HIV is brought to lymph nodes by dendritic cells or macrophages.
Infects T helper cells (CD4 lymphocytes).
CD4 cell count is <200 cell/mm
-HIV can mimic mononucleosis (fever, HA, sore throat, lymphadenopathy, rash, joint ache, myalgia) and my be accompanied by diarrhea and weight loss.
Key Receptors
CD4 Receptor: Primary receptor required for HIV to bind to T helper cells
Co-receptors: CCR5 (preferred) and CXCR4.
HIV Entry Mechanism
Gp120 Protein on HIV envelope binds CD4 receptor. Lock (CD4) and key (Gp120) receptors.
Induces conformational change in CD4, allowing CCR5/CXCR4 to pull viral and T cell membranes together. The CD4, CCRS receptor pulls the viral membrane closer to bind
Gp120 protein stalk pierces T cell membrane, pulling the two closer together fusing the membranes.
HIV injects its genetic material (viral RNA) into T cell.
Viral RNA to DNA Conversion
Reverse Transcriptase: Converts viral RNA into single-stranded DNA, then into double-stranded DNA.
High error rate leads to mutations, complicating vaccine development.
Integration into Host DNA
Integrase Enzyme: Integrates viral DNA is carried into T cell nucleus then cuts or snips a section in the DNA to integrate itself into the persons DNA.
Either remains latent or the DNA transcribed into mRNA.
HIV Replication and Budding
Viral mRNA leads to creation of new viral proteins.
Polyproteins: Long protein strands including viral enzymes (reverse transcriptase, integrase).
Protease enzyme: Cleaves polyproteins into functional viral components.
New virions bud off T cell, becoming mature HIV particles.
T Helper Cell Death
Not due to budding off virions.
Often due to self-destruct mechanism triggered by HIV production.
Implications
High mutation rate from reverse transcriptase hinders medication and vaccine development.
Chronic infection as viral DNA integrates into host DNA.