Macrophages: Hideouts for HIV and Drivers of Inflammation
Human immunodeficiency virus (HIV) is a chronic infection that causes acquired immunodeficiency syndrome (AIDS) and currently infects over 38 million people. Despite the success of antiretroviral therapy (ARV), almost 700,000 people died from AIDS-related deaths in 2019, and for people with access to ARVs, infection-associated inflammation persists — increasing the risk of co-morbidities such as cardiovascular disease and HIV-associated neurocognitive disorder.
While CD4+ helper T cells are the main cell type infected by HIV, tissue-resident macrophages also become infected and persist despite ARV treatment. This session looks at how macrophages persist in the presence of killer immune cells.
Key Learning Objectives
- CD8+ T cells and natural killer (NK) cells have more difficulty killing HIV-infected macrophages than HIV-infected CD4+ T cells
- Poor killing of HIV-infected macrophages further drives inflammation that could contribute to co-morbidities
- Current work on how macrophages inhibit CD8+ T cell and NK cell killer activity
Watch Now: Macrophages: Hideouts for HIV and Drivers of Inflammation
This webinar is available on demand. Fill in the form to watch the full recording — we'll email you the link too.
- May 31, 2022
- kbiinfo@krishgen.com
- +91 22 49198700
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