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a harmful or corrupting agency; "bigotry is a virus that must not be allowed to spread"; "the virus of jealousy is latent in everyone"
(virology) ultramicroscopic infectious agent that replicates itself only within cells of living hosts; many are pathogenic; a piece of nucleic acid (DNA or RNA) wrapped in a thin coat of protein
a software program capable of reproducing itself and usually capable of causing great harm to files or other programs on the same computer; "a true virus cannot spread to another computer without human assistance" (同)computer virus

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/02/15 19:29:33」(JST)

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Hantaviruses are single-stranded, enveloped, negative sense RNA viruses in the Bunyaviridae family. Humans may become infected with hantaviruses through contact with rodent urine, saliva, or feces. Some strains of hantaviruses cause potentially fatal diseases in humans, such as Hantavirus hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS), while others have not been associated with known 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, for which Hantaan virus is named. It was isolated in the late 1970s by Karl M. Johnson and Ho-Wang Lee.^[2]^[3]^[4]^[5]

1 History
2 Two major clinical syndromes
- 2.1 Hemorrhagic fever with renal syndrome
- 2.2 Hantavirus pulmonary syndrome
3 Epidemiology
- 3.1 Asia
- 3.2 South America
- 3.3 North America
- 3.4 Europe
- 3.5 Africa
4 Prevention and treatment
5 Virology
- 5.1 Classification
- 5.2 Genome
- 5.3 Virions
- 5.4 Life cycle
- 5.5 Pathogenesis
6 Transmission
7 Evolution
8 Vaccine Research
9 See also
10 References
11 External links

History[edit]

The hantaviruses are a relatively newly discovered genus of viruses. An outbreak of Korean Hemorrhagic Fever among American and Korean soldiers during the Korean War (1951–1953) was later found to be caused by a hantavirus infection. More than 3000 troops became ill with symptoms that included renal failure, generalized hemorrhage, and shock. It had a 10% mortality rate. This outbreak sparked a 25-year search for the etiologic agent. Ho-Wang Lee, a South Korean virologist, Karl M. Johnson, an American tropical virologist, and his colleagues isolated Hantaan virus in 1976 from the lungs of striped field mice.^[6]^[7]

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.^[8]^[9] 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.^[10] Limited transmission via human-to-human contact has since been shown in Hantavirus outbreaks in Argentina.^[11]

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.^[12]

Two major clinical syndromes[edit]

Hemorrhagic fever with renal syndrome[edit]

Main article: Hantavirus hemorrhagic fever with renal syndrome (HFRS)

Hemorrhagic fever with renal syndrome (HFRS) is a group of clinically similar illnesses caused by species of hantaviruses from the family Bunyaviridae. It is also known as Korean hemorrhagic fever, epidemic hemorrhagic fever, and nephropathis epidemica. The species that cause HFRS include Hantaan River, Dobrava-Belgrade, Saaremaa, Seoul, and Puumala. It is found in Europe, Asia, and Africa.

In hantavirus induced hemorrhagic fever, incubation time is between two to four weeks in humans before symptoms of infection present. Severity of symptoms depends on the viral load.^[13]

Hantavirus pulmonary syndrome[edit]

Main article: Hantavirus pulmonary syndrome

Hantavirus pulmonary syndrome (HPS) is found in North, Central and South America.^[14] It is an often fatal pulmonary disease. In the United States, the causative agent is Sin Nombre virus carried by deer mice. Prodromal symptoms include flu-like symptoms such as fever, cough, myalgia, headache, and lethargy. It is characterized by a sudden onset of shortness of breath with rapidly evolving pulmonary edema that is often fatal despite mechanical ventilation and intervention with potent diuretics. It has a fatality rate of 38%.^[15]

Hantavirus pulmonary syndrome was first recognized during the 1993 outbreak in the Four Corners region of the southwestern United States. It was identified by Dr. Bruce Tempest. It was originally called "Four Corners disease," but the name was changed to Sin Nombre virus after complaints by Native Americans that the name 'Four Corners' stigmatized the region.^[16] It has since been identified throughout the United States. Rodent control in and around the home remains the primary prevention strategy.

