Recent publications:

CONSTRUCTION OF A GREEN FLUORESCENT PROTEIN LABELED gE MUTANT OF HSV FOR STUDIES OF INTERCELLULAR VIRAL SPREAD. M.S. Chin, T.P. Margolis*, N.T. M endoza and J.H. LaVail. Abst. Soc. Neurosci. (in press).

Corneal infection by Herpes simplex virus, type-1 (HSV) is the most common cause of infectious blindness in the United States. HSV may initially infect epithelial cells, replicate and then spread to trigeminal nerve endings. Little is known about how HSV or other viruses spread between trigeminal nerve endings and corneal epithelial cells or between corneal cells following viral reactivation from the latent state. The spread of virus from c ell-to-cell may occur by two possible mechanisms: (1) enveloped virus is released from the first neuron into the extracellular space and attaches and fuses with the plasma membrane of the second cell; or (2) virus spreads to neighboring cells via cellular junctions. We have begun to investigate the role of trigeminal innervation on the spread of virus in recurrent corneal infection, using HSV mutants which have the green fluorescent protein (GFP) of Aequorea victoria fused to either the amino or carboxyl terminus of viral glycoprotein E. After infecting Vero cultures with equivalent titers, the mutant with GFP fused to the amino terminus of gE (GFP-gE) formed smaller plaques than the wild-type virus (strain F) or the mutant fused to the carboxyl terminuso f gE (gE-GFP). Twenty-four hours after corneal scarification and inoculation with equivalent titers of the strains, we found all 3 strains infected the corneal epithelium, including: the squamous-like cells coupled by tight junctions; wing cells; and basa l cells. Efforts to determine the temporal sequence of spread of the viral strains from squamous-like cells to underlying epithelial and stromal cells are underway.

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