Title A Restrictive Virus Tropism, Latency and Reactivation of Pseudorabies Virus Following Irreversible Deletion of BsrI Restriction Site in the Thymidine-kinase Gene
Author Mohd Lila Mohd Azmi *, Nazariah Allaudin Zeenathul, Abdel-Wahid Saeed Ali, Che Abdul Rahim Mohamed, and Awang Isa Kamarudin
Address Faculty of Veterinary Medicine Universiti Putra Malaysia 43400 UPM Serdang, Selangor, Malaysia
Bibliography Journal of Microbiology, 40(1),1-10, 2002,
DOI
Key Words pseudorabies virus, thymidine kinase, latency, reactivation, tropism
Abstract At the dose of 1000 p.f.u. per mouse, 100% mortality occurred in mice inoculated with wild-type pseudorabies virus (PrV). In contrast, upon stable deletion of 10 bp nucleotides at the BsrI site within the TK gene, PrV was rendered to be completely apathogenic. The deletion also caused the virus to be less capable of replicating in respiratory as well as in nervous system tissues. Although animals were exposed to high titers of TK-deleted PrVs, the virus failed to replicate to a high titer as compared to the pathogenic parental virus. In contrast to previous studies, the deletion in the TK gene did not prevent the virus from establishing latency. Upon immunosuppression, the latent virus, however, reactivated but replicated at low titers. Interestingly, TK-deleted virus established latency and reactivation, that are occurred only in trigeminal ganglia and the cerebrum, and no other tissues involved. Following reactivation, there was no indication of virus shedding in respiratory tissues as confirmed by virus isolation and polymerase chain reaction (PCR) technique targeting at the gB gene of PrV. The non-pathogenic virus with non-shedding characteristics, upon reactivation of the latent virus, would be the important feature of a live virus vaccine candidate.
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