Corrigendum to“African swine fever virus protein E199L promotes cell autophagy through the interaction of PYCR2”[Virol Sin 36(2021)196–206]

Due to our negligence,the original version of this article,published online on April 08,2021,contained a mistake in Fig.1E.The lane ofβ-actin in Western blotting was misused.The correct Fig.1 is given below.We apologize for our oversight when preparing the figure and state that this does not change the scientific conclusions of the article in any way.

African Swine Fever Virus Protein E199L Promotes Cell Autophagy through the Interaction of PYCR2

African swine fever virus(ASFV),as a member of the large DNA viruses,may regulate autophagy and apoptosis by inhibiting programmed cell death.However,the function of ASFV proteins has not been fully elucidated,especially the role of autophagy in ASFV infection.One of three Pyrroline-5-carboxylate reductases(PYCR),is primarily involved in conversion of glutamate to proline.Previous studies have shown that depletion of PYCR2 was related to the induction of autophagy.In the present study,we found for the first time that ASFV E199 L protein induced a complete autophagy process in Vero and HEK-293 T cells.Through co-immunoprecipitation coupled with mass spectrometry(Co IP-MS)analysis,we firstly identified that E199 L interact with PYCR2 in vitro.Importantly,our work provides evidence that E199 L down-regulated the expression of PYCR2,resulting in autophagy activation.Overall,our results demonstrate that ASFV E199 L protein induces complete autophagy through interaction with PYCR2 and down-regulate the expression level of PYCR2,which provide a valuable reference for the role of autophagy during ASFV infection and contribute to the functional clues of PYCR2.

The Efficacy of a Live Attenuated TW I-Type Infectious Bronchitis Virus Vaccine Candidate

Infectious bronchitis(IB) is a highly contagious avian disease caused by infection with infectious bronchitis virus(IBV),which seriously affects the development of the global poultry industry. The distribution of TW I-type IBV in China has increased in recent years, becoming a widespread genotype. We previously isolated a TW I-type IBV strain termed CK/CH/GD/GZ14 in 2014, but its pathogenicity and possibility for vaccine development were not explored. Therefore, this research aimed to develop a live-attenuated virus vaccine based on the CK/CH/GD/GZ14 strain. The wild type IBV CK/CH/GD/GZ14 strain was serially passaged in SPF embryos for 145 generations. The morbidity and mortality rate of wildtype strain in 14 day-old chickens is 100% and 80% respectively, while the morbidity rate in the attenuated strain was 20%in the 95 th and 105 th generations and there was no death. Histopathological observations showed that the pathogenicity of the 95th and 105th generations in chickens was significantly weakened. Further challenge experiments confirmed that the attenuated CK/CH/GD/GZ14 strain in the 95th and 105 th generations could resist CK/CH/GD/GZ14(5th generation)infection and the protection rate was 80%. Tracheal cilia stagnation, virus shedding, and viral load experiments confirmed that the 95 th and 105th generations provide good immune protection in chickens, and the immunogenicity of the 105th generation is better than that of the 95th generation. These data suggest that the attenuated CK/CH/GD/GZ14 strain in the105th generation may be applied as a vaccine candidate against TW I-type IBV.

Semen extracellular vesicles mediate vertical transmission of subgroup J avian leukosis virus

Subgroup J avian leukosis virus(ALV-J) is a highly oncogenic retrovirus that has been devastating the global poultry industry since the late 1990s. The major infection model of ALV-J is vertical transmission, which is responsible for the congenital infection of progeny from generation to generation. Increasing evidence has suggested that extracellular vesicles(EVs) derived from virus-infected cells or biological fluids have been thought to be vehicles of transmission for viruses. However, the role of EVs in infection and transmission of ALV-J remains obscure. In the present study, semen extracellular vesicles(SE) were isolated and purified from ALV-J-infected rooster seminal plasma(SE-ALV-J), which was shown to contain ALV-J genomic RNA and partial viral proteins, as determined by RNA sequencing, reverse transcription-quantitative PCR and Western blotting. Furthermore, SE-ALV-J was proved to be able to transmit ALV-J infection to host cells and establish productive infection.More importantly, artificial insemination experiments showed that SE-ALV-J transmitted ALV-J infection to SPF hens, and subsequently mediated vertical transmission of ALV-J from the SPF hens to the progeny chicks. Taken together, the results of the present study suggested that ALV-J utilized host semen extracellular vesicles as a novel means for vertical transmission, enhancing our understanding on mechanisms underlying ALV-J transmission.