Epidemiology[edit]

Regions especially affected by hemorrhagic fever with renal syndrome 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 hantavirus pulmonary syndrome include Patagonia Argentina, Chile, Brazil, the United States, Canada, and Panama.

Asia[edit]

In China, the Korean Peninsula, and Russia, hemorrhagic fever with renal syndrome is caused by Hantaan, Puumala and Seoul viruses. Korean Hemorrhagic Fever was first documented during the Korean War when American troops became ill.

South America[edit]

The two agents of HPS 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.^[17]

North America[edit]

In the U.S., minor cases of HPS include Sin Nombre virus, 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^[18] – 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.^[19] In Long Island there is another confirmed death, David Hartstein, MD. He died in June 2011, after contracting hantavirus. His story is featured in the HBO documentary Hard Times, Lost on Long Island.http://www.newsday.com/entertainment/tv/hard-times-lost-on-long-island-review-1.3824405

In addition to infecting rodents hantaviruses are known to be carried by shrews (order Soricomorpha, family Soricidae) and moles (family Talpidae).^[20]

In Mexico a number of rodents have been found to carry hantaviruses: Megadontomys thomasi, Neotoma picta, Peromyscus beatae, Reithrodontomys megalotis and Reithrodontomys sumichrasti.^[21]

In Canada, there was one confirmed death in Northern British Columbia in January, 2013 and at least one confirmed death in Kindersley, Saskatchewan, in June 2013.^[22] Another death in the Kindersley area (June 2013) may also be linked to Hantavirus. One confirmed case (July 2013) in Burr, Saskatchewan (near Kindersley); the patient was gravely ill but survived.

Europe[edit]

In Europe three hantaviruses - Puumala, Dobrava and Saaremaa viruses - are known to cause haemorrhagic fever with renal syndrome.^[23] 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 through 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[edit]

A novel hantavirus, Sangassou virus has been isolated in Africa that causes hemorrhagic fever with renal syndrome.^[24]

Prevention and treatment[edit]

There is no known antiviral treatment, but natural recovery from the virus is possible with supportive treatment. Patients with suspected hantavirus are usually admitted to the hospital and given oxygen and mechanical ventilation support to help them breathe during the acute pulmonary stage.^[25] 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.^[25]

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[edit]

Classification[edit]

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,^[26] but hantaviruses are thought to be transmitted to humans mainly through inhalation of aerosolized rodent excreta or rodent bites.

Genome[edit]

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).^[26]^[27]

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 3'-terminal nucleotide sequence (AUCAUCAUC), which is complementary to the 5' terminal sequence and is distinct from those of the other four genera in the family.^[28] These sequences appear to form panhandle structures which seem likely to play a role in replication and encapsidation facilitated by binding with the viral nucleocapsid (N) protein.^[29] 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[edit]

Hantavirus virions are about 120-160 nanometers (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 Gn and Gc, 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[edit]

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[edit]

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.^[25]

Transmission[edit]

The species that cause hantavirus hemorrhagic fever have not been shown to transfer from person to person. Transmission by aerosolized rodent excreta still remains the only known way the virus is transmitted to humans. Similar negative-stranded RNA viruses, such as Marburg and Ebola hemorrhagic fevers, can be transmitted by contact with infected blood and body fluids, and are known to spread to patient-care workers in African hospitals. But those viruses do not transfer readily in the modern hospital setting with universal precautions. Fomite transfer has not been shown in the hantaviruses in either the hemorrhagic or pulmonary forms.^[30]^[31]

Evolution[edit]

Findings of significant congruence between phylogenies of hantaviruses and phylogenies of their rodent reservoirs have led to the theory that rodents, although infected by the virus are not harmed by it because of long-standing hantavirus-rodent host coevolution.^[26]^[32] However, recent findings have led to scientific debate and new hypotheses regarding hantavirus evolution.^[27]^[33]

Various hantaviruses have been found to infect multiple rodent species, and cases of cross-species transmission (host switching) have been recorded.^[34]^[35]^[36] Additionally, rates of substitution based on nucleotide sequence data reveal that hantavirus clades and rodent subfamilies may not have diverged at the same time.^[33]^[37] Furthermore, hantaviruses have been found in multiple species of shrews and moles.^[33]^[38]^[39]^[40]

