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Panbio Dengue Duo IgM & IgG Capture ELISA(E-DEN01D)

广州健仑生物科技有限公司

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Panbio Dengue Duo IgM & IgG Capture ELISA(E-DEN01D)

非洲工作用登革热试纸

热带国家旅游用登革热检测试纸

登革热IgM抗体、登革热IgG抗体、登革热NS1抗原、登革热早期检测试剂盒

登革热核酸检测试剂盒

Panbio公司简介:
1、1988年成立，2001年在澳大利亚证券交易所上市。
2、Panbio系关于虫媒感染性疾病及热带感染性疾病的专业供货商。
3、产品面向虫媒感染性疾病的检测，在国内疾控系统具有*的认知和认可度。
4、2010年销售800万检测试剂，为30多种疾病提供诊断。

Panbio登革热介绍：

1、登革热快速检测试剂(Dengue Duo Cassette R-DEN03D)
用于定性的快速检测人群血清、血浆或全血中登革病毒的IgM及IgG抗体。可在15分钟内检测结果。

2、登革IgM捕捉ELISA(Dengue IgM Capture ELISA E-DEN01M)
用于定性的检测人群血清中登革病毒的IgM抗体，用于临床实验室对具有持续发烧的登革热症状的病人的辅助诊断。

3、登革IgG捕捉ELISA(Dengo IgG Capture ELISA E-DEN02G)
用于定性检测血清中登革病毒(血清型1、2、3及4型)的IgG抗体。用于临床实验室对继发登革热感染的辅助诊断。

4、登革早期ELISA(Dengue Early ELISA E-DEN01P)
用于定性检测血清中登革病毒的NS1抗原(血清型1、2、3及4型)。用于临床实验室对有持续发烧的登革热症状病人的辅助性诊断。

5、登革IgG间接ELISA(Dengue IgG Indirect ELISA E-DEN01G)
用于定性检测血清中登革病毒(血清型1、2、3及4型)的IgG抗体，用于临床实验室对具有持续发烧的登革感染症状或接触史的患者的辅助性诊断。

6、登革IgM & IgG联检ELISA(Dengue Duo IgM & IgG Capture ELISA E-DEN01D)
用于定性检测血清中登革病毒的IgM和IgG抗体。可以区分原发感染与继发感染。

Dengue产品介绍

Panbio Dengue Duo IgM & IgG Capture ELISA(E-DEN01D)

