Development of duck hepatitis A virus type 3 vaccine and its use to protect ducklings against infections

Kim, Min‐Chul; Kim, Minjeong; Kwon, Yong-Kuk; Lindberg, Anders; Joh, Seong-Joon; Kwon, Hyuk-Man; Lee, Youn‐Jeong; Kwon, Jun-Hun

doi:10.1016/j.vaccine.2009.08.092

Cited by 48 publications

(22 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The epidemiology, clinical symptoms, and pathological changes of DHAV-C infection are very similar to those of DHAV-A infections, making molecular biological methods necessary to distinguish DHAV-C infection from other DHV infections (8,16). DHAV strains were categorized into three distinct genetic groups based on the phylogenetic analysis of complete VP1, VP0, and VP3 and partial 3D sequences (24).…”

Section: Discussionmentioning

confidence: 99%

Development of a Real-Time Quantitative PCR for Detecting Duck Hepatitis A Virus Genotype C

et al. 2012

View full text Add to dashboard Cite

Recently, duck hepatitis A virus genotype C (DHAV-C), a causative agent of duck viral hepatitis, has been responsible for increasing economic losses in the duck industry in China and South Korea. In this study, a real-time PCR assay targeting the 2C gene for detecting DHAV-C was developed. The assay was confirmed to be specific and sensitive, and the minimum detection limit was 3.36 ؋ 10 3 copies per reaction, making this assay suitable for rapid diagnosis of DHAV-C infection from clinical samples. In addition, the dynamics of the viral loads in tissues of specific-pathogen-free (SPF) ducklings infected with DHAV-C were investigated using this method. The DHAV-C could be detected earliest in the liver within 12 h postinfection. Moreover, high viral loads were identified in the heart, liver, spleen, lung, kidney, bursa of Fabricius, thymus, pancreas, brain, and small intestine after 24 h postinfection. Taking the data collectively, the study described in this report is the first to have developed a realtime PCR method for detection of DHAV-C and thus contributes to pathogenicity research.

show abstract

Section: Discussionmentioning

confidence: 99%

Development of a Real-Time Quantitative PCR for Detecting Duck Hepatitis A Virus Genotype C

et al. 2012

View full text Add to dashboard Cite

show abstract

“…So far, attenuated vaccine derived from serial passages in embryonated chicken eggs has been reported for DHAV-1, DHAV-3, DHV-2 and DHV-3 (Asplin, 1965; Woolcock and Fabricant, 1991; Kim et al, 2007, 2009; Knowles et al, 2012). These vaccines have been proven to be highly efficacious in controlling DVH caused by homologous virus.…”

Section: Introductionmentioning

confidence: 99%

Host Differences Affecting Resistance and Susceptibility of the Second Generation of a Pekin Duck Flock to Duck Hepatitis A Virus Genotype 3

et al. 2017

View full text Add to dashboard Cite

Earlier work suggested the possibility to anti duck hepatitis A virus genotype 3 (DHAV-3) using the resistance breeding strategy. Here, we report the creation of the second generations of a resistant Pekin duck flock (designated Z8R2) and a highly susceptible Pekin duck flock (designated Z8S2) and the investigation of their responses to DHAV-3. Experimental infection with DHAV-3 at 7 days of age resulted in a high mortality (66.3%) in 11 susceptible Z8S2 families and an extremely low mortality rate (2.67%) in 32 Z8R2 families, indicating that Z8R2 exhibits strong resistance to DHAV-3, while Z8S2 is highly susceptible to the virus. Detection of DHAV-3 in the liver between 1 and 60 hours post inoculation (hpi) suggests that DHAV-3 can be replicated rapidly and efficiently in the liver of Z8S2, whereas the replication of the virus in the liver of Z8R2 is suppressed greatly. High levels of serum biochemical markers (e.g., ALT, AST, ALP and GGT) were detected in Z8S2 at 24 hpi, which were significantly higher than those in Z8R2. Analysis of transcripts in the liver revealed that the expression levels of several pattern recognition receptors (PRRs) (e.g., TLR4/7, RIG-1 and MDA5) and cytokines (e.g., IL-2, IL-6, IL-8, IFN-α, and IFN-γ) in Z8S2 were significantly higher than those in Z8R2 at 12 and 24 hpi. Together these findings suggest that Z8R2 and Z8S2 Pekin ducks, which were derived from the same Z8 line, exhibit disparate pathogenic outcomes following DHAV-3 infection. Therefore, it is possible to select a Pekin duck flock resistant to DHAV-3 employing the strategy described here. It is likely that the high viral load and the strong inflammatory response correlate with the high susceptibility of Z8S2 Pekin ducks to DHAV-3.

