Shokrollah Elahi PhD Associate Professor at University of Alberta

Study Sheds Light On How Immune System Allows HIV Infection to Be Chronic Interview with:

Shokrollah Elahi PhD Associate Professor at University of Alberta

Dr. Elahi

Shokrollah Elahi PhD
Associate Professor at University of Alberta  What is the background for this study? 

Response: CD8+T cells (killer T cells) play an important role against virally infected and cancer cells, however, their functional properties get compromised during the course of HIV infection and cancer. CD73, is one of molecules that influences killer T cell functions but its role in the context of viral infections has not been well defined.

In this study, we analyzed the presence of this protein (CD73) on killer T cells in a cohort of 102 HIV-infected individuals. We found that the proportion of killer T cells expressing this protein was substantially lower among different killer T cell subsets obtained from the blood of HIV-infected individuals compared to individuals who were not infected with HIV. Notably, CD73 was decreased at the intracellular protein and gene levels. This suggests that the CD73 gene gets suppressed by a specific mechanism in HIV-infected individuals.

Furthermore, we decided to better understand the difference between killer T cells having CD73 versus those who do not. We found that CD73 was essential for the migratory capacity of killer T cells. It means killer T cells without this protein have impaired ability to move into the tissues. This implies that lack of CD73 prevents killer T cells from homing into the tissue where HIV reservoirs are hidden.  What are the main findings?

Response: On the other hand, it has been reported that HIV-infected individuals have lower risk of developing multiple sclerosis (MS). As proof of concept, we investigated the proportion of killer T cells in the cerebrospinal fluids (CSF) of relapsing-remitting multiple sclerosis (MS) patients at the time of disease remission versus relapse. Interestingly, we found a significantly higher abundance of killer T cells having CD73 in the CSF of MS patients at time of relapse. These observations suggest that CD73 enhances the trafficking capacity of killer T cells to cross the blood-brain barrier.

Finally, we observed that chronic inflammation results in the accumulation of ATP, which provides energy to cells ” also called the energy currency of the cell”.

ATP via a complex mechanism suppresses the CD73 gene in killer T cells resulting in a lower production of CD73 protein. What should readers take away from your report? 

Response: The main message is that our immune system is complex and fascinating! Our study has shed some light on one potential mechanism for the chronicity of HIV infection. We believe that HIV infection by reducing the CD73 gene through a complex mechanism evades the immune system, in particular, killer T cells. Lack of killer T cells trafficing capacity impaires killer T cells from finding and eliminating hidden infected cells in different tissues. What recommendations do you have for future research as a result of this work?

Response: Further studies are required to better understand how to manipulate the CD73 gene to enhance its activity in HIV and suppress its activity in MS.


Shima Shahbaz, Isobel Okoye, Gregg Blevins, Shokrollah Elahi. Elevated ATP via enhanced miRNA-30b, 30c, and 30e downregulates the expression of CD73 in CD8 T cells of HIV-infected individuals. PLOS Pathogens, 2022; 18 (3): e1010378 DOI: 10.1371/journal.ppat.1010378

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Last Updated on March 29, 2022 by Marie Benz MD FAAD