易感性
人类普遍易感。在新流行区各年龄组均易感，但以青壮年发病者居多，年龄在20～40岁，临床上以panbio登革热为主要表现。如1999年我国福州市所发生的自新中国成立以来*暴发流行的1649例panbio登革热患者中，青壮年占76.11%。而在地方性流行区发病者中，以儿童为多见，并且以登革出血热为主要表现。机体一次得病后对同一亚型的免疫力可持续多年，但仍可感染另一亚型。感染两种亚型后可获持久的免疫力。
（四）流行特征
本病呈世界性分布，尤其在热带和亚热带地区。东南亚地区好发，其次是北非、非洲赤道地区、南非北部、澳洲、地中海地区、太平洋岛屿、加勒比海岛屿等地。本病已广泛分布100 多个国家和地区，对25亿人健康构成危险。据世界卫生组织估计，世界上每年约发生1亿例panbio登革热，50万例登革出血热，25 000 人死亡，而且在亚、非、南美的热带地区发病率呈上升趋势，成为继疟疾之后zui重要的热带病。我国广东、海南等地区从1978年以来曾有过14次规模不等的panbio登革热流行，1999年福州市发生Ⅱ型panbio登革热流行。2004年，浙江省慈溪市也发生了由泰国输入所引起的panbio登革热暴发疫情，共发病83例，由panbio登革热Ⅰ型病毒引起。我国的流行病学资料表明，本病流行间隔时间约为3年，每次流行持续2～4年，并且地域有不断扩大之势。本病系由蚊传播，故流行有一定的季节性，一般在每年的5～11月份，高峰在7～9月份。
发病机制病理 
（一）发病机制
panbio登革热和登革出血热的发病机制迄今尚未*阐明。登革病毒通过伊蚊叮咬进入人体后，在单核‐巨噬细胞系统增殖达一定数量后进入血液循环，形成*次病毒血症。继而再侵入单核‐巨噬细胞和淋巴组织中，复制后再释放入血液，形成第二次病毒血症。登革病毒与血液中已存在的抗登革病毒抗体结合形成免疫复合物，并激活补体系统，引起血管通透性增加、血浆外渗，血液浓缩。同时病毒可抑制骨髓，使血小板和白细胞减少，发生出血倾向。该病的发病机制有两个学说。*种学说是抗体依赖增强作用。血清学研究证实，登革病毒表面存在两种不同的抗原决定簇，即群特异性决定簇和型特异性决定簇。群特异性决定簇为黄病毒属（包括登革病毒在内）所共有，其产生的抗体有助于登革病毒感染的发展，称增强性抗体；型特异性决定簇产生的抗体具有较强的中和作用，称中和抗体，能中和同一型登革病毒的再感染，对异型病毒也有一定中和能力。再次感染同一型病毒时，血清中增强性抗体活性弱，而中和抗体活性强，足以中和入侵病毒，则病毒血症迅速被清除，患者可不发病，反之，若再次感染异型病毒时，体内增强性抗体活性强，可促进病毒在单核‐巨噬细胞中大量复制，出现抗体依赖姓感染增强现象（antibody dependent enhancement，ADE）。此时病毒抗原与抗体形成免疫复合物，后者与单核‐巨噬细胞表面的Fc 受体结合，使这些细胞被激活并释出可裂解补体C3 的蛋白酶、凝血活酶和血管通透因子，引起血管通透性增加、血浆外渗、血容量减少，导致血液浓缩和休克。活化的凝血系统可引起播散性血管内凝血（DIC），加重了休克；登革病毒抗原可与又病毒受体的血小板相结合，登革病毒抗体再与血小板上的病毒抗原结合，均导致血小板聚集、破坏，引起血小板减少及患者骨髓被抑制，使血小板生成减少，各系统易于出血。有人发现Ⅱ型登革病毒株有多个与抗体依赖姓感染增强现象有关的抗原决定簇，而其他型病毒株则无这种增强性抗原决定簇，故Ⅱ型登革病毒比其他型病毒易引起登革出血热。第二种学说认为与感染病毒的毒力、变异有关。通过对塔希提、斐济等太平洋岛屿的流行病学观察，发现不少初次感染的panbio登革热患者也出现登革出血热临床经过，患者的血清反应也属初次感染类型，且儿童占多数，这提示登革病毒有可能通过变异产生毒力更强的病毒株，从而引起登革出血热的发生。各型登革病毒均可引起登革出血热，其中以血清Ⅱ型病毒引起病变zui为明显，Ⅲ型和Ⅳ型次之，Ⅰ型相对较轻。此外激活的T 细胞本身亦可释放一系列细胞因子，如IL‐2、IFN‐γ、组胺、过敏素C3a、C5a 等，可引起感染加重、休克、循环衰竭和出血等表现。

Panbio Dengue Duo IgM & IgG Capture ELISA(E-DEN01D)

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【公司名称】 广州健仑生物科技有限公司
【市场部】    杨永汉

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【腾讯  】 2042552662
【公司地址】 广州清华科技园创新基地番禺石楼镇创启路63号二期2幢101-103室

