2 English reference hemorrhagic fever with renal syndrome, HFRS.
Note that hemorrhagic fever with renal syndrome (hfrs) is an acute viral infectious disease, which is caused by HFRS virus and spread through rats and other natural foci. In the past, this disease was called epidemic hemorrhagic fever in China and Japan, Korean hemorrhagic fever in Korea and South Korea, Far East hemorrhagic fever and hemorrhagic nephritis in the former Soviet Union, and epidemic nephropathy in Scandinavian countries. 1980, which was named as hemorrhagic fever with renal syndrome by the World Health Organization.
Hfrs virus was first isolated from the lung tissue of Apodemus agrarius captured by Li Haowang and others in Korea in 1978, and it was called Hantaan virus according to the separation site. Since then, many virus strains have been isolated from different animals and patients around the world, which is now commonly known as hfrs virus in the world. According to the morphological and molecular biological characteristics of the virus. At present, it has been classified as Bunyaviridae and established as a new genus, named Hantavirus.
The virus body is round or oval, with a diameter of 90 ~ 1 10 nm, and has an envelope with protrusions on it. The nucleic acid of hfrs virus is single-stranded rna, which is divided into L, M and S segments with molecular weights of 2.7× 106,10.4×106 and 0.6× 106 daltons respectively. The base sequences of the three fragments are different from each other, but they all have the same 3' end, that is, "3'aucaucaucugg", which is different from other viruses of Bunyaviridae. Hfrs virus consists of four proteins: N, g 1, g2 and L. N is a nuclear protein and encoded by S fragment. Its main function is to wrap three fragments of viral rna, and protein has strong immunogenicity. G 1 and g2 are glycoproteins, which are encoded by M fragments and have neutralizing antigen sites and hemagglutination active sites. These two antigenic sites exist independently, but they can also partially overlap. L is rna polymerase, which is encoded by L fragment and plays an important role in virus replication. The mature mode of hfrs virus is bud maturation, and its mature process is related to Golgi apparatus and endoplasmic reticulum of cells. The virus can agglutinate goose red blood cells at pH 5.6 ~ 6.4. Many passaged, primary and diploid cells are sensitive to hfrs virus. African green monkey kidney cells (veroe6) and human lung cancer passaged cells (a549) are commonly used to isolate and culture the virus in the laboratory. Viruses generally do not cause visible cytopathic changes in cells, and usually need to be detected and confirmed by immunological methods. There are many susceptible animals, such as Apodemus agrarius, Mongolian gerbils, mice and rats. However, there are no obvious symptoms except that mice and suckling mice will get sick and die after infection. Hfrs virus has strong resistance. Sensitive to acid (ph3) and fatty solvents such as acetone, chloroform and ether. General disinfectants such as Lysol and bromogeramine can also inactivate the virus. The virus has weak heat resistance and can be inactivated at 56 ~ 60℃ for 30 minutes. Ultraviolet radiation (50 cm, 30 minutes) can also inactivate the virus.
The incubation period is generally about two weeks, with acute onset and rapid development. Typical cases have three main symptoms, namely fever, bleeding and kidney damage. The clinical course is divided into fever stage, hypotensive shock stage, polyuria stage, polyuria stage and recovery stage. The pathogenesis of hemorrhagic fever with renal syndrome is very complicated, and some links have not been fully understood. At present, it is generally believed that the direct action of virus is the initial link of the disease, and immunopathological injury also plays an important role. Virus infection causes viremia and systemic capillary and small blood vessel damage, causing high fever, chills, fatigue, systemic soreness, bleeding spots or spots on skin and mucosa, and serious cases of cavity or organ bleeding, renal damage, hematuria, proteinuria and electrolyte disorder. Hemorrhage, plasma exudation and microcirculation disturbance caused by large area capillary and small blood vessels injury cause hypotension or shock. The level of lge in blood increased at the early stage of the disease, suggesting that type ⅰ allergic reaction may dilate small blood vessels and increase exudation through the action of vasoactive substances. In addition, a large number of circulating immune complexes can appear in early patients, which are deposited on blood vessel walls, platelets, glomeruli and renal tubules, and the serum complement level decreases; Anti-basement membrane and anti-myocardial antibodies can also be detected in serum, which indicates that the immunopathological damage caused by type ⅲ and type ⅱ allergic reactions also participates in the pathogenesis of hfrs.
People are usually susceptible to hfrs virus. Only a few people get sick after infection, and most of them are in a state of recessive infection, especially in type II epidemic areas. Antibodies appeared early after infection, and lgm antibodies could be detected on fever 1 ~ 2 days, reaching the peak on the 7th ~10 day. Lgg antibody can be detected on the 2nd ~ 3rd day, and the peak value of14th ~ 20th day. lgg antibody can persist in the body for more than 30 years. In recent years, the research results show that the neutralizing antibody and hemagglutination inhibition antibody produced by g 1 and g2 glycoprotein * * * are the main immunoprotective agents, and the specific antibody produced by N protein * * * also plays a certain role in immunoprotection. Cellular immunity also plays an important role in immune protection against hfrs virus infection. In particular, it is observed that the function of suppressor T cells in hfrs patients is low, which leads to the relative enhancement of killer T cells and B cells. Levels of some cytokines (such as interleukin 1, interferon, tumor necrosis factor, interleukin -2 receptor, pre-mitogen e2, etc.). ) there are also significant changes in different stages of hemorrhagic fever with renal syndrome. It is worth pointing out that the above-mentioned fine chest immunity (including some cytokines), like specific antibodies, not only participates in anti-infection immunity and has the function of resisting and clearing viruses, but also participates in allergic reactions, which may also be one of the reasons for the immunopathological donation damage of this disease. After the onset of hfrs, continuous immunity can be obtained, and reinfection usually does not occur, but the immunity produced by recessive infection is mostly not lasting.
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