Sin Nombre orthohantavirus

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Sin Nombre orthohantavirus
Sin Nombre hanta virus TEM PHIL 1136 lores.jpg
Transmission electron micrograph of Sin Nombre orthohantavirus
Virus classification OOjs UI icon edit-ltr.svg
(unranked): Virus
Realm: Riboviria
Kingdom: Orthornavirae
Phylum: Negarnaviricota
Class: Ellioviricetes
Order: Bunyavirales
Family: Hantaviridae
Genus: Orthohantavirus
Species:
Sin Nombre orthohantavirus
Member viruses
Synonyms
  • Four Corners virus
  • Sin Nombre hantavirus
  • Sin Nombre virus
Sin Nombre virus
Specialty Virology

Sin Nombre orthohantavirus (SNV) (from Spanish, meaning "without a name"), a member of the genus Orthohantavirus , is the prototypical etiologic agent of hantavirus cardiopulmonary syndrome (HCPS). [1]

Contents

Discovered in 1993 near the Cañon de la Muerte on the Navajo Reservation, it was originally named the Muerto Canyon hantavirus, in keeping with the convention for naming new pathogens. [2] However, the Navajo Nation objected to the name in 1994. [3] It was also near the Four Corners point in the United States, so the virologists then tried naming it the "Four Corners virus". The name was changed after local residents raised objections. [4] In frustration, the virologists changed it to Sin Nombre, meaning "without a name" in Spanish.

History

It was first isolated in 1993 from rodents collected near the home of one of the initial patients with hantavirus pulmonary syndrome (HPS) in the Four Corners region of the western United States. Isolation was achieved through a blind passage in Peromyscus maniculatus (eastern deermouse) and subsequent adaptation to growth in Vero E6 cells. Additional viral strains have also been isolated from P. maniculatus associated with a fatal case in California and P. leucopus from the vicinity of probable infection of a New York case. Black Creek Canal virus was isolated from S. hispidus collected near the residence of a human case in Dade County, Florida. Another etiologic agent of HCPS, Bayou virus, was first isolated from the vicinity of Monroe, Louisiana. [5]

Epidemiology

SNV occurs wherever its reservoir rodent carrier, the deer mouse Peromyscus maniculatus , [6] is found, which includes essentially the entire populated area of North America, except for the far southeastern region from eastern Texas through Florida, Alaska, and the far northern reaches of Canada. SNV and HCPS are especially common in western states; peak incidences for HCPS have been reported in regions in which there is a lot of contact between humans and mice (New Mexico, Arizona) and in states with exceptionally large rural populations such as California. All of the western provinces of Canada have also reported cases. SNV can be contracted through the inhalation of virus-contaminated deer mouse excreta.[ citation needed ]

While transmission from the deer mouse carrier to humans is understood to occur primarily through contact with mouse urine and feces, transmission within the vector population is believed to occur through direct contact, in contrast to the understood vector transmission for other species in the Orthohantavirus genus. [7]

The case fatality ratio of SNV-induced HCPS in the USA was reported to be about 66.7% (CDC, 1993). However, since that time the case fatality ratio has steadily declined as more mild cases came to be recognized. By 2007 the CFR had declined to about 35%.[ citation needed ]

Virus sequencing

As with other Orthohantavirus species, SNV has a tripartite single-stranded negative-sense RNA genome. The entire genomic sequence of SNV has subsequently been determined by using RNA extracted from autopsy material as well as RNA extracted from cell culture-adapted virus. The L RNA is 6562 nucleotides (nt) in length; the M RNA is 3696 nt long; and the S RNA is 2059 to 2060 nt long. When the prototype sequence (NMH15) of SNV detected in tissues from an HPS case was compared with the sequence of the SNV isolate (NMR11; isolated in Vero E6 cells from Peromyscus maniculatus trapped in the residence of the same case), only 16 nucleotide changes were found, and none of these changes resulted in alterations in amino acid sequences of viral proteins. It had been assumed that in the process of adaptation to cell culture, selection of SNV variants which grow optimally in cell culture would occur, and selected variants would differ genetically from the parental virus. Though NMH10 and NMR11 are identical in protein sequence, nucleotide substitutions in nontranslated regions of the genome could be responsible for altered viral phenotypes, as could changes in protein glycosylation or virus membrane components.[ citation needed ]

The nested RT-PCR assay developed during the initial HCPS outbreak provided a rapid method for the genetic characterization of novel hantaviruses that did not require a virus isolate. Numerous new hantaviruses have been detected by RT-PCR in rodent tissues but have yet to be associated with human disease. These include El Moro Canyon virus associated with the western harvest mouse, Reithrodontomys megalotis , Tula virus with Microtus arvalis and M. rossiaemeridionalis , Rio Segundo virus with the Mexican harvest mouse, R. mexicanus, Isla Vista virus with the California vole, M. californicus , and Prospect Hill-like viruses in Microtus species.[ citation needed ]

