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In the United States, as of July 2010 eight states had reported 30 or more cases of Hantavirus since 1993<ref>[http://www.cdc.gov/ncidod/diseases/hanta/hps/noframes/epislides/episls.htm "Hantavirus Pulmonary Syndrome (HPS) Cases, by State"], CDC Website, July 9, 2010, accessed November 9, 2010.</ref> - [[New Mexico]] ([[Sin Nombre virus|84]]), [[Colorado]] (70), [[Arizona]] (62), [[California]] (42), [[Washington (U.S. state)|Washington]] (41), [[Texas]] (37), [[Utah]] (31) and [[Montana]] (30). Other states reporting a significant number of cases include [[Idaho]] (16), [[Kansas]] (15), [[South Dakota]] (15), and [[North Dakota]] (12). With only 11 cases, [[Oregon]] has a notably lower attack rate overall and relative to population, compared to other Western states.
In the United States, as of July 2010 eight states had reported 30 or more cases of Hantavirus since 1993<ref>[http://www.cdc.gov/ncidod/diseases/hanta/hps/noframes/epislides/episls.htm "Hantavirus Pulmonary Syndrome (HPS) Cases, by State"], CDC Website, July 9, 2010, accessed November 9, 2010.</ref> - [[New Mexico]] ([[Sin Nombre virus|84]]), [[Colorado]] (70), [[Arizona]] (62), [[California]] (42), [[Washington (U.S. state)|Washington]] (41), [[Texas]] (37), [[Utah]] (31) and [[Montana]] (30). Other states reporting a significant number of cases include [[Idaho]] (16), [[Kansas]] (15), [[South Dakota]] (15), and [[North Dakota]] (12). With only 11 cases, [[Oregon]] has a notably lower attack rate overall and relative to population, compared to other Western states.


In August of 2012, four new cases of Hantavirus were confirmed in the [[Curry Village, California|Curry Village]] area of [[Yosemite National Park]].{{cite news |title=Third case of Hantavirus confirmed in Yosemite |author=KFSN-30 |url=http://abclocal.go.com/kfsn/story?section=news/local&id=8787968 |newspaper= |date=27 August 2012 |accessdate=28 August 2012}}
In August of 2012, four new cases of Hantavirus were confirmed in the [[Curry Village, California|Curry Village]] area of [[Yosemite National Park]].<ref>{{cite news|title=Third case of Hantavirus confirmed in Yosemite|author=KFSN-30|url=http://abclocal.go.com/kfsn/story?section=news/local&id=8787968 |newspaper=|date=27 August 2012|accessdate=28 August 2012}}</ref>


== {{anchor|Symptoms}}Symptoms ==
== {{anchor|Symptoms}}Symptoms ==

Revision as of 09:32, 28 August 2012

Orthohantavirus

Hantavirus
Transmission electron micrograph of the Sin Nombre Hantavirus
Virus classification
Group:
Group V ((−)ssRNA)
Order:
Unassigned
Family:
Bunyaviridae
Genus:
Hantavirus
Type species
Hantaan virus
Species

Andes virus
Amur virus
Azagny virus
Bayou virus
Black Creek Canal virus
Cano Delgadito virus
Calabazo virus
Carrizal virus
Catacamas virus
Choclo virus
Dobrava-Belgrade virus
El Moro Canyon virus
Hantaan virus
Huitzilac virus
Imjin virus
Isla Vista virus
Khabarovsk virus
Laguna Negra virus
Limestone Canyon virus
Magboi virus
Monongahela virus
Montano virus
Mouyassue virus
Muleshoe virus
Muju virus
New York virus
Nova virus
Oran virus
Playa de Oro virus
Prospect Hill virus
Puumala virus
Rio Mamore virus
Rio Segundo virus
Sangassou virus
Saaremaa virus
Seoul virus
Sin Nombre virus
Soochong virus
Tanganya
Thailand virus
Thottapalayam virus
Topografov virus
Tula virus

