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Hantaviruses belong to the Bunyaviridae family of viruses. There Bunyaviridae family is divided into 5 genera: Orthobunyavirus, Nairovirus, Phlebovirus, Tospovirus, and Hantavirus. Like all members of this family, hantaviruses have genomes comprised of three negative-sense, single-stranded RNA segments, and so are classified as negative sense RNA viruses. Viruses in the genus Hantavirus are unique in that they are transmitted by aerosolized rodent excreta or rodent bites, whereas all other genera in the Bunyaviridae family are arthropod-borne viruses.
The name hantavirus is derived from the Hantan River, where the Hantaan virus (the etiologic agent of Korean hemorrhagic fever) was first isolated by Dr. Ho-Wang Lee and colleagues. The disease associated with Hantaan virus is called hemorrhagic fever with renal syndrome (HFRS), a term that is accepted by the World Health Organization. It was formerly called Korean hemorrhagic fever (a term that is no longer in use).
The hantaviruses constitute a relatively newly discovered genus of viruses; the disease entity HFRS was first recognized by Western medicine during the Korean War in the early 1950s. In 1993, a newly-recognized species of hantavirus was found to be behind the Hantavirus cardiopulmonary syndrome (HCPS, also called HPS) caused by the Sin Nombre virus (Spanish for “nameless virus”) in New Mexico and other Four Corners states. In addition to Hantaan virus and Sin Nombre virus, several other hantaviruses have been implicated as etiologic agents for either HFRS or HCPS.
Like other members of the bunyavirus family, hantaviruses are enveloped viruses with a genome that consists of three single-stranded, negative sense RNA segments designated S (small), M (medium), and L (large). The S RNA encodes the nucleocapsid (N) protein. The M RNA encodes a polyprotein that is cotranslationally cleaved to yield the envelope glycoproteins G1 and G2. The L RNA encodes the L protein, which functions as the viral transcriptase/replicase. Within virions, the genomic RNAs of hantaviruses are thought to complex with the N protein to form helical nucleocapsids, the RNA component of which circularizes due to sequence complementarity between the 5′ and 3′ terminal sequences of genomic segments.
Entry into host cells is thought to occur by attachment of virions to cellular receptors and subsequent endocytosis. Nucleocapsids are introduced into the cytoplasm by pH-dependent fusion of the virion with the endosomal membrane. Transcription of viral genes must be initiated by association of the L protein with the three nucleocapsid species. In addition to transcriptase and replicase functions, the viral L protein is also thought to have an endonuclease activity that cleaves cellular messenger RNAs (mRNAs) for the production of capped primers used to initiate transcription of viral mRNAs. As a result of this “cap snatching,” the mRNAs of hantaviruses are capped and contain nontemplated 5′ terminal extensions. The G1 (aka Gn) and G2 (Gc) glycoproteins form hetero-oligomers and are then transported from the endoplasmic reticulum to the Golgi complex, where glycosylation is completed. The L protein produces nascent genomes by replication via a positive-sense RNA intermediate. Hantavirus virions are believed to assemble by association of nucleocapsids with glycoproteins embedded in the membranes of the Golgi, followed by budding into the Golgi cisternae. Nascent virions are then transported in secretory vesicles to the plasma membrane and released by exocytosis.
The pathogenesis of Hantavirus infections is unclear as there is a lack of animal models (rats and mice do not seem to acquire severe disease). While the primary replication site is not clear, in both HFRS and HPS, the main effect is in the blood vessels. There is increased vascular permeability and decreased blood pressure due to endothelial dysfunction. In HFRS, the most dramatic damage is seen in the kidneys, whereas in HPS, the lungs and spleen are most affected.
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