Immune Memory Formation Seen In Early Stages Of Viral Infection

In an acute viral infection, most of the white blood cells known as T cells differentiate into cells that fight the virus and die off in the process. But a few of these “effector” T cells survive and become memory T cells, ensuring that the immune system can respond faster and stronger the next time around.

Scientists have identified a molecule that defines which cells are destined to become memory T cells just a few days after a viral infection begins. The finding could guide the development of more effective vaccines for challenging infections such as HIV/AIDS and also cancer.

The results were published online by the journal Immunity. The senior author is Rafi Ahmed, PhD, director of the Emory Vaccine Center, a Georgia Research Alliance Eminent Scholar and a member of the National Academy of Sciences.

Working with Ahmed, postdoctoral fellows Vandalia Kalia and Surojit Sarkar tracked memory T cell formation in mice infected with lymphocytic choriomeningitis virus, a virus that causes an acute infection. They observed that a few days after infection begins, T cells separate into two groups: one with high levels of the molecule CD25 on their surfaces and one with low levels of CD25. Later on, all T cells reduce their levels of CD25 and the differences disappear as the infection is cleared.

“The outstanding question in our field has been: when do T cells commit to becoming memory cells,” Kalia says. “This is one of the earliest points where we have been able to see these groups of cells with distinct fates.” Read more

Drug Kills Cells Through Novel Mechanism

MIT and Boston University researchers have discovered that the drug hydroxyurea kills bacteria by inducing them to produce molecules toxic to themselves -a conclusion that raises the possibility of finding new antibiotics that use similar mechanisms.

Hydroxyurea inhibits the enzyme critical for making the building blocks for DNA, so for decades it has been used to study the consequences of inhibiting DNA replication in E. coli, yeast and mammalian cells. It is also sometimes used in chemotherapy to halt the growth of cancer cells.

The research team, led by biologist Graham Walker of MIT and bioengineer James Collins of Boston University, showed that cells don’t die after hydroxyurea treatment because their DNA replication is blocked, but because the blockage sets in motion a chain of cellular events that culminates in the production of hydroxyl radicals. Those radicals are highly reactive and can damage cellular molecules such as nucleic acids, lipids and proteins. Read more

Immune Therapy Can Protect Against Or Treat Later Lymphoma

Specially developed immune system cells that target the common Epstein-Barr virus can protect immune-suppressed bone marrow transplant recipients against lymph system disease and cancers that arise from the viral infection, said a group of researchers led by those from Baylor College of Medicine, The Methodist Hospital and Texas Children’s Hospital.

“Therapy with EBV-specific CTLs (cytotoxic lymphocytes) was effective for these patients who were severely immune-compromised, as the cells successfully reached the tumor, multiplied and were able to kill tumor cells” said Dr. Helen Heslop, lead author of the study and professor of pediatrics and medicine and a member of the Center for Cell and Gene therapy at BCM, The Methodist Hospital and Texas Children’s. The cell remained in the body for up to nine years, providing long-term protection.

Patients who undergo the transplants are often immune-suppressed. Because most people have been infected with Epstein-Barr virus, the lack of immune protection makes their lymph system vulnerable to adverse effects of the virus, especially lymphomas that can be traced directly back to the infection.

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