Antibodies (by target):
Fig.1 Structure and genome organization of hantaviruses.
Fig.2 HTNV replication cycle.
Hantaan virus (HTNV) infection is an important cause of hemorrhagic fever with renal syndrome (HFRS) in Eurasia and of hantavirus pulmonary syndrome in the Americas. About 200,000 clinical cases of hantavirus disease are reported every year. Usually, HFRS occurs in 5 consecutive stages: febrile, hypotensive, oliguric, diuretic, and convalescent. Clinical symptoms also include thrombocytopenia and, in severe cases, bleeding due to capillary leak syndrome. HTNV is transmitted to humans by inhalation of aerosols extracted from rodent excreta. Its natural hosts are various small mammals, including rodents, shrews, moles, and bats.
HTNVs have been classified as category A pathogens by CDC (Centers for Disease Control and Prevention). It is the prototypic member of the genus Hantavirus within the family Bunyaviridae, which includes five genera: Bunyavirus, Hantavirus, Nairovirus, Phlebovirus, and Tospovirus. HTNV is a kind of enveloped negative-sense RNA virus, which contains three-part segmented genomes. The three genomic RNA segments, S, M, and L, encode a nucleocapsid protein (N), a precursor glycoprotein, which is processed into two envelope glycoproteins (Gn and Gc), and virus RNA-dependent RNA polymerase (RdRp). N protein is the main structural component of the virus. Its main function is to protect and envelop the three genomic RNAs that form the ribonucleocapsid of three viruses.
HTNV infects many cell lines, including endothelial cells, epithelial cells, macrophages, dendritic cells and lymphocytes. The replication cycle begins when the virus particles attach to integrin receptors on the surface of host cells. After attachment, the cells enter into the pore mediated by clatherin-coated pits, and the virus body is finally delivered to the lysosome. In the lysosomal compartment, the virus is not enveloped, and three viral capsids are released into the cytoplasm. RdRp starts transcription and produces three mRNA, which are translated by host cell translation mechanism to generate virus protein. The virus genome is synthesized by RdRp through the cRNA intermediate, then packaged into new virus particles, and germinated from the host cells.
Currently, there is no antiviral therapy or vaccine available for HTNV related diseases. Understanding the molecular details of HTNV life cycle will help to determine the target of antiviral therapy and design potential antiviral drugs for the treatment of HFRS.
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