Understanding why virus can’t replicate in human cells could improve vaccines

The identification of a gene that helps to restrict the host range of the modified vaccinia virus Ankara (MVA) could lead to the development of new and improved vaccines against diverse infectious agents, according to a study published May 30 in the open-access journal PLOS Pathogens by Bernard Moss of the National Institutes of Health, and colleagues.

Poxvirus vectors have outstanding properties for the development of vaccines against various infectious agents. Safety concerns have led to a preference for attenuated poxviruses that have lost the ability to produce infectious progeny in human cells. The most widely used poxvirus vector is MVA, which exhibits extreme host-range restriction, having lost the inability to efficiently produce infectious virus in most mammalian cells. Despite ongoing clinical testing of MVA-vectored vaccines, the basis for its host-range restriction remains unknown. In the new study, Moss and colleagues set out to identify specific genes that contribute to the host-range defect of MVA.

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