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Wistar Science Highlights: New Discoveries on HIV Latency and How Cancer Cells Talk With Their Neighboring Normal Cells

August 24, 2020

Antiretroviral therapy (ART) has dramatically increased the health and life expectancy of HIV-infected individuals, suppressing virus replication in the host immune cells and stopping disease progression; however, low yet persistent amounts of virus remain in the blood and tissues despite therapy. Virus persistency limits immune recovery and is associated with chronic levels of inflammation so that treated HIV-infected individuals have higher risk of developing a number of diseases.

This persistent infection stems from the ability of HIV to hide in a rare population of CD4 T cells. Finding new markers to identify the virus reservoir is of paramount importance to achieve HIV eradication.

The lab of Mohamed Abdel-Mohsen, Ph.D., assistant professor in the Vaccine & Immunotherapy Center, may have discovered a new way of identifying and targeting hidden HIV reservoirs during ART.

The sugar molecules present on the surface of immune cells play a critical role in regulating their functions and fate. Researchers explored the role of the sugar component on the surface of host cells and described a “glycomic — or sugar — signature” that can impact HIV persistence.

Published in Cell Reports, the findings may have translational implications for improving the long-term care of HIV positive people.

The crosstalk between cancer cells and their neighboring normal cells is important to promote cancer progression.

The lab of Dario C. Altieri, M.D., Wistar president and CEO, director of the Institute’s Cancer Center and the Robert & Penny Fox Distinguished Professor, studied how this exchange happens to gain more clues on how tumors “hijack” their microenvironment and promote disease progression and recurrence.

Researchers cultured breast cancer cells in low-oxygen to mimic a condition known as hypoxia, which is a hallmark of the microenvironment surrounding most solid tumors. In this setting, they discovered that cancer cells package oncogenic messages into tiny particles called extracellular vesicles and send them to neighboring normal epithelial cells. This results in reprogramming of the shape and position of their mitochondria — the cell’s powerhouse — to ultimately alter tissue structure.

These findings, published in the journal Developmental Cell, suggest novel therapeutic targets to disrupt the pro-tumorigenic changes caused by cancer cells to the microenvironment.