Development and evaluation of a gp85 protein-based subgroup-specific indirect enzyme-linked immunosorbent assay for the detection of anti-subgroup J avian leukosis virus antibodies

2020 ◽  
Vol 104 (4) ◽  
pp. 1785-1793
Author(s):  
Fangfang Chang ◽  
Lixiao Xing ◽  
Zhifeng Xing ◽  
Mengmeng Yu ◽  
Yuanling Bao ◽  
...  
2021 ◽  
Vol 71 (4) ◽  
pp. 451-461
Author(s):  
Nuhu Abdulazeez Sani ◽  
Iniobong Chukwuebuka Ugochukwu ◽  
Ahmadu Saleh ◽  
Samson Eneojo Abalaka ◽  
Muhammed Shuaib Muhammed ◽  
...  

Abstract Previous reports indicate high seroprevalence of avian leukosis virus (ALV) p72 antigen in layer flocks suspected to have Marek’s disease (MD) in Kaduna and Plateau States. However, the specific subgroups responsible for ALV infection in layers in the States are still unknown, hence the need for this study. Therefore, the objective of this study was to determine the antibody profiles of ALV subgroups A/B and J in layer flocks suspected to have MD in Kaduna and Plateau States. Sera from 7 and 16 layer flocks suspected to have MD in Kaduna and Plateau States respectively, were screened for the presence of antibodies to ALV subgroups A/B and J using IDEXX enzyme linked immunosorbent assay (ELISA) kits. Out of the seven layer flocks screened in Kaduna State, antibodies to ALV subgroup A/B was detected in six of the flocks (85.7%), while antibodies to ALV subgroup J was detected in only one flock (14.3%). Antibodies to both ALV subgroups A/B and J were detected in one flock (14.3%), which suggests co-infection of the two ALV subgroups. Out of the 16 flocks screened in Plateau State, antibodies to ALV subgroup A/B were detected in 15 flocks (93.8%), while antibodies to ALV subgroup J were detected in six flocks (37.5%). Antibodies to both ALV subgroups A/B and J were detected in five flocks (31.3%). The high detection of antibodies to ALV A/B suggests that ALV infection in layers is mostly due to ALV subgroup A or B in the study areas.


1985 ◽  
Vol 29 (4) ◽  
pp. 1118 ◽  
Author(s):  
K. Tsukamoto ◽  
Y. Kono ◽  
K. Arai ◽  
H. Kitahara ◽  
K. Takahashi

1989 ◽  
Vol 62 (04) ◽  
pp. 1078-1082 ◽  
Author(s):  
Burt Adelman ◽  
Patricia Ouynn

SummaryThis report describes the binding of plasminogen to fibrinogen adsorbed onto polystyrene wells. Binding was determined by enzyme linked immunosorbent assay. Both glu- and lys-plasminogen bound to immobilized fibrinogen in a dose-dependent fashion. However, more lys- than glu-plasminogen bound when equal concentrations of either were added to immobilized fibrinogen. Plasminogen binding was inhibited by epsilon aminocaproic acid indicating that binding was mediated via lysine-binding regions of plasminogen. Soluble fibrinogen added in excess of immobilized fibrinogen did not compete for plasminogen binding but fibrinogen fragments produced by plasmin digestion of fibrinogen did. Treatment of immobilized fibrinogen with thrombin caused a small but significant (p <0.01) increase in plasminogen binding. These studies demonstrate that immobilized fibrinogen binds both glu- and lys-plasminogen and that binding is mediated via lysine-binding regions. These interactions may facilitate plasminogen binding to fibrinogen adsorbed on to surfaces and to cells such as platelets which bind fibrinogen.


1995 ◽  
Vol 74 (04) ◽  
pp. 1045-1049 ◽  
Author(s):  
P Butthep ◽  
A Bunyaratvej ◽  
Y Funahara ◽  
H Kitaguchi ◽  
S Fucharoen ◽  
...  

SummaryAn increased level of plasma thrombomodulin (TM) in α- and β- thalassaemia was demonstrated using an enzyme-linked immunosorbent assay (ELISA). Nonsplenectomized patients with β-thalassaemia/ haemoglobin E (BE) had higher levels of TM than splenectomized cases (BE-S). Patients with leg ulcers (BE-LU) were found to have the highest increase in TM level. Appearance of larger platelets in all types of thalassaemic blood was observed indicating an increase in the number of younger platelets. These data indicate that injury of vascular endothelial cells is present in thalassaemic patients.


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