references：

Susceptibility
Human generally susceptible. In the new endemic areas are susceptible to all age groups, but the majority of young adults, aged 20 to 40 years old, clinical panbio dengue fever as the main performance. Such as 1999 China's Fuzhou City since the founding of China since the first outbreak of 1649 cases of panbio dengue fever, young adults accounted for 76.11%. In the endemic areas of the incidence of children, the children are more common, and to dengue hemorrhagic fever as the main performance. The body after a disease on the same subtype of immunity for many years, but still infected with another subtype. Infection of two subtypes can be sustained after the immune system.
(D) popular characteristics
The disease is distributed worldwide, especially in tropical and subtropical regions. Southeast Asia, followed by North Africa, the African equatorial region, northern South Africa, Australia, the Mediterranean region, the Pacific Islands, the Caribbean islands and other places. The disease has been widely distributed in more than 100 countries and regions, 2.5 billion people constitute a dangerous health. According to the World Health Organization estimates that there are about 100 million cases of panbio dengue fever in the world each year, 500,000 cases of dengue haemorrhagic fever, 25,000 deaths, and in Asia, Africa, South America, the incidence of tropical areas was on the rise, The most important tropical disease. China's Guangdong, Hainan and other regions since 1978, there have been 14 times the scale of panbio dengue epidemic, in 1999 occurred in Fuzhou, type Ⅱ panbio dengue epidemic. In 2004, Cixi City, Zhejiang Province, also occurred by the Thai input caused by panbio dengue fever outbreak, a total of 83 cases, caused by panbio dengue virus type Ⅰ virus. China's epidemiological data show that the epidemic interval of about 3 years, each epidemic for 2 to 4 years, and the region has been expanding trend. The disease is spread by the mosquito, so the epidemic has a certain seasonal, generally in the annual 5 to 11 months, the peak in the 7 to 9 months.
Pathogenesis pathology
(A) the pathogenesis
The pathogenesis of dengue fever and dengue hemorrhagic fever has not yet been fully elucidated. Dengue virus through the Aedes bite into the human body, the mononuclear - macrophage system to a certain number of proliferation into the blood circulation, the formation of the first viremia. And then invade the mononuclear - macrophages and lymphoid tissue, replicate and then released into the blood, the formation of a second viremia. Dengue virus and blood in the existing anti-dengue virus antibodies to form immune complexes, and activation of the complement system, causing increased vascular permeability, plasma extravasation, blood concentration. At the same time the virus can inhibit bone marrow, so that plaets and leukopenia, bleeding tendency. The pathogenesis of the disease has two doctrines. The first theory is antibody-dependent enhancement. Serological studies have shown that there are two different antigenic determinants on the surface of dengue virus, namely, group-specific determinants and type-specific determinants. Group-specific determinants are common to flaviviruses (including dengue virus), and their antibodies contribute to the development of dengue virus infection, called enhanced antibodies; type-specific determinants produce antibodies that are strong Of the neutralization of the role, said neutralizing antibodies, and in the same type of dengue virus re-infection, the virus also has a certain ability to neutral. Once again infected with the same type of virus, the serum enhanced antibody activity is weak, and neutralizing antibody activity is strong enough to neutralize the virus, the viremia quickly cleared, the patient may not disease, on the contrary, if again infected with heterotypic virus, Enhanced antibody activity, can promote the virus in mononuclear - macrophages in a large number of replication, antibody dependent surname infection enhancement phenomenon (antibody dependent enhancement, ADE). Where the viral antigen forms an immune complex with the antibody that binds to the Fc receptor on the surface of the monocyte-macrophage so that these cells are activated and release the cleavable complement C3 protease, thromboplastin and vascular permeability factor , Causing increased vascular permeability, plasma extravasation, reduced blood volume, resulting in blood concentration and shock. The activation of the coagulation system can cause disseminated intravascular coagulation (DIC), increased shock; dengue virus antigen can be combined with the virus receptor plaets, dengue virus antibodies and plaet virus antigen binding, Plaet aggregation, destruction, causing thrombocytopenia and bone marrow suppression in patients with plaet production is reduced, the system is easy to bleeding. It has been found that type II dengue virus strains have multiple antigenic determinants associated with antibody-dependent surgeries, whereas other virus strains do not have this enhanced epitope, so the type II dengue virus is superior to other viruses Causing dengue hemorrhagic fever. The second theory is related to the virulence and variation of the infected virus. Through the epidemiological observations of Pacific islands such as Tahiti and Fiji, it has been found that many patients with panbio dengue fever who are initially infected have also experienced dengue haemorrhagic fever. The patient's serum response is also the type of primary infection and the majority of children Suggesting that dengue virus may produce more virulent strains by mutation, causing dengue hemorrhagic fever. Dengue virus can cause dengue hemorrhagic fever, of which the serum type Ⅱ virus caused by the most obvious lesions, type Ⅲ and Ⅳ followed, Ⅰ type is relatively light. In addition, activated T cells can also release a series of cytokines, such as IL-2, IFN-γ, histamine, allergens C3a, C5a, can cause infection, shock, circulatory failure and bleeding and other performance.