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.^[33] Ulrich et al. (2010) have proposed that the observed geographical clustering of hantavirus sequences may have been caused by an isolation-by-distance mechanism.^[36] 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.^[38]

A Bayesian analysis suggests a common origin for these viruses ~2000 years ago.^[41] The association with particular rodent families appears to have been more recent. The viruses carried by the Arvicolinae and Murinae subfamilies originated in Asia 500–700 years ago. These subsequently spread to Africa, Europe, North America and Siberia possibly carried by their hosts. The species infecting the Neotominae subfamily evolved 500–600 years ago in Central America. These species then spread toward North America. The species infecting Sigmodontinae evolved in Brazil 400 years ago. Their ancestors may have been a Neotominae associated virus from northern South America.

Vaccine Research[edit]

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.^[42]

References[edit]

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^ Johnson KM (2001). "Hantaviruses: history and overview". Current topics in microbiology and immunology (256): 1–14. PMID 11217399.
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^ Kariwa, H.; Yoshida, H.; Sánchez-Hernández, C.; Romero-Almaraz Mde, M. A. D. L.; Almazán-Catalán, J. A.; 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 Research 163 (2): 486–494. doi:10.1016/j.virusres.2011.11.013. PMID 22138671.
^ http://www.newstalk650.com/story/death-caused-hantavirus-west-central-saskatchewan/117291
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^ ^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.
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External links[edit]

Wikimedia Commons has media related to Hantaviruses.

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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1. ハンタウイルス感染の疫学および診断 epidemiology and diagnosis of hantavirus infections
2. ハンタウイルス心肺症候群 hantavirus cardiopulmonary syndrome
3. ハンタウイルス感染による腎疾患（腎症候性出血熱） renal involvement with hantavirus infection hemorrhagic fever with renal syndrome
4. ハンタウイルス感染の病因 pathogenesis of hantavirus infections
5. 東アジアへの旅行によって感染する可能性のある疾患 diseases potentially acquired by travel to east asia

English Journal

Hemorrhagic Fever with Renal Syndrome, Zibo City, China, 2006-2014.

Wang L, Wang T, Cui F, Zhai SY, Zhang L, Yang SX, Wang ZQ, Yu XJ.
Emerging infectious diseases.Emerg Infect Dis.2016 Feb;22(2):274-6. doi: 10.3201eid/2202.151516.
Analysis of hemorrhagic fever with renal syndrome cases in Zibo City, China, during 2006-2014 showed that it occurred year-round. Peaks in spring and fall/winter were caused by Hantaan and Seoul viruses, respectively. Rodent hosts were the striped field mouse for Hantaan virus and the brown rat and
PMID 26812444

Development of a TaqMan Array Card for Acute-Febrile-Illness Outbreak Investigation and Surveillance of Emerging Pathogens, Including Ebola Virus.

Liu J1, Ochieng C2, Wiersma S3, Ströher U4, Towner JS4, Whitmer S4, Nichol ST4, Moore CC1, Kersh GJ5, Kato C5, Sexton C5, Petersen J5, Massung R4, Hercik C6, Crump JA7, Kibiki G8, Maro A8, Mujaga B8, Gratz J8, Jacob ST9, Banura P10, Scheld WM1, Juma B11, Onyango CO11, Montgomery JM12, Houpt E13, Fields B14.
Journal of clinical microbiology.J Clin Microbiol.2016 Jan;54(1):49-58. doi: 10.1128/JCM.02257-15. Epub 2015 Oct 21.
Acute febrile illness (AFI) is associated with substantial morbidity and mortality worldwide, yet an etiologic agent is often not identified. Convalescent-phase serology is impractical, blood culture is slow, and many pathogens are fastidious or impossible to cultivate. We developed a real-time PCR-
PMID 26491176

CD8low CD100- T Cells Identify a Novel CD8 T Cell Subset Associated with Viral Control during Human Hantaan Virus Infection.

