A study on the infection status and transmission of avian leukosis virus subgroup J in Hy-line brown roosters.

Avian leukosis virus subgroup J (ALV-J) is the most prevalent subgroup in chickens and exhibits increased pathogenicity and stronger horizontal and vertical transmission ability among different breeds. Although vertical transmission of ALV-J from infected hens through artificial insemination has been inferred from the detection of the p27 antigen in swabs and serum, there has been no further research on the transmission pattern of ALVs in roosters. In the present study, the positive rate of ALV increased significantly in an indigenous flock after detecting the p27 antigen via enzyme-linked immunosorbent assay (ELISA) and virus isolation in DF-1 cells. Viral sequence comparisons and an indirect fluorescent antibody assay showed that these isolates belonged to the ALV-J subgroup but formed a new branch in a phylogenetic tree when compared to domestic and foreign referential strains. The gp85 gene of the ALV-J isolated from hens and albumen was 94.1-99.7% identical to that in roosters, revealing that these isolates were quite likely transmitted to the hens and their offspring through the semen of ALV-infected roosters by artificial insemination from the Hy-line brown roosters. In addition, we defined four ALV-J infection states in plasma and semen of roosters (P+S+, P-S+, P+S-, and P-S-), which suggests that, in order to eradicate ALV in roosters, it is necessary to perform virus isolation using both semen and plasma. Additionally, ALV detection in semen by ELISA produced false-positive and false-negative results when compared to virus isolation in DF-1 cells. Collectively, our results suggested that an incomplete process of eradication of ALV from ALV-positive roosters led to the sporadic presence of ALV-J in laying hens.

Lethal infection caused by Tetratrichomonas gallinarum in black swans (Cygnus atratus).

BACKGROUND: Tetratrichomonas gallinarum is parasitic protozoa with a wide host range. However, its lethal infection is rare reported. CASE PRESENTATION: Here, we described the first lethal cases of T. gallinarum infection in black swans in China. Five black swans died within a week in succession without obvious symptoms except mild diarrhea. At necropsy, severe lesions were observed in caeca with thickened caecal walls and hemorrhages in the mucosa. A large number of moving trophozoites were found in the contents of the cecum by microscopic examination. The livers were enlarged with multiple bleeding spots on the surface. Histopathology of the livers showed mononuclear cell infiltration and moderate hyperplasia of fibrous tissue. The histopathology of the cecum showed that the villi of the cecum were edematous. Finally, the presence of T. gallinarum was determined by specific PCR andin-situ hybridization assay. Additionally, common pathogens that can cause similar symptoms were excluded. CONCLUSIONS: The death of the black swan was caused by T. gallinarum, suggesting that the parasite might be a new threat to the Cygnus birds.

Geldanamycin Reduces Acute Respiratory Distress Syndrome and Promotes the Survival of Mice Infected with the Highly Virulent H5N1 Influenza Virus.

Infections with lethal influenza viruses lead to acute lung injury (ALI) or acute respiratory distress syndrome (ARDS), which may be related to the activation of the host's immune system. Here, in our study, male C57BL/6 mice were infected with 10 LD50 of the H5N1 influenza virus and treated with geldanamycin or oseltamivir 2 h after infection. Lung injury was assessed by histopathology on days 4 and 7. The viral load was quantified by measuring the NP gene expression level on days 2, 4, and 7. Levels of cytokines and chemokines in bronchoalveolar lavage fluids and inflammatory cells were analyzed at different time points. Geldanamycin administration prolonged survival in mice and dramatically reduced lung injury and pulmonary inflammatory compared with other mice. Viral loads in geldanamycin-treated mice also significantly reduced compared with non-treated mice, but not to the extent as the oseltamivir-treated mice. Furthermore, the geldanamycin treatment markedly reduced the production of major proinflammatory cytokines and chemokines and attenuated the infiltration and activation of immune cells, but it did not alter the generation of virus-neutralizing antibodies. In conclusion, geldanamycin plays an important role in attenuating virus infection-induced ALI/ARDS by reducing the host's inflammatory responses and may provide an important reference for clinical treatments.