| Hantavirus |
| Classification and external resources |
| ICD-10 |
B33.4 |
| ICD-9 |
079.81 |
| MedlinePlus |
001382 |
| MeSH |
D018778 |
| 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 urine, saliva or contact with rodent waste products. Some hantaviruses cause potentially fatal diseases in humans, such as hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS), but others have not been associated with human disease.[1]
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]
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Contents
- 1 History
- 2 Symptoms
- 2.1 Hemorrhagic fever with renal syndrome
- 2.2 Hantavirus (cardio-)pulmonary syndrome
- 3 Epidemiology
- 3.1 South America
- 3.2 North America
- 3.3 Europe
- 3.4 Africa
- 4 Prevention and treatment
- 5 Virology
- 5.1 Classification
- 5.2 Genome
- 5.3 Virions
- 5.4 Life cycle
- 5.5 Pathogenesis
- 6 Weaponization
- 7 Evolution
- 8 Vaccine Research
- 9 See also
- 10 References
- 11 External links
|
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.
In late Medieval England a mysterious sweating sickness swept through the country in 1485 just before the Battle of Bosworth Field. Noting the similar symptoms which overlap with Hantavirus pulmonary syndrome (HPS, see below), several scientists have theorised that the virus may have been the cause of the disease.[4][5] The hypothesis was criticised because sweating sickness was recorded as being transmitted human-to-human whereas hantaviruses were not known to spread in this way.[6] However, infection via human-to-human contact has since been proven in Hantavirus outbreaks in Argentina. [7]
In 1993, an outbreak of Hantavirus pulmonary syndrome 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, the Deer mouse (Peromyscus maniculatus), was first identified by Terry Yates, a professor at the University of New Mexico.[8]
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.
Symptoms
Hemorrhagic fever with renal syndrome
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This section does not cite any references or sources. (October 2012) |
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.
- 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.[9]
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.
Epidemiology
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.
South America
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.
Rodents that have been shown to carry hantaviruses include Abrothrix longipilis and Oligoryzomys longicaudatus.[10]
North America
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[11] – 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), North Dakota (12) and Oregon (11).
In late August and early September of 2012, eight new cases of Hantavirus were confirmed, including three deaths, in the Curry Village area of Yosemite National Park.[12]
In addition to infecting rodents hantaviruses are known to be carried by shrews (order Soricomorpha, family Soricidae) and moles (family Talpidae).[13]
In Mexico a number of rodents have been found to carry hantaviruses: Megadontomys thomasi, Neotoma picta, Peromyscus beatae, Reithrodontomys megalotis and Reithrodontomys sumichrasti.[14]
Europe
In Europe three hantaviruses - Puumala, Dobrava and Saaremaa viruses - are known to cause haemorrhagic fever with renal syndrome.[15] Puumala usually causes a generally mild disease - nephropathia epidemica - which typically presents with fever, headache, gastrointestinal symptoms, impaired renal function and blurred vision. Dobrava infections while similar often also have haemorrhagic complications. There are few reports of confirmed Saaremaa infections but these appear to be similar to those caused by Puumala and less pathogenic than Dobrava.
Puumala is carried by its rodent host, the bank vole (Clethrionomys glareolus) and is present throught most of Europe excluding the Mediterranean region. Dobrava and Saaremaa carried respectively by the yellow necked mouse (Apodemus flavicollis) and the striped field mouse (Apodemus agrarius) are reported mainly in eastern and central Europe.
Africa
A hantavirus (Sangassou virus) has been isolated in Africa.[16]
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.[9] 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, setting up traps, laying down poisons or using natural predators such as cats in the home.[9]
Leptospirosis causes similar symptoms and is also carried by rodent vectors, but it is due to a bacterial spirochete rather than 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.