Liu B1, Ma Y1, Zhang Y1, Zhang C1, Yi J2, Zhuang R1, Yu H3, Yang A1, Zhang Y4, Jin B4.
Journal of virology.J Virol.2015 Dec 1;89(23):11834-44. doi: 10.1128/JVI.01610-15. Epub 2015 Sep 16.
Hantaan virus (HTNV) infection can cause a severe lethal hemorrhagic fever with renal syndrome (HFRS) in humans. CD8(+) T cells play a critical role in combating HTNV infections. However, the contributions of different CD8(+) T cell subsets to the immune response against viral infection are poorly u
PMID 26378166

Japanese Journal

Role of nucleocapsid protein of hantaviruses in intracellular traffic of viral glycoproteins

Shimizu Kenta,Yoshimatsu Kumiko,Koma Takaaki,Yasuda Shumpei P.,Arikawa Jiro
Virus
… Double staining of viral and host proteins in Hantaan virus (HTNV)-infected Vero E6 cells showed that Gn and Gc were localized to cis-Golgi, in which virus particles are thought to be formed. … Co-expression of HTNV GPC with NPs of other hantaviruses, such as Seoul virus, Puumala virus and Sin Nombre virus, also reduced the ratios of diffused Gc-positive cells to 13.5%, 25.2%, and 11.6%, respectively. …
NAID 120005372351

Epidemiology of Hantavirus Infection in Thousand Islands Regency of Jakarta, Indonesia

IBRAHIM Ima-Nurisa,SHIMIZU Kenta,YOSHIMATSU Kumiko [他],YUNIANTO Andre,SALWATI Ervi,YASUDA Shumpei P.,KOMA Takaaki,ENDO Rika,ARIKAWA Jiro
Journal of Veterinary Medical Science 75(8), 1003-1008, 2013
… A total of 170 rodents were captured in 2005, and 27 (15.9%) of the rodents were antibody-positive against Hantaan virus antigen in an immunofluorescence assay (IFA) and Western blotting. … To identify the virus in rodents genetically, a total of 59 rodents were captured in 2009. … Genetic analysis showed that the viruses belonged to Seoul virus and formed a cluster with those in Vietnam and Singapore. …
NAID 130003362164

Studies on Hantavirus Infection in Small Mammals Captured in Southern and Central Highland Area of Vietnam

LUAN Vu Dinh,YOSHIMATSU Kumiko,ENDO Rika [他],TARUISHI Midori,HUONG Vo Thi,DAT Dang Tuan,TIEN Pham Cong,SHIMIZU Kenta,KOMA Takaaki,YASUDA Shumpei P.,NHI Le,HUONG Vu Thi Que,ARIKAWA Jiro
Journal of Veterinary Medical Science 74(9), 1155-1162, 2012
… A total of 1066 serum samples from rats were examined for IgG antibodies against Hantaan virus, and there were 30 antibody-positive serum samples from rats that had been captured mainly in a port area and urban area in Ho Chi Minh City (HCMC) (2.8%). … All of the antibody-positive rats were Rattus norvegicus, and they had Seoul virus (SEOV) genome in their lungs. …
NAID 130001879745

Related Pictures

★リンクテーブル★

「virus」

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; Asama virus; Azagny virus; Bayou virus; Black Creek Canal virus; Bloodland Lake virus; Blue River virus; Cano Delgadito virus; Calabazo virus; Carrizal virus; Catacamas virus; Choclo virus; Dobrava-Belgrade virus; El Moro Canyon virus; Gou virus; Hantaan River virus; Huitzilac virus; Imjin virus; Isla Vista virus; Khabarovsk virus; Laguna Negra virus; Limestone Canyon virus; Magboi virus; Maripa virus; Monongahela virus; Montano virus; Mouyassue virus; Muleshoe virus; Muju virus; New York virus; Nova virus; Oran virus; Oxbow virus; Playa de Oro virus; Prospect Hill virus; Puumala virus; Rockport virus; Rio Mamore virus; Rio Segundo virus; Sangassou virus; Saaremaa virus; Seoul virus; Serang virus; Sin Nombre virus; Soochong virus; Tanganya virus; Thailand virus; Thottapalayam virus; Topografov virus; Tula virus; Xuan Son virus

Hantavirus
	Classification and external resources
ICD-10	B33.4
ICD-9	079.81
DiseasesDB	5629
MedlinePlus	001382
MeSH	D018778

　　[★] ウイルス

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hantaan virus