scholarly journals Virological confirmation of concurrent dengue virus serotypes 1 and 4 by virus isolation using Fc-gamma receptor-expressing BHK cells

2015 ◽  
Vol 33 ◽  
pp. 177-178 ◽  
Author(s):  
Meng Ling Moi ◽  
Yasuko Honma ◽  
Satomi Mori ◽  
Toshiki Kuze ◽  
Masumi Kanekawa ◽  
...  
Author(s):  
Roudhotul Ismaillya Noor ◽  
Aryati Aryati ◽  
Puspa Wardhani

Dengue virus infection (DVI) currently is detected by using dengue virus NS1 antigen (NS1 Ag). The sensitivity of NS1 Ag is 27.8%–93.4%,but recent study of Kumarasamy the sensitivity of NS1 Ag is better than the virus isolation and polymerase chain reaction (PCR). This studyis focussed on the evaluation of the validity of Panbio Dengue Early Rapid for the diagnosis of DVI and the NS1 Ag sensitivity associated withdengue virus serotypes. The sera was obtained from 65 DVI patients which diagnosed by the clinicians. The resulted diagnosis was foundby serology tests (positive IgM/IgG antidengue/NS1 Ag ELISA) and 1997 WHO criteria as the gold standard, and which also found 35 nonDVI patients (typhoid fever, HAV, malaria, UTI, tuberculosis and bronchopneumonia). The samples were examined by Panbio Dengue EarlyRapid. PCR was performed on each positive serological test result to determine the dengue virus serotypes. The sensitivity and specificity ofPanbio Dengue Early Rapid was 49.2% and 100%. The PCR results of 65 sera showed positive PCR in 49.2% (positive NS1 Ag was 62.5%).Meanwhile, and negative PCR in 50.8% (positive NS1 Ag was 36.4%). The predominance of serotypes (positive NS1 Ag) were DEN-3 (37.5%),DEN-4 (28.1%), DEN-1 (21.9%) and DEN-2 (12.5%). The Panbio Dengue Early Rapid can be used as early detection of DVI, although itshould be used in conjunction with other dengue serological tests as well. Unfortunately there is still not enough evidence about the NS1 Agsensitivity associated with the dengue virus serotypes.


2011 ◽  
Vol 108 (30) ◽  
pp. 12479-12484 ◽  
Author(s):  
K. R. Chan ◽  
S. L.-X. Zhang ◽  
H. C. Tan ◽  
Y. K. Chan ◽  
A. Chow ◽  
...  

2021 ◽  
Vol 22 (3) ◽  
pp. 1377
Author(s):  
Thansita Bhunyakarnjanarat ◽  
Kanyarat Udompornpitak ◽  
Wilasinee Saisorn ◽  
Bhumdhanin Chantraprapawat ◽  
Peerapat Visitchanakun ◽  
...  

A high dose of NSAIDs, a common analgesic, might induce lupus activity through several NSAIDs adverse effects including gastrointestinal permeability defect (gut leakage) and endotoxemia. Indomethacin (25 mg/day) was orally administered for 7 days in 24-wk-old Fc gamma receptor IIb deficient (FcgRIIb-/-) mice, an asymptomatic lupus model (increased anti-dsDNA without lupus nephritis), and age-matched wild-type (WT) mice. Severity of indomethacin-induced enteropathy in FcgRIIb-/- mice was higher than WT mice as demonstrated by survival analysis, intestinal injury (histology, immune-deposition, and intestinal cytokines), gut leakage (FITC-dextran assay and endotoxemia), serum cytokines, and lupus characteristics (anti-dsDNA, renal injury, and proteinuria). Prominent responses of FcgRIIb-/- macrophages toward lipopolysaccharide (LPS) compared to WT cells due to the expression of only activating-FcgRs without inhibitory-FcgRIIb were demonstrated. Extracellular flux analysis indicated the greater mitochondria activity (increased respiratory capacity and respiratory reserve) in FcgRIIb-/- macrophages with a concordant decrease in glycolysis activity when compared to WT cells. In conclusion, gut leakage-induced endotoxemia is more severe in indomethacin-administered FcgRIIb-/- mice than WT, possibly due to the enhanced indomethacin toxicity from lupus-induced intestinal immune-deposition. Due to a lack of inhibitory-FcgRIIb expression, mitochondrial function, and cytokine production of FcgRIIb-/- macrophages were more prominent than WT cells. Hence, lupus disease-activation from NSAIDs-enteropathy-induced gut leakage is possible.


Blood ◽  
1992 ◽  
Vol 79 (11) ◽  
pp. 2960-2964 ◽  
Author(s):  
T Berney ◽  
T Shibata ◽  
R Merino ◽  
Y Chicheportiche ◽  
V Kindler ◽  
...  

Abstract We have evaluated the therapeutic activity of recombinant erythropoietin (rEpo), in comparison with recombinant interleukin-3 (rIL-3) and granulocyte-macrophage colony-stimulating factor (rGM-CSF), on a lethal form of acute anemia resulting from Fc gamma receptor- mediated erythrophagocytosis after a single injection (500 micrograms) of a monoclonal anti-mouse red blood cell (MRBC) autoantibody. Continuous perfusion of rEpo before the administration of anti-MRBC monoclonal antibody completely protected animals from death due to anemia with a rapid recovery, while no protection was obtained by rIL-3 perfusion. In contrast, rGM-CSF perfusion markedly accelerated the progression of anemia and the mortality rate. This was found to result from an enhancement of erythrophagocytosis by Kupffer cells and by polymorphonuclear leukocytes that massively infiltrated the livers. Even after the injection of a sublethal dose (100 micrograms) of anti- MRBC monoclonal antibody, rGM-CSF-perfused mice died of a severe form of acute anemia. Furthermore, we have shown that rEpo was able to treat efficiently a spontaneous form of autoimmune hemolytic anemia in a majority of anemic NZB mice, whereas rGM-CSF markedly aggravated anemia. This may be of clinical importance, because GM-CSF administration could exhibit an adverse effect in some autoimmune diseases that involve autoimmune anemia.


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