University Times

Climate research funded

Civil and environmental engineering professor Xu Liang has been awarded a Department of Energy grant to study megadrought and its implications for climate change. As PI, she receives $300,691 for three years.

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Wastewater research published

Civil and environmental engineering professor Willie Harper has made a breakthrough in the understanding of the biochemistry and microbial ecology of bacteria that remove ammonia from wastewater. The results were reported online in the journal Biotechnology and Bioengineering.

Harper has been studying nitrification, a biochemical process for removing ammonia from wastewater that is critical to most municipal water pollution control facilities.

Working with microbiology and chemistry researchers, Harper discovered that hydroxylamine, which forms during nitrification, can cause the microbial communities to become inhibited and disaggregated, interfering with the removal of ammonia. The discovery may explain why nitrification suddenly fails. A better understanding of nitrification could lead to better technologies for wastewater treatment.

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Herpes research published

Pitt researchers are challenging the once-common notion that latent herpes simplex virus type I (HSV-1) in sensory neurons is invisible to the immune system. Instead, said Robert L. Hendricks, Joseph F. Novak professor and vice chair for research in the Department of Ophthalmology and professor in the departments of immunology and molecular microbiology and genetics at the School of Medicine, immune cells keep the infection under close surveillance, actively holding HSV-1 in check without destroying the neurons harboring it. In a paper published in the Oct. 10 issue of Science, teams led by Hendricks and ophthalmology professor Paul R. Kinchington show one way this balancing act is carried out.

Typically, immune cells called CD8 T cells carry lytic granules (packets of potentially toxic enzymes) into virus-infected cells to induce a form of cellular suicide called apoptosis. 

However, according to the researchers’ experiments, that isn’t the case when CD8 T cells target infected sensory neurons. Sensory neurons may not regenerate, so an immune system attack that destroys them could do more harm than good.

Instead, the lytic granules attack the virus in neurons without killing them. One way is by targeting one of the proteins the virus needs to reproduce. “That means the neuron and the virus survive, but the infection can’t spread to other cells,” Hendricks said.

A common infection, HSV-1 typically causes mild symptoms or none at all initially, but the virus remains in the neurons for a lifetime, occasionally activating to cause disease. It can cause bouts of cold sores, blindness and potentially lethal encephalitis when it reawakens in infected nerve cells. 

Previous studies showed CD8 T cells can use interferon-gamma to block reactivation without killing the neuron, but only some sets of neurons are controlled in this manner, Hendricks said. His team will continue to try to identify how immune cells, HSV-1 and neurons interact, which could have implications for treatment and vaccine development for HSV-1 infections, as well as for gene therapy applications that use harmless versions of the herpes virus as a vector to ferry treatment genes into cells. 

The paper’s lead author was Jared E. Knickelbein of ophthalmology. Other Pitt co-authors were Michael B. Yee of ophthalmology and Catherine J. Baty of cell biology and physiology.  

The research was supported by the Eye and Ear Foundation of Pittsburgh, the New York-based Research to Prevent Blindness and the National Eye Institute.

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