DELETION OF GLYCOPROTEIN GE REDUCES THE PROPAGATION OF PSEUDORABIES VIRUS IN THE NERVOUS-SYSTEM OF MICE AFTER INTRANASAL INOCULATION

A pseudorabies virus (PrV) mutant, deficient in the nonessential glyco protein E (gE) and expressing the LacZ gene (gE(-) beta gal(+) PrV), a nd its rescued virus were inoculated intranasally in mice. The median lethal dose of gE(-) beta gal(+) PrV was similar to that of the parent al Kaplan strain, but mice survived longer and did not develop symptom s of pseudorabies. In the nasal mucosa, gE(-) beta gal(+) PrV replicat ed less efficiently than rescued virus. gE(-) beta gal(+) PrV could in fect first-order trigeminal and sympathetic neurons innervating the na sal mucosa. However, transneuronal transfer to second-order cells grou ps did not occur in trigeminal pathways and was severely reduced in sy mpathetic pathways. The mutant was also unable to propagate in the par asympathetic system. In contrast, gE-rescued virus was transferred tra nsneuronally in trigeminal, sympathetic, and parasympathetic pathways, like wild-type PrV. These findings provide further evidence that dele tion of gE specifically affects transneuronal transfer of PrV more tha n penetration and multiplication of the virus in first-order neurons. (C) 1996 Academic Press, Inc.