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,[17] 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).[17][18]
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.[9]
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 discontinuing its biological weapons program in 1969.[19]
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.[17][20] However, recent findings have led to scientific debate and new hypotheses regarding hantavirus evolution.[18][21]
Various hantaviruses have been found to infect multiple rodent species, and cases of cross-species transmission (host switching) have been recorded.[22][23][24] Additionally, rates of substitution based on nucleotide sequence data reveal that hantavirus clades and rodent subfamilies may not have diverged at the same time.[21][25] Furthermore, hantaviruses have been found in multiple species of shrews and moles.[21][26][27][28]
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.[21] Ulrich et al. (2010) have proposed that the observed geographical clustering of hantavirus sequences may have been caused by an isolation-by-distance mechanism.[24] 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.[26]
Vaccine Research
The Korean Army is one of the largest consumers of the hantavirus vaccine, second only to public health centers. There are more than 20 recognized hantaviruses, some of which are associated with one of two serious human diseases: hemorrhagic fever with renal syndrome (HFRS) or hantavirus pulmonary syndrome (HPS). Efforts are continuing to develop safe and effective hantavirus vaccines. Several classical and molecular vaccine approaches are in pre-clinical stages of development. The development of hantavirus vaccines is hampered by the lack of adequate animal models of hantavirus-associated disease. No specific antiviral therapy is yet available. No hantavirus vaccine has been approved for use in the US, and no WHO-approved vaccine has gained widespread acceptance.
See also
- Sweating sickness, which may have been caused by a hantavirus
- List of cutaneous conditions
References
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This article needs additional citations for verification. Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and removed. (January 2008) |
- ^ a b Martinez, V. P.; Bellomo, C.; San Juan, J.; Pinna, D.; Forlenza, R.; Elder, M.; Padula, P. J. (2005). "Person-to-person transmission of Andes virus". Emerging Infectious Diseases 11 (12): 1848–1853. PMID 16485469. edit
- ^ Lee, HW; Lee, PW; Johnson, KM (1978). "Isolation of the etiologic agent of Korean Hemorrhagic fever". The Journal of infectious diseases 137 (3): 298–308. PMID 24670. edit
- ^ a b Jonsson, C. B.; Figueiredo, L. T. M.; Vapalahti, O. (2010). "A Global Perspective on Hantavirus Ecology, Epidemiology, and Disease". Clinical Microbiology Reviews 23 (2): 412–441. doi:10.1128/CMR.00062-09. PMC 2863364. PMID 20375360. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2863364/. edit
- ^ Thwaites, Guy; Taviner, Mark; Gant, Vanya (1997). "The English Sweating Sickness, 1485 to 1551". New England Journal of Medicine 336 (8): 580–582. doi:10.1056/NEJM199702203360812. PMID 9023099. edit
- ^ M. Taviner, G. Thwaites, and V. Gant (1998). "The English sweating sickness, 1485-1551: a viral pulmonary disease?". Medical History (Department of Modern History. St Andrews University, London) 42 (1): 96–98. PMC 1043971. PMID 9536626. //www.ncbi.nlm.nih.gov/pmc/articles/PMC1043971/.
- ^ Bridson, Eric (2001). "English 'sweate' (Sudor Anglicus) and Hantavirus pulmonary syndrome, The". British Journal of Biomedical Science. http://www.findarticles.com/p/articles/mi_qa3874/is_200101/ai_n8939673.
- ^ Padula, P; Edelstein A, Miguel SD, López NM, Rossi CM, Rabinovich RD. (February 15, 1998). "Hantavirus pulmonary syndrome outbreak in Argentina: molecular evidence for person-to-person transmission of Andes virus" (in English). Virology (London: Elsevier) 241 (2): 323–330. doi:10.1006/viro.1997.8976. PMID 9499807.
- ^ Schudel, Matt (2007-12-24). "Terry Yates, 57; biologist found source of hantavirus". Washington Post (Boston Globe). http://www.boston.com/bostonglobe/obituaries/articles/2007/12/24/terry_yates_57_biologist_found_source_of_hantavirus/. Retrieved 2007-01-04.
- ^ a b c d "Hantavirus: Canadian Lung Association". Canadian Lung Association. 18 August 2009. http://www.lung.ca/diseases-maladies/a-z/hantavirus-hantavirus/index_e.php. Retrieved 17 March 2011.
- ^ Medina RA, Torres-Perez F, Galeno H, Navarrete M, Vial PA, Palma RE, Ferres M, Cook JA, Hjelle B (2009) Ecology, genetic diversity, and phylogeographic structure of andes virus in humans and rodents in Chile. J Virol 83(6):2446-2459
- ^ "Hantavirus Pulmonary Syndrome (HPS) Cases, by State", CDC Website, July 9, 2010, accessed November 9, 2010.