show abstract

“…This DHV was recently classified as a member of Picornaviridae and renamed duck hepatitis A virus (DHAV) (28). Complete genome sequence determination showed that DHAVs form a genetically distinct group within the picornaviruses.…”

mentioning

confidence: 99%

Duck Hepatitis A Virus Possesses a Distinct Type IV Internal Ribosome Entry Site Element of Picornavirus

Pan

Yang

Zhou

et al. 2012

J Virol

View full text Add to dashboard Cite

Sequence analysis of duck hepatitis virus type 1 (DHV-1) led to its classification as the only member of a new genus, Avihepatovirus, of the family Picornaviridae, and so was renamed duck hepatitis A virus (DHAV). The 5= untranslated region (5= UTR) plays an important role in translation initiation and RNA synthesis of the picornavirus. Here, we provide evidence that the 651-nucleotide (nt)-long 5= UTR of DHAV genome contains an internal ribosome entry site (IRES) element that functions efficiently in vitro and within BHK cells. Comparative sequence analysis showed that the 3= part of the DHAV 5= UTR is similar to the porcine teschovirus 1 (PTV-1) IRES in sequence and predicted secondary structure. Further mutational analyses of the predicted domain IIId, domain IIIe, and pseudoknot structure at the 3= end of the DHAV IRES support our predicted secondary structure. However, unlike the case for the PTV-1 IRES element, analysis of various deletion mutants demonstrated that the optimally functional DHAV IRES element with a size of approximately 420 nt is larger than that of PTV-1 and contains other peripheral domains (Id and Ie) that do not exist within the type IV IRES elements. The domain Ie, however, could be removed without significant loss of activity. Surprisingly, like the hepatitis A virus (HAV) IRES element, the activity of DHAV IRES could be eliminated by expression of enterovirus 2A protease. These findings indicate that the DHAV IRES shares common features with type IV picornavirus IRES elements, whereas it exhibits significant differences from type IV IRESs. Therefore, we propose that DHAV possesses a distinct type IV IRES element of picornavirus.T he internal ribosome entry site (IRES) elements have the function to direct cap-independent internal initiation of protein synthesis, which is mechanistically quite different from the canonical cap-dependent mechanism for the translation initiation of the majority of cellular mRNAs (3). Earlier studies have indicated that all cytoplasmic cellular mRNAs possess a 5= terminal cap structure (m7GpppG. . .) that is recognized by the translation initiation factor complex-eukaryotic initiation factor 4 (eIF4F), which contains three proteins including eIF4E (cap-binding protein); eIF4A (ATP-dependent RNA helicase); and eIF4G, which acts as a protein scaffold. This complex of proteins acts as a bridge between the mRNA and the 40S ribosomal subunit via its interaction with eIF3 by multiple protein-protein interactions (23). In contrast to the cellular mRNAs, no cap structure exists at the 5= terminus of some viral mRNAs, such as those of picornaviruses and relevant viruses like hepatitis C virus (HCV). Initiation of protein synthesis for these viruses which rely on cap structure is termed internal initiation; in this case, the IRES element located within the 5= untranslated region (5= UTR) of the viral genome can exert the function to direct translation initiation (4, 19). Previous studies have showed that these IRES elements contain diverse secondary structures with ...

show abstract

Development of duck hepatitis A virus type 3 vaccine and its use to protect ducklings against infections

Cited by 48 publications

References 21 publications

Development of a Real-Time Quantitative PCR for Detecting Duck Hepatitis A Virus Genotype C

Development of a Real-Time Quantitative PCR for Detecting Duck Hepatitis A Virus Genotype C

Host Differences Affecting Resistance and Susceptibility of the Second Generation of a Pekin Duck Flock to Duck Hepatitis A Virus Genotype 3

Duck Hepatitis A Virus Possesses a Distinct Type IV Internal Ribosome Entry Site Element of Picornavirus

Contact Info

Product

Resources

About