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一種假單孢菌屬細菌：具生物農藥潛能以防治登革熱病媒蚊之細菌

為了解決killing mosquito mem的問題，作者李琵亞 這樣論述：

Dengue virus is mainly transmitted by female Aedes aegypti and less by Ae. albopictus. These two mosquitoes also transmit Chikungunya, Yellow fever and Zika virus. They can be found in tropical and sub-tropical countries mostly in urban and semi-urban areas. Synthetic insecticides, such as syntheti

c pyrethroids, are commonly used to control these mosquitoes; however insecticide resistant is a growing problem in control of these mosquito vectors worldwide. From this point of view, microbial control, one kind of biological controls, becomes an alternative way to control insect pests, including

mosquitos. In this study, I demonstrated that the culture of Pseudomonas bacterium could kill the larvae of Ae. aegypti. The killing activity occurred after at least 6-h culture and decreased gradually over 24-h culture. Moreover, the supernatant of the culture killed over 70% larvae after 8-h treat

ments and increased to over 80% after 16-h, yet there was no killing activity of the resuspended pellets (bacteria only). Besides, storage temperatures can affect the killing activity of the culture. After storage for 7 days, the culture and their supernatants remained very similar killing activity

as their stored at 4 and 28 °C, respectively; nonetheless, the killing activity were entirely lost when they were stored at -20 or 37°C for the same period. In conclusion, these results indicate that this Pseudomonas bacterium should have the potential to be developed as an alternative bio-insectici

de to control dengue fever vectors in the future.

探討登革病毒複製機轉：蛋白酶在登革病毒複製所扮演之角色

為了解決killing mosquito mem的問題，作者邱琦 這樣論述：

登革病毒感染引起的症狀有輕微的登革熱、可能致死的登革出血熱以及登革休克症候群，截至目前為止，臨床上仍然沒有發展出可以有效抑制登革病毒複製的疫苗或是藥物，其中最主要的原因為缺乏一個適合用來篩選抗病毒藥物的平台，因此，我們構築了以分泌性鹼性去磷酸酶 (secreted alkaline phosphatase, SEAP) 結合登革病毒蛋白酶NS2B-NS3的報導系統，連接上pEGFP-C1載體之後，利用暫時性轉染的方式表現在HuH7和HT29細胞中，接著以觀察綠色螢光蛋白 (EGFP) 的方式來推測pEG(Δ2B3)SEAP在細胞內的表現情形，從結果可以得知EGFP的表現量會隨著細胞代數的增加

而有下降的趨勢，由於之前有研究顯示在埃及斑蚊的腸道中，蛋白酶的活性會影響登革病毒的感染能力，因此我們認為宿主細胞表現的蛋白酶可能會對病毒的多蛋白進行切割，於是利用蛋白酶抑制劑來觀察蛋白酶在登革病毒複製中的作用，從結果可以得知胰蛋白酶抑制劑 (TI) 和胰凝乳蛋白酶抑制劑 (TPCK) 可以抑制登革病毒多蛋白NS2B-NS3被切割的情形，由於TPCK除了能夠抑制胰凝乳蛋白酶之外，同時也可以抑制細胞核轉錄因子 (nuclear factor kappa B, NF-κB) 的活化，而有研究顯示NF-κB活化參與了登革病毒感染引起的細胞自噬及細胞凋亡，所以我們接著利用其他NF-κB抑制劑進行實驗，由

於文獻指出NF-κB活化與引起細胞自噬和細胞凋亡有關，而細胞自噬會使得登革病毒複製量上升，同時登革病毒感染會引發許多不同種類細胞的凋亡，這些現象在NF-κB被抑制之後都有顯著下降的情形，而且抑制NF-κB也可以抑制細胞激素-巨噬細胞移動抑制因子 (macrophage migration inhibitory factor, MIF) 的生成，使得發炎反應不會加劇。總結來說，我們發現宿主細胞胰蛋白酶會幫助登革病毒複製，同時NF-κB活化也會參與登革病毒感染引起的細胞自噬、細胞凋亡以及發炎激素產生，因此未來或許可以在臨床上合併使用胰蛋白酶以及NF-κB抑制劑治療受到登革病毒感染的患者。