The study appears in the Sept. 25 issue of the Journal of Cell Biology.
Both strains of the herpes virus -- HSV-1, the strain that causes cold sores on the mouth, and HSV-2, genital herpes -- can infect the cornea, the clear, domed surface that forms the eye's outermost layer. Ocular herpes is the leading cause of infectious blindness in the United States, with 50,000 new or recurring cases each year.
In about one quarter of cases, the virus penetrates the first layer of the cornea to infect an inner layer, the stroma, making the disease much more difficult to treat.
Effective treatment is hampered by poor understanding of how the virus infects the stroma, says Deepak Shukla, assistant professor of ophthalmology and visual science and microbiology and immunology, and senior author of the paper. In their study, he and his coworkers determined that the HSV-1 virus enters stroma cells in a process similar to the way bacteria, viruses and other foreign invaders are engulfed by immune cells called phagocytes.
"In the electron microscope pictures, it looks like the stroma cells form long arms that reach out and collect the virus particles, and then wrap around them, forming a sac, and bring them into the cell body," Shukla said.
In phagocytes, ingested foreign particles are destroyed in the sacs, which are highly acidic. But even though the sacs formed by the stroma cells were similar to the phagocyte's sacs, Shukla said, the envelope containing the herpes virus genome emerges from the sac undamaged and able to infect the cell. "This raises the interesting possibility that herpes may be able to evade the immune system defenses in the same way," he said.
"Understanding herpes' unusual pathway for infe cting the stroma cells opens up new strategies for developing therapies against this potentially blinding disease and has implications for understanding other herpes virus infections," Shukla said.