• 농약과학회지
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• 제15권4호
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• pp.490-494
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• 2011

벼줄무늬잎마름병(Rice stripe tenuivirus; RSV)은 벼에 발생하는 주요 바이러스병으로 2000년대 이후 서해안을 중심으로 벼에 발생하여 큰 피해를 주고 있다. RSV는 벼의 주요 해충인 애멸구에 의해 영속적으로 전염되기 때문에 애멸구의 적절한 방제로 피해를 경감시킬 수 있다. RSV의 방제전략을 수립하기 위해서는 RSV와 애멸구 간의 생태학적 연구가 필요하며, 특히 애멸구의 흡즙 및 감염생태가 결정적인 키포인트가 될 수 있다. 따라서 본 연구에서는 RSV에 감염된 벼에서 애멸구의 흡즙 및 감염특성을 조사하였다. 애멸구의 영기별 RSV 전염능력을 조사한 결과, RSV 감염주에서 3일 이상 흡즙한 4령충 이상에서 바이러스 전염능력이 높았다. RSV 이병주를 3일간 흡즙하였을 때 성충의 전염능력은 44.8%인데 비해 4령충과 5령충의 전염능력은 69.2%와 67.9%로 성충보다 4, 5령충의 전염능력이 높았다. 이병주 흡즙시 온도에 따른 보독충의 전염능력 조사 결과에서는 $30^{\circ}C$에서 전염능력이 가장 높았으며, $30^{\circ}C$에서 3일간 흡즙하였을 때 전염능력은 93.3%로 $25^{\circ}C$와 $20^{\circ}C$의 70.6%, 43.8%에 비해 현저히 높았다.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• 제5권1호
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• pp.39-50
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• 2002

Hepatitis B viral infection which affect about 10% of Korean population manifests asymptomatic carrier, chronic hepatitis and liver cirrhosis and even associates with hepatocellular carcinoma. Clinical manifestations induced by hepatitis B virus vary depending on the degree of immune response by cytotoxic T cells against viral epitope-presenting liver cells. Since hepatitis B virus presents high rate of mutaton that might change the presented epitope and eventually alter immune response, viral mutations, especially in promoters and enhancers, have an important implication in hepatic inflammation and viral replication. To identify mutations related to the hepatic inflammation, we investigated sequence variations of hepatitis B viral promotor regions in the presence or absence of symptoms in hepatitis B carriers. For this, sera from persistently hepatitis B virus-infected mother-child pairs were collected. After PCR amplifiation of all hepatitis B viral promoters (C promoter, S1 promoter, S2/S promoter, X promoter) using serum DNA from each pair, viral promotors were sequenced by automatic sequencer and then sequence data were analyzed by ClustalW. In most cases, the dominant type of maternal virus was transmitted to the child. However, in some children, some new host specific viral variants could be observed in Cp, S1p and S2/Sp. The mutations in C promoter did not seem to be vertically transmitted but arose in new host independently after the wild type had been transmitted. Enhancer I containing X promoter revealed high host specific variations as has been reported before. Two S promoters, S1p and S2/Sp, have shown some point mutations in children, but no deletion mutations were detected as in chronic hepatitis patients in whom deletion mutations are frequently found. In conclusion, the children with the vertically transmitted hepatitis B virus mostly retain the dominant type virus that had been transmitted. However, host specific variants tended to accumulate over time, possibly as clinical symptoms develop.