gastrointestinal cells checked and virus subjugated to inert status by riddance of infective agents in these places Reorganization of anti retroviral drugs to accommodate latent reservoirs

Clinical progression of HIV CD4+T cells prevention of replication HIV copies viral load prevention of metastasis thymus spleen lymph nodes genetic material of the cell protected from integration of the virus examination of acute phase latency Examination for flu-like symptoms CD4+T cells regulation and (additives to fight infection to antibodies)modified CD$+T cells regulated(2to4 weeks) Prevention of replication in the lymphoid organs Prevention of increase of viral load in blood Regulation of CD4+Tcells Prevention of further infections Factors that affect disease progression CCR5 +CD4 molecule prevention of infection of cells CXCR4 prevented from entering a cell a look at mutations-examination HIV in blood viral load controlled by cleansing of the blood transfusions etc HAART highly active antiretroviral therapy introduced okays progression of drugs.