- ^ "Yosemite extends hantavirus warning; death toll rises". 7 September 2012. http://news.yahoo.com/yosemite-extends-hantavirus-warning-death-toll-rises-020953730.html. Retrieved 7 September 2012.
- ^ Kang HJ, Bennett SN, Hope AG, Cook JA, Yanagihara R (2011) Shared ancestry between a newfound mole-borne hantavirus and hantaviruses harbored by cricetid rodents. J Virol 85 (15) 7496-7503 10.1128/JVI.02450-10
- ^ Kariwa H, Yoshida H, Sánchez-Hernández C, Romero-Almaraz Mde L, Almazán-Catalán JA, Ramos C, Miyashita D, Seto T, Takano A, Totani M, Murata R, Saasa N, Ishizuka M, Sanada T, Yoshii K, Yoshimatsu K, Arikawa J, Takashima I (2012) Genetic diversity of hantaviruses in Mexico: identification of three novel hantaviruses from Neotominae rodents. Virus Res 163(2):486-494
- ^ Vapalahti O, Mustonen J, Lundkvist A, Henttonen H, Plyusnin A, Vaheri A (2003) Hantavirus infections in Europe. Lancet Infect Dis 3(10):653-661
- ^ Klempa B, Witkowski PT, Popugaeva E, Auste B, Koivogui L, Fichet-Calvet E, Strecker T, Ter Meulen J, Krüger DH (2012) Sangassou virus, the first hantavirus isolate from Africa, displays genetic and functional properties distinct from those of other murinae-associated hantaviruses. J Virol 86(7):3819-3827
- ^ a b c Plyusnin, A.; Vapalahti, O.; Vaheri, A. (1996). "Hantaviruses: Genome structure, expression and evolution". Journal of General Virology 77 (11): 2677. doi:10.1099/0022-1317-77-11-2677. edit
- ^ a b Jonsson, C. B.; Figueiredo, L. T. M.; Vapalahti, O. (2010). "A Global Perspective on Hantavirus Ecology, Epidemiology, and Disease". Clinical Microbiology Reviews 23 (2): 412–441. doi:10.1128/CMR.00062-09. PMC 2863364. PMID 20375360. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2863364/. edit
- ^ "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.
- ^ Jackson, A. P.; Charleston, M. A. (2003). "A Cophylogenetic Perspective of RNA-Virus Evolution". Molecular Biology and Evolution 21 (1): 45–57. doi:10.1093/molbev/msg232. PMID 12949128. edit
- ^ a b c d Ramsden, C.; Holmes, E. C.; Charleston, M. A. (2008). "Hantavirus Evolution in Relation to Its Rodent and Insectivore Hosts: No Evidence for Codivergence". Molecular Biology and Evolution 26 (1): 143–153. doi:10.1093/molbev/msn234. PMID 18922760. edit
- ^ Delfraro, A.; Tomé, L.; d'Elía, G.; Clara, M.; Achával, F.; Russi, J. C.; Rodonz, J. R. (2008). "Juquitiba-like Hantavirus from 2 Nonrelated Rodent Species, Uruguay". Emerging Infectious Diseases 14 (9): 1447–1451. doi:10.3201/eid1409.080455. PMC 2603116. PMID 18760017. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2603116/. edit
- ^ Plyusnina, A.; Ibrahim, I. -N.; Plyusnin, A. (2009). "A newly recognized hantavirus in the Asian house rat (Rattus tanezumi) in Indonesia". Journal of General Virology 90 (Pt 1): 205–209. doi:10.1099/Vir.0.006155-0. PMID 19088290. edit
- ^ a b Schmidt-Chanasit, J.; Essbauer, S.; Petraityte, R.; Yoshimatsu, K.; Tackmann, K.; Conraths, F. J.; Sasnauskas, K.; Arikawa, J. et al. (2009). "Extensive Host Sharing of Central European Tula Virus". Journal of Virology 84 (1): 459–474. doi:10.1128/Jvi.01226-09. PMC 2798396. PMID 19889769. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2798396/. edit
- ^ Ramsden, C.; Melo, F. L.; Figueiredo, L. M.; Holmes, E. C.; Zanotto, P. M. A.; Vgdn, C. (2008). "High Rates of Molecular Evolution in Hantaviruses". Molecular Biology and Evolution 25 (7): 1488–1492. doi:10.1093/molbev/msn093. PMID 18417484. edit
