Moru Xu

Upon infection, viruses reprogram the host metabolic system to hijack metabolic resources for proliferation. Avian leukosis virus subgroup J (ALV-J), an avian oncogenic virus, poses significant challenges to the poultry industry. ALV-J infection upgrades monosaccharide N-acetylgalactosamine (GalNAc) and galactosyltransferase (core 1 β3-Gal-T) in DF-1 cells, both of which are crucial for O-linked glycosylation. Addition of GalNAc or overexpression of core 1 β3-Gal-T in DF-1 cells can promote ALV-J replication. ALV-J envelope protein (Env) undergoes complex post-translational modifications. Two O-linked glycosylation sites (T32 and T271) located in the head region of the ALV-J Env have been identified for the first time using liquid chromatography–mass spectrometry (LC–MS). The results of coimmunoprecipitation and flow cytometry indicate that mutations in T32 or T271 diminish ALV-J infection by affecting viral internalization, rather than attachment. The viral internalization efficiency was partially restored under a low pH environment. Incorporation of T32A and T271A into ALV-J led to significantly reduced replication capacity in vivo and viral shedding of the recombinant virus. These findings are valuable for our understanding of the roles of glycans in the ALV-J infection cycle, as well as for providing potential anti-ALV-J strategies.

Marek’s disease (MD), caused by the Marek’s disease virus (MDV), is a common infectious tumor disease in chickens and was the first neoplastic disease preventable by vaccination. However, the vaccine cannot completely prevent virulent MDV infections, allowing both the vaccine and virulent MDV to coexist in the same chicken for extended periods. This study aims to investigate the changes in viral load of the very virulent strain Md5 and the rHVT-IBD vaccine in different chicken tissues using a real-time PCR assay. The results showed that the rHVT-IBD vaccine significantly reduced the viral load of MDV-Md5 in different organs, while the load of rHVT-IBD was significantly increased when co-infected with Md5. Additionally, co-infection with Md5 and rHVT-IBD in chickens not only changed the original viral load of both viruses but also affected the positive rate of Md5 at 14 days post-vaccination. The positive rate decreased from 100% to 14.29% (feather tips), 0% (skin), 33.33% (liver), 16.67% (spleen), 28.57% (thymus), 33.33% (bursa), and 66.67% (PBL), respectively. This study enhances our understanding of the interactions between HVT vector vaccines and very virulent MDV in chickens and provides valuable insights for the future development of MD vaccines.

Newcastle disease (ND) is a significant infectious disease in poultry, causing substantial economic losses in developing countries. To control ND, chickens must be vaccinated multiple times a year. In order to develop an improved vaccine that provides long-term protection, the F gene from genotype VII NDV was inserted into the herpesvirus of turkey (HVT) vaccine virus using CRISPR/Cas9-mediated NHEJ repair and Cre/LoxP technology. The immunogenicity and protective efficacy of the resulting recombinant vaccines were evaluated through antibody assays and virus challenge experiments. Two recombinant vaccines, rHVT-005/006-F and rHVT-US2-F, were generated, both exhibiting growth rates comparable with those of HVT in vitro and consistently expressing the F protein. One-day-old specific pathogen-free (SPF) chickens immunized with 2000 PFU/bird of either rHVT-005/006-F or rHVT-US2-F developed robust humoral immunity and were completely protected against challenge with the NDV F48E8 strain at 4 weeks post-vaccination (wpv). Furthermore, a single dose of these vaccines provided sustained protection for at least 52 wpv. Our study identifies rHVT-005/006-F and rHVT-US2-F as promising ND vaccine candidates, offering long-term protection with a single administration. Moreover, HVT-005/006 demonstrates promise for accommodating additional foreign genes, facilitating the construction of multiplex vaccines.