Hantaan Virus Antibody Products by Targets
Fig.1 Structure and genome organization of hantaviruses.
Fig.2 HTNV replication cycle.
Hantaan Virus Background
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.
Structure of HTNV
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.
Replication cycle of HTNV
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.
As an expert in antibody field, Creative Biolabs not only grasps the relevant knowledge of HTNV, but also provides anti-HTNV antibodies for antiviral treatment research. Our expert team has the ability to provide comprehensive services for specific project needs, including ViroAntibody discovery, ViroAntibody engineering, ViroAntibody customized and ViroAntibody neutralization assays services. If you are interested in our anti-HTNV antibody products or services, please feel free to contact us for more details.
References
- Hussein, I. T., et al. “Recent Advances in Hantavirus Molecular Biology and Disease.” Advances in Applied Microbiology (2011): 35-75.
- Razzauti M, Plyusnina A, Henttonen H, et al. Microevolution of Puumala hantavirus during a Complete Population Cycle of Its Host, the Bank Vole (Myodes glareolus). PLOS ONE. 2013.
