Abstract
In China, the re-emerging pseudorabies virus (PRV) variant has caused large-scale outbreaks of pseudorabies in swine herds with classical PRV vaccine immunization since late 2011. Here, a recombinant PRV with TK/gI/gE/11k/28k deletion was constructed based on variant HN1201 strain isolated in 2012, by the bacterial artificial chromosome infectious clones. Compared with the parental virus, the recombinant PRV rHN1201TK−/gE−/gI−/11k−/28k− showed a similar virus grown curve and exhibited smaller plaques. The vaccination of rHN1201TK−/gE−/gI−/11k−/28k− could elicit an earlier and higher level of gB antibody, and the neutralizing antibodies elicited by rHN1201TK−/gE−/gI−/11k−/28k− were effective against both PRV classical and variant strains. Clinically, the body temperature of the pigs immunized with rHN1201TK−/gE−/gI−/11k−/28k− was significantly lower than that of the classical PRV vaccine immunized pigs, and the recombinant PRV could provide effective protection against the challenge with the PRV variant. These results imply that the rHN1201TK−/gE−/gI−/11k−/28k− could be a promising vaccine candidate for the prevention of the current epidemic of pseudorabies in China.
Highlights
Pseudorabies (PR), called Aujeszky’s disease, is caused by the infection of an alpha-herpesvirus Pseudorabies virus (PRV) [1]
The 5-gene deleted plasmid pBACHN1201TK−/gE−/gI−/11k−/28k−/Amp+ was selected on an agar plate containing chloramphenicol and ampicillin, and further confirmed by sequencing
After digestion using ISceI, the linear plasmid was transformed into E. coli DY380 to remove the Amp gene, and the plasmid pBACHN1201TK−/gE−/gI−/11k−/28k− was generated
Summary
Pseudorabies (PR), called Aujeszky’s disease, is caused by the infection of an alpha-herpesvirus Pseudorabies virus (PRV) [1]. The double-stranded DNA genomic sequence of PRV is ∼145 kb in size, containing almost 70 open reading frames (ORFs) that encode 70–100 viral proteins [2]. The herpesvirus PRV has a broad host range, which is known to cause acute fatal disease in a variety of mammals [3–5]. The PRV infection may lead to acute symptoms and even death in piglets, and the clinical signs of coughing, sneezing, lethargy, nervousness, uncoordinated movements, and abortion in sows [1], resulting in heavy economic losses in the pig industry. Like other alpha-herpesviruses, PRV is characterized by a lifelong latent infection in the host peripheral nervous system. Stress-induced reactivation of latent PRV is a difficulty for PR prevention [6]
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