The interactions between the subgroup A avian leukosis virus [ALV(A)] envelope glycoproteins and soluble forms of the ALV(A) receptor Tva were analyzed both in vitro and in vivo by quantitating the ability of the soluble Tva proteins to inhibit ALV(A) entry into susceptible cells. Two soluble Tva proteins were tested: the 83-amino-acid Tva extracellular region fused to two epitope tags (sTva) o...

Avian leukosis virus subgroup J (ALV-J) infection can cause tumors and immunosuppression. Endogenous viruses integrate into host genomes and can recombine with exogenous avian leukosis virus (ALV). In this study, we analyzed the interaction of endogenous retrovirus 21 (ev21) with the ALV-J in late-feathering Chinese yellow chicken. Two ALV-J strains M180 and K243 were isolated from late-feather...

Cell killing by avian leukosis virus subgroup B (ALV-B) in cultures has been extensively studied, but the molecular basis of this process has not been established. Here we show that superinfection, which has been linked to cell killing by ALV-B, plays no crucial role in cell death induction. Instead, we show that signaling by the ALV-B receptor, TVB(S3), a member of the tumor necrosis factor re...

avian leukosis virus subgroup-j (alv-j). mycoplasma gallisepticum (mg) and mycopjasma synviae (ms) are important pathogens in chickens that cause severe economical losses in poultry industry throughout the world. seven broiler grandparent flocks of iran (six broiler strains) were sampled randomly at the ages of 8-63 wk (100 samples from each flock) for antibody detection to alv-j, mg, and ms by...

Avian leukosis virus subgroup J (ALV-J) was first isolated from meat-type chickens in 1988. No field cases of ALV-J infection or tumors in layer chickens were observed worldwide until 2004. However, layer flocks in China have experienced outbreaks of this virus in recent years. The molecular epidemiology of ALV-J strains isolated from layer flocks was investigated. The env genes of 77.8% (21/27...

Cell killing by avian leukosis virus subgroup B (ALV-B) in cultures has been extensively studied, but the molecular basis of this process has not been established. Here we show that superinfection, which has been linked to cell killing by ALV-B, plays no crucial role in cell death induction. Instead, we show that signaling by the ALV-B receptor, TVB, a member of the tumor necrosis factor recept...

23 Avian leukosis virus subgroup J (ALV-J) was first isolated from meat-type 24 chickens in 1988. No field cases of ALV-J infection and tumors in layer chickens were 25 observed worldwide until 2004. However, layer flocks in China have experienced 26 outbreaks of this virus in recent years. The molecular epidemiology of ALV-J strains 27 isolated from layer flocks was investigated. The env genes...

Exploration of the abnormal expression exosomal molecules during infection avian leukosis virus subgroup J (ALV-J) is essential to provide a deeper understanding exosome’s role in viral pathogenesis involved. The study aimed investigate differentially expressed proteins and miRNAs exosomes derived from DF-1 cells infected by ALV-J, their gene function involved signal pathways. We isolated ALV-J...

Eight Chinese field strains of subgroup J avian leukosis viruses (ALV-J) were isolated from broilers or parent stocks during January 1999 to April 2001. One strain, SD9902, was an acute transforming virus, able to induce typical myelocytomatosis in 22-38 days after inoculation of 1-day-old meat-type chicks. The envelope protein and 3'-untranslated region (UTR) of the eight field strains were co...

Avian leukosis virus (ALV) is detrimental to poultry health and causes substantial economic losses from mortality and decreased performance. Because tumorigenesis is a complex mechanism, the regulatory architecture of the immune system is likely to include the added dimensions of modulation by miRNAs and long-noncoding RNA (lncRNA). To characterize the response to ALV challenge, we developed a ...