Hantaviruses are negative sense RNA viruses in the Bunyaviridae family. Humans may be infected with hantaviruses through rodent bites, urine, saliva or contact with rodent waste products. Some hantaviruses cause potentially fatal diseases in humans, hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS), but others have not been associated with human disease. Human infections of hantaviruses have almost entirely been linked to human contact with rodent excrement, but recent human-to-human transmission has been reported with the Andes virus in South America.[1] The name hantavirus is derived from the Hantan River area in South Korea, which provided the founding member of the group: Hantaan virus (HTNV), isolated in the late 1970s by Ho-Wang Lee and colleagues.[2] HTNV is one of several hantaviruses that cause HFRS, formerly known as Korean hemorrhagic fever.[3]

History

The hantaviruses are a relatively newly discovered genus of viruses. Several thousand United Nations soldiers became ill with "Korean haemorrhagic fever" (now called HFRS) during the Korean War. This outbreak sparked a 25-year search for the etiologic agent. The isolation of Hantaan virus, or HTNV, was reported by Ho-Wang Lee of South Korea in 1978.

It has been proposed that the mysterious sweating sickness was caused by a previously unknown hantavirus, therefore making the first appearance of this pathogen before the Battle of Bosworth Field. This has yet to be confirmed, however.[citation needed]

In 1993, an outbreak of Hantavirus pulmonary syndrome (HPS, see below) occurred in the Four Corners region in the southwestern United States. The viral cause of the disease was found only weeks later and was called the Sin Nombre virus (SNV, in Spanish, "Virus sin nombre", for "nameless virus"). Its rodent host, Peromyscus maniculatus, was first identified by Terry Yates, a professor at the University of New Mexico.[4] In addition to Hantaan virus and Sin Nombre virus, several other hantaviruses have been implicated as etiologic agents for either HFRS or HPS. Other identified hantaviruses have not been associated with disease.

Virology

Classification

Hantaviruses are Bunyaviruses. The Bunyaviridae family is divided into five genera: Orthobunyavirus, Nairovirus, Phlebovirus, Tospovirus, and Hantavirus. Like all members of this family, hantaviruses have genomes comprising three negative-sense, single-stranded RNA segments, and so are classified as negative sense RNA viruses. Members of other Bunyaviridae family genera are generally arthropod-borne viruses,[5] but hantaviruses are thought to be transmitted to humans mainly through inhalation of aerosolized rodent excreta or rodent bites.

Genome

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 Gn (formerly G1) and Gc (formerly G2).[5][6] 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.

As with other Bunyaviridae, each of the three segments has a consensus 39-terminal nucleotide sequence (AUCAUCAUC), which is complementary to the 59 terminal sequence and is distinct from those of the other four genera in the family. These sequences may form panhandle structures which seem likely to play a role in replication. The large segment is 6530-6550 nucleotides (nt) in length, the medium is 3613-3707 nt in length and the small is 1696-2083 nt in length. No nonstructural proteins are known unlike the other genera in this family. At the 5' and 3' of each segment are short noncoding sequences: the noncoding segment in all sequences at the 5' end is 37-51 nt. The 3' noncoding regions differ: L segment 38-43 nt; M segment 168-229 nt; and S segment 370-730 nt. The 3'end of the S segment is conserved between the genera suggesting a functional role.

Virions

Hantavirus virions are about 100 nanometres (nm) in diameter. The lipid bilayer of the viral envelope is about five nm thick and is embedded with viral surface proteins to which sugar residues are attached. These glycoproteins, known as G1 and G2, are encoded by the M segment of the viral genome. They tend to associate (heterodimerize) with each other and have both an interior tail and an exterior domain that extends to about six nm beyond the envelope surface. Inside the envelope are the nucleocapsids. These are composed of many copies of the nucleocapsid protein N, which interact with the three segments of the viral genome to form helical structures. The virally encoded RNA polymerase is also found in the interior. By mass, the virion is greater than 50% protein, 20-30% lipid and 2-7% carbohydrate. The density of the virions is 1.18 gram per cubic centimeter. These features are common to all members of the Bunyaviridae.

Life cycle

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. Subsequent to release of the nucleocapsids into cytoplasm, the complexes are targeted to the ER-Golgi Intermediate compartments (ERGIC) through microtubular associated movement resulting in the formation of viral factories at ERGIC. These factories then facilitate transcription and subsequent translation of the viral proteins. 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 cotton rat Sigmodon hispidus is a hantavirus carrier that becomes a threat when it enters human habitation in rural and suburban areas.

