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HSV vectors with vhs gene deletion offer dendritic cell immunotherapy.

Vaccine Weekly

| May 07, 2003 | COPYRIGHT 2003 NewsRX. This material is published under license from the publisher through the Gale Group, Farmington Hills, Michigan.  All inquiries regarding rights should be directed to the Gale Group. (Hide copyright information)Copyright

2003 MAY 7 - (NewsRx.com & NewsRx.net) -- Deletion of the virion host shutoff protein (vhs) from the herpes simplex virus (HSV) relieved the viral block to dendritic cell activation.

According to recent research published in the Journal of Virology, "Herpes simplex virus (HSV) infects dendritic cells (DC) efficiently but with minimal replication. HSV, therefore, appears to have evolved the ability to enter DC even though they are nonpermissive for virus growth. This provides a potential utility for HSV in delivering genes to DCs for vaccination purposes and also suggests that the life cycle of HSV usually includes the infection of DCs."

"However, DCs infected with HSV usually lose the ability to become activated following infection," stated Laila Samady and collaborators at University College London. "We report that for DCs to retain the ability to become activated following HSV infection, the virion host shutoff protein (vhs) must be deleted. vhs usually functions to destabilize mRNA in favor of the production of HSV proteins in permissive cells. We have found that it also plays a key role in the inactivation of DCs and is therefore likely to be important for immune evasion by the virus. Here, vhs would be anticipated to prevent DC activation in the early stages of infection of an individual with HSV, reducing the induction of cellular immune responses ...

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