Cell-to-Cell Spread of HIV and Viral Pathogenesis
K M Law1, N Satija1, A M Esposito1
1Immunology Institute Icahn School of Medicine at Mount Sinai, New York, NY, United States.
Advances in Virus Research
|April 27, 2016
Summary
Human immunodeficiency virus type 1 (HIV-1) infection depletes CD4(+) T cells. Cell-to-cell interactions, like virological and infectious synapses, enhance HIV-1 spread and immune evasion.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Human immunodeficiency virus type 1 (HIV-1) causes chronic infection, progressively depleting CD4(+) T lymphocytes, crucial for adaptive immunity.
- Cell-free HIV-1 is a prognostic indicator, but cell-to-cell transmission via interactions can significantly enhance viral spread.
- HIV-1 utilizes viral Env protein for cell adhesion and fusion, forming virological synapses that promote replication under immune and therapeutic pressure.
Purpose of the Study:
- To investigate the role of cell-cell interactions in HIV-1 infection dynamics.
- To understand how virological and infectious synapses contribute to viral spread and persistence.
- To elucidate the mechanisms by which HIV-1 evades immune responses through cell-mediated transmission.
Main Methods:
- Analysis of T cell interactions in lymphoid compartments and effector sites.
- Investigating the function of viral Env protein as a cell adhesion molecule.
- Characterizing virological and infectious synapses in HIV-1 infection.
Main Results:
- HIV-1-induced interactions between infected and uninfected T cells (virological synapses) enhance viral replication.
- Infectious synapses between antigen-presenting cells and T cells also promote viral spread.
- These cell-cell interactions facilitate HIV-1 persistence and immune evasion.
Conclusions:
- Cell-to-cell interactions are critical mechanisms for HIV-1 dissemination and persistence.
- Virological and infectious synapses contribute to viral spread, potentially overcoming therapeutic and immune pressures.
- Further research is needed to fully define the roles of these interactions throughout HIV-1 infection stages.
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