Pathogenesis

The pathogenesis of Hantavirus infections is unclear as there is a lack of animal models to describe it (rats and mice do not seem to acquire severe disease). While the primary site of viral replication in the body is not known, in HFRS the main effect is in the blood vessels while in HPS most symptoms are associated with the lungs. In HFRS, there are increased vascular permeability and decreased blood pressure due to endothelial dysfunction and the most dramatic damage is seen in the kidneys, whereas in HPS, the lungs, spleen, and gall bladder are most affected. Early symptoms of HPS tend to present similarly to the flu (muscle aches, fever and fatigue) and usually show up around 2 to 3 weeks after exposure. Later stages of the disease (about 4 to 10 days after symptoms start) will include difficulty breathing, shortness of breath and coughing.[7]

Prevalence

Regions especially affected by HFRS include China, the Korean Peninsula, Russia (Hantaan, Puumala and Seoul viruses), and northern and western Europe (Puumala and Dobrava virus). Regions with the highest incidences of HCPS include Patagonian Argentina, Chile, Brazil, the United States, Canada, and Panama, where a milder form of disease that spares the heart has been recognized. The two agents of HCPS in South America are Andes virus (also called Oran, Castelo de Sonhos, Lechiguanas, Juquitiba, Araraquara, and Bermejo viruses, among many other synonyms), which is the only hantavirus that has shown (albeit uncommonly) an interpersonal form of transmission, and Laguna Negra virus, an extremely close relative of the previously-known Rio Mamore virus. In the U.S., minor cases of HCPS include New York virus, Bayou virus, and possibly Black Creek Canal virus.

In the United States, as of July 2010 eight states had reported 30 or more cases of Hantavirus since 1993[8] - New Mexico (84), Colorado (70), Arizona (62), California (42), Washington (41), Texas (37), Utah (31) and Montana (30). Other states reporting a significant number of cases include Idaho (16), Kansas (15), South Dakota (15), and North Dakota (12). With only 11 cases, Oregon has a notably lower attack rate overall and relative to population, compared to other Western states.

In August of 2012, four new cases of Hantavirus were confirmed in the Curry Village area of Yosemite National Park.[9]

Symptoms

Hemorrhagic fever with renal syndrome

Hantavirus has an incubation time of two to four weeks in humans before symptoms of infection occur. The symptoms of HFRS can be split into five phases:

  • Febrile phase: Symptoms include fever, chills, sweaty palms, diarrhea, malaise, headaches, nausea, abdominal and back pain, respiratory problems such as the ones common in the influenza virus, as well as gastro-intestinal problems. These symptoms normally occur for three to seven days and arise about two to three weeks after exposure.[7]
  • Hypotensive phase: This occurs when the blood platelet levels drop and symptoms can lead to tachycardia and hypoxemia. This phase can last for 2 days.
  • Oliguric phase: This phase lasts for three to seven days and is characterised by the onset of renal failure and proteinuria occurs.
  • Diuretic phase: This is characterized by diuresis of three to six litres per day, which can last for a couple of days up to weeks.
  • Convalescent phase: This is normally when recovery occurs and symptoms begin to improve.

Formerly known as Korean hemorrhagic fever, HFRS is the term accepted by the World Health Organization.

Hantavirus (cardio-)pulmonary syndrome

Hantavirus pulmonary syndrome (HPS) is an often fatal disease caused by hantavirus infection. The symptoms are very similar to those of HFRS and include tachycardia and tachypnea. Additionally, patients will develop difficulty breathing, coughing and shortness of breath.[7] Such conditions can lead to a cardiopulmonary phase, where cardiovascular shock can occur, and hospitalization of the patient is required. HPS was first recognized in 1993 in the southwest of the United States by Bruce Tempest MD, and was originally called "Four Corners disease". It has since been identified throughout the United States. Although rare, HPS is fatal in up to 60% of cases.[3] Rodent control in and around the home remains the primary strategy for preventing hantavirus infection. People suspecting illness are encouraged to contact their local health department.