- ^ a b Kang, H. J.; Bennett, S. N.; Hope, A. G.; Cook, J. A.; Yanagihara, R. (2011). "Shared Ancestry between a Newfound Mole-Borne Hantavirus and Hantaviruses Harbored by Cricetid Rodents". Journal of Virology 85 (15): 7496–7503. doi:10.1128/Jvi.02450-10. PMC 3147906. PMID 21632770. //www.ncbi.nlm.nih.gov/pmc/articles/PMC3147906/. edit
- ^ Song, J. W.; Baek, L. J.; Schmaljohn, C. S.; Yanagihara, R. (2007). "Thottapalayam Virus, a Prototype Shrewborne Hantavirus". Emerging Infectious Diseases 13 (7): 980–985. PMC 2254531. PMID 18214168. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2254531/. edit
- ^ Song, J. W.; Kang, H. J.; Song, K. J.; Truong, T. T.; Bennett, S. N.; Arai, S.; Truong, N. U.; Yanagihara, R. (2007). "Newfound Hantavirus in Chinese Mole Shrew, Vietnam". Emerging Infectious Diseases 13 (11): 1784–1787. PMC 2262106. PMID 18217572. //www.ncbi.nlm.nih.gov/pmc/articles/PMC2262106/. edit
External links
- Sloan Science and Film / Short Films / Muerto Canyon by Jen Peel 29 minutes
- "Hantaviruses, with emphasis on Four Corners Hantavirus" by Brian Hjelle, M.D., Department of Pathology, School of Medicine, University of New Mexico
- CDC's Hantavirus Technical Information Index page
- Viralzone: Hantavirus
- Virus Pathogen Database and Analysis Resource (ViPR): Bunyaviridae
- Occurrences and deaths in North and South America
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Zoonotic viral diseases (A80–B34, 042–079)
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|
| Arthropod-borne |
| Mosquito-borne |
| Bunyaviridae |
- Arbovirus encephalitides: La Crosse encephalitis
- California encephalitis
- Viral hemorrhagic fevers: Rift Valley fever
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|
| Flaviviridae |
- Arbovirus encephalitides: Japanese encephalitis
- Australian encephalitis
- Saint Louis encephalitis
- West Nile fever
- Viral hemorrhagic fevers: Dengue fever
- Yellow fever
- ZIKV
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|
| Togaviridae |
- Arbovirus encephalitides: Eastern equine encephalomyelitis
- Western equine encephalomyelitis
- Venezuelan equine encephalomyelitis
- Chikungunya
- O'Nyong-nyong fever
- Ross River fever
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|
|
| Tick-borne |
| Bunyaviridae |
- Viral hemorrhagic fevers: Crimean-Congo hemorrhagic fever
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| Flaviviridae |
- Arbovirus encephalitides: Tick-borne encephalitis
- Powassan encephalitis
- Viral hemorrhagic fevers: Omsk hemorrhagic fever
- Kyasanur forest disease
- Langat virus (LGTV)
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| Reoviridae |
|
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| Mammal-borne |
| Rodent-borne |
| Arenaviridae |
- Viral hemorrhagic fevers: Lassa fever
- Venezuelan hemorrhagic fever
- Argentine hemorrhagic fever
- Brazilian hemorrhagic fever
- Bolivian hemorrhagic fever
- LUJV
- CHPV
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|
| Bunyaviridae |
- Hemorrhagic fever with renal syndrome
- Hantavirus pulmonary syndrome
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| Bat-borne |
| Filoviridae |
- Viral hemorrhagic fevers: Ebola virus disease
- Marburg virus disease
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| Rhabdoviridae |
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| Paramyxoviridae |
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| Multiple vectors |
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cutn/syst (hppv/hiva, infl/zost/zoon)/epon
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drug(dnaa, rnaa, rtva, vacc)
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