Jamil Mahmud, PhD, spent years researching a virus that infects thousands of newborns each year and is a leading cause of death among transplant patients. His work led to uncovering the mechanisms the virus uses to infect and hide within humans and, earned him a spot as one of four finalists for the SUNY Chancellor’s Distinguished PhD Dissertation Award competition.

As a member of the lab of Gary Chan, PhD, Mahmud investigated human cytomegalovirus, known as HCMV. The virus is a member of the herpesvirus family and infects more than 70 percent of Americans, and is near universal in less-developed countries, Mahmud said.

For the vast majority of healthy people, the virus is not a problem. For those with an underdeveloped immune system, or one compromised by an illness or injury, HCMV can be deadly or debilitating. Mahmud said some 400 infants die from the virus each year in the United States. Other infants, perhaps as many as 9,000, suffer neurological damage, including blindness and loss of hearing.

In adults, HCMV has been linked to breast cancer and glioblastomas. “It’s not the cause,” he said, “but it can contribute to the progression of cancers.”

The only medication currently used to combat HCMV is only partially effective and has serious side effects.

HCMV has been a particularly challenging pathogen because it infects a person and then hides inside monocytes, a type of white blood cell, eventually moving into bone marrow where it awaits an opportunity to inflict illness on its host.

Mahmud’s work brought to light the way the virus works its way into monocytes, cells that usually help fight infections. The key, he explained is a protein called Akt. The virus uses Akt to get into the monocyte. Once inside the blood cell, it is virtually invisible to the body’s immune system. Worse, it turns the monocyte into a “zombie” cell, continuing to live long past the regular 24- 48-hour lifespan of a regular monocyte.

But Mahmud discovered a way to uncover the virus, which could expose it to the body’s defenses. When activated by an infectious threat, monocytes are converted to macrophages, the cells that actively combat infections. The conversion involves the same Akt protein, but the defense system activates the monocyte at two spots, while the HCMV slips in by activating at only one spot.

HCMV’s success depends on a gene, US28. If US28 can be blocked, Mahmud said, the virus can be kept from hiding inside the monocyte in the first place,  as the human immune system would be able to detect and kill the infected monocytes along with the viruses within. Mahmud recalled when it became clear what he had found. “This is how the virus hides. This is what we can utilize.” 

Success in blocking US28, he said, “could keep HCMV from ever happening.”

Now involved in post-doctoral work at Northwestern University, Mahmud praised his time at Upstate Medical University and Central New York. A native of Bangladesh, he came to Upstate with his wife and fellow PhD student, Farzana Tuli, in 2016. 

The two enjoyed life in the region, particularly camping in the Adirondacks. 

Mahmud said work in the Chan lab was very rewarding. He praised Chan for his mentorship and for the way he made work-life balance an integral part of the lab experience. “He’s my idol,” Mahmud said. 

College of Graduate Studies Dean Mark Schmitt, PhD, gave some context for the importance of the chancellor’s award. “This is a fantastic achievement considering SUNY granted 1,283 PhDs last year,” he said.

As one of four finalists for the Chancellor’s award, Mahmud received $1,000. First place went to Hamed Rahimi-Nasrabadi of SUNY Optometry for his dissertation on “Neural Mechanisms of Luminance Perception."