Weaponization

Korean hemorrhagic fever (Hantavirus) was one of three hemorrhagic fevers and one of more than a dozen agents that the United States researched as potential biological weapons before suspending its biological weapons program.[10]

Prevention and treatment

There is no known antiviral treatment, but natural recovery from the virus is possible. Patients with suspected hantavirus are usually admitted to hospital and given oxygen to help them breathe.[7] As the virus can be transmitted by rodent saliva, excretia, and bites, control of rats and mice in areas frequented by humans is key for disease prevention. General prevention can be accomplished by disposing of rodent nests, sealing any cracks and holes in homes where mice or rats could get in, laying down poisons or using natural predators such as cats in the home.[7]

Leptospirosis causes similar symptoms and is also carried by rodent vectors, but it is due to a bacterial spirochete (instead of a virus). Presumptive treatment of leptospirosis with penicillin (and other) antibiotics is often started for severe symptoms when a diagnostic dilemma between the two diseases is encountered.

Evolution

Findings of significant congruence between phylogenies of hantaviruses and phylogenies of their rodent reservoirs have led to the theory – well-accepted until recently – of long-standing hantavirus–rodent host coevolution.[5][11] However, recent findings have led to scientific debate and new hypotheses regarding hantavirus evolution.[6][12]

Various hantaviruses have been found to infect multiple rodent species, and cases of cross-species transmission (host switching) have been recorded.[13][14][15] Additionally, rates of substitution based on nucleotide sequence data reveal that hantavirus clades and rodent subfamilies may not have diverged at the same time.[12][16] Furthermore, hantaviruses have been found in multiple species of shrews and moles.[12][17][18][19]

Taking into account the inconsistencies in the theory of coevolution, Ramsden et al. (2009) have proposed that the patterns seen in hantaviruses in relation to their reservoirs could be attributed to preferential host switching directed by geographical proximity and adaptation to specific host types.[12] Ulrich et al. (2010) have proposed that the observed geographical clustering of hantavirus sequences may have been caused by an isolation-by-distance mechanism.[15] Upon comparison of the hantaviruses found in hosts of orders Rodentia and Soricomorpha, Yanagihara et al. (2011) have proposed that the evolutionary history of the hantavirus consists of a complex mix of both host switching and codivergence and suggest that ancestral shrews or moles rather than rodents may have been the early original hosts of ancient hantaviruses.[17]

See also

References

  1. ^ Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 16485469, please use {{cite journal}} with |pmid=16485469 instead.
  2. ^ Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 24670, please use {{cite journal}} with |pmid=24670 instead.
  3. ^ a b Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 20375360, please use {{cite journal}} with |pmid=20375360 instead.
  4. ^ Schudel, Matt (2007-12-24). "Terry Yates, 57; biologist found source of hantavirus". Washington Post. Boston Globe. Retrieved 2007-01-04.
  5. ^ a b c Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1099/0022-1317-77-11-2677, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1099/0022-1317-77-11-2677 instead.
  6. ^ a b Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1128/CMR.00062-09, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1128/CMR.00062-09 instead.
  7. ^ a b c d e "Hantavirus: Canadian Lung Association". Canadian Lung Association. 18 August 2009. Retrieved 17 March 2011.
  8. ^ "Hantavirus Pulmonary Syndrome (HPS) Cases, by State", CDC Website, July 9, 2010, accessed November 9, 2010.
  9. ^ KFSN-30 (27 August 2012). "Third case of Hantavirus confirmed in Yosemite". Retrieved 28 August 2012.{{cite news}}: CS1 maint: numeric names: authors list (link)
  10. ^ "Chemical and Biological Weapons: Possession and Programs Past and Present", James Martin Center for Nonproliferation Studies, Middlebury College, April 9, 2002, accessed November 14, 2008.
  11. ^ Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1093/molbev/msg232, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1093/molbev/msg232 instead.
  12. ^ a b c d Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1093/molbev/msn234, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1093/molbev/msn234 instead.
  13. ^ Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.3201/eid1409.080455, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.3201/eid1409.080455 instead.
  14. ^ Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1099/Vir.0.006155-0, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1099/Vir.0.006155-0 instead.
  15. ^ a b Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1128/Jvi.01226-09, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1128/Jvi.01226-09 instead.
  16. ^ Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1093/molbev/msn093, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1093/molbev/msn093 instead.
  17. ^ a b Attention: This template ({{cite doi}}) is deprecated. To cite the publication identified by doi:10.1128/Jvi.02450-10, please use {{cite journal}} (if it was published in a bona fide academic journal, otherwise {{cite report}} with |doi=10.1128/Jvi.02450-10 instead.
  18. ^ Template:Cite PMID
  19. ^ Template:Cite PMID
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