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Neoprobe reports positive feedback from FDA for RIGScan development

January 22, 2016

"What was really striking is that Nrf2 is a kind of master switch controlling the machinery of these antioxidant enzymes, and it appears the virus blocks its activity," said UTMB Health professor Dr. Roberto Garofalo, also a lead author on the study. "This is interesting because genetic factors have been shown to be associated with other airway diseases, and the obvious question now is do the children who develop the most severe disease in response to RSV also have an Nrf2 gene that favors a low level of expression of these antioxidant enzymes? Are we seeing a combination of two hits, one from the virus and one from genetics?"

The apparent involvement of Nrf2 also opens an intriguing therapeutic possibility, Garofalo said, because compounds that induce cells to make more of the transcription factor are already in clinical trials as potential cancer therapies. Another possibility is the delivery of short-term genetic therapy via a genetically engineered virus licensed by the National Heart, Lung and Blood Institute.

Any such intervention will have to await further human studies like the one described in the AJRCCM paper. In that part of the investigation, the researchers measured biochemical markers of reactive oxygen species and levels of antioxidant enzymes in nasal samples from 30 infants with RSV infections. The severity of the babies' disease ranged from relatively minor upper respiratory tract infections to full-blown lung disease requiring respiratory support from a ventilator.

"Our findings in patients were very consistent with what we saw in mice, " Garofalo said. "We found a significant increase in markers of oxidative injury and a significant decrease in antioxidant enzyme expression corresponding to the severity of the disease."

Source: University of Texas Medical Branch at Galveston