Reverse transcribing viruses - Retroviruses - HIV

9 important questions on Reverse transcribing viruses - Retroviruses - HIV

How is viral entry of HIV mediated?

By the binding of the viral envelope to CD4 and CCR5 coreceptor on resident memory T cells in the genital mucosa

Describe the life cycle of HIV

1. Fusion of HIV to the host cell surface (gp120/CD4 and coreceptor CCR5 or CXCR4)
2. HIV RNA, reverse transcriptase, integrase, and other viral proteins enter the host cell.
3. Viral DNA is formed by reverse transcription
4. Viral DNA is transported across the nucleus and integrates into the host DNA
5. New viral RNA is used as genomic RNA and to make viral proteins
6. New viral RNA and proteins move to the cell surface and a new, immature HIV forms
7. The virus matures by protease releasing individual HIV proteins

What is the potential role of the innate immune system in immunity to HIV?

- Prevention of viral transmission
- Immune-mediated T cell death and progression of infection
- Defence against established infection
- Chronic immune activation
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In which ways is HIV recognised by the innate immune system?

- Pathogen recognition receptors
         - Toll-like receptors on cell surface and endosomes - viral DNA and RNA
         - RIG-I-like receptors in cytosol - viral RNA
         - cGAS - cytosolic viral DNA
- Recognition of HIV PAMPs: ssRNA - TLR7/8, cGAS

What happens when there is ligand engagement of PRRs in HIV infection?

Proinflammatory antimicrobial response. Signal transduction via transcription factors NF-kB, interferon regulatory factor) leads to production of type 1 IFN, cytokines, chemokines.

What are the effects of type I interferon in HIV infection?

- Restricts viral replication
        - e.g. through unregulation of host restriction factors - APOBEC3G
- Activation of NK cells
- Initiation of adaptive responses
- Recruits target cells to mucosa
- Apoptosis of CD4+ T cells
- Chronic immune activation

What are the mechanisms of NK cell antiviral activity in HIV infection?

- Direct killing upon activation: preferential expansion of licensed NK cells expressing some KIRs e.g. KIR2DL1 modulated by HLA-C alleles
- Antibody-dependent cellular cytotoxicity via FCyRIII (CD16) receptor
- Cytokine production
- Immune regulation - elimination of dendritic cells, virus-specific T cells
- Slow disease progression in subjects expressing protective HLA class I alleles (HLA-B57) together with activating KIR3DS1 - possible role of NK cells in controlling immune activation in primary infection

How does HIV escape from the antibody response?

- High antigenic variability
- Low Env density
- Glycan shield
- Decoy nonfunctional Env (misfolded and degraded Env)
- Steric occlusion (antibodies cannot engage with the epitope)
- Cryptic epitopes

What is the effect of HIV on the gut-associated lymphoid tissue during acute infection?

Massive depletion of CD4+ CCR5+ cells

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