Virion morphology

In contrast to members of the Orthohantavirus genus endemic outside of the Americas, whose virions are predominately round or pleomorphic, SNV virions have a greater propensity for tubular and irregular virion morphologies. This finding suggests that the genus is more diverse in terms of morphology than previously assumed, which may help explain differences in epidemiology between species. Within the Sin Nombre species, morphologic variability exists between strains, with virions of an elongated phenotype associated with higher virulence. Sin Nombre virions have an average diameter of 90 nm for round particles and 85 nm for tubular particles, with an average length of 180 nm for tubular particles, making them somewhat smaller than closely related members of the genus. [8]

See also

Related Research Articles

<i>Orthohantavirus</i> Genus of viruses

Orthohantavirus is a genus of single-stranded, enveloped, negative-sense RNA viruses in the family Hantaviridae within the order Bunyavirales. Members of this genus may be called orthohantaviruses or simply hantaviruses.

<i>Bunyavirales</i> Order of RNA viruses

Bunyavirales is an order of segmented negative-strand RNA viruses with mainly tripartite genomes. Member viruses infect arthropods, plants, protozoans, and vertebrates. It is the only order in the class Ellioviricetes. The name Bunyavirales derives from Bunyamwera, where the original type species Bunyamwera orthobunyavirus was first discovered. Ellioviricetes is named in honor of late virologist Richard M. Elliott for his early work on bunyaviruses.

<i>Andes orthohantavirus</i> Species of virus

Andes orthohantavirus (ANDV), a species of Orthohantavirus, is a major causative agent of hantavirus cardiopulmonary syndrome (HCPS) and hantavirus pulmonary syndrome (HPS) in South America. It is named for the Andes mountains of Chile and Argentina, where it was first discovered. Originating in the reservoir of rodents, Andes orthohantavirus is easily transmitted to humans who come into contact with infected rodents or their fecal droppings. However, infected rodents do not appear ill, so there is no readily apparent indicator to determine whether the rodent is infected or not. Additionally, Andes orthohantavirus, specifically, is the only hantavirus that can be spread by human to human contact via bodily fluids or long-term contact from one infected individual to a healthy person.

Playa de Oro virus (OROV) is a probable species of orthohantavirus found in the rodents Oryzomys couesi and Sigmodon mascotensis in the Mexican state of Colima. The former is thought to be the main host. The sequences of parts of the virus's RNA-based genome have been determined; they differ by 7–10% in amino acid composition and 22–24% in nucleotide composition from closely related viruses.

New York orthohantavirus or New York virus is an Orthohantavirus. It is considered a strain of Sin Nombre orthohantavirus. It was first isolated from a white-footed mouse caught on an island off New York. The virus is associated with typical hantavirus pulmonary syndrome.

Black Creek Canal orthohantavirus (BCCV) is a single-stranded, negative sense RNA virus species of New World Orthohantavirus. It was first isolated in cotton rats found in the Black Creek Canal area of Dade County, Florida, in 1995. The discovery followed from an isolated case of Hantavirus pulmonary syndrome diagnosed in a Dade County resident.

<span class="mw-page-title-main">1993 Four Corners hantavirus outbreak</span> 1993 disease outbreak

The 1993 Four Corners hantavirus outbreak was an outbreak of hantavirus that caused the first known human cases of hantavirus disease in the United States. It occurred within the Four Corners region – the geographic intersection of the U.S. states of Utah, Colorado, New Mexico, and Arizona – of the Southwestern United States in mid-1993. This region is largely occupied by Native American tribal lands, including the Hopi, Ute, Zuni, and Navajo reservations, from which many of the cases were reported.

Sangassou orthohantavirus(SANGV) is single-stranded, negative-sense RNA virus species of the genus Orthohantavirus in the Bunyavirales order. It was first isolated in an African wood mouse (Hylomyscus simus) in the forest in Guinea, West Africa in 2010. It is named for the village near where the mouse was trapped. It is the first indigenous Murinae-associated African hantavirus to be discovered.

<span class="mw-page-title-main">Hantavirus hemorrhagic fever with renal syndrome</span> Group of clinically similar illnesses caused by species of hantaviruses

Hantavirus hemorrhagic fever with renal syndrome (HFRS) is a group of clinically similar illnesses caused by species of hantaviruses. It is also known as Korean hemorrhagic fever and epidemic hemorrhagic fever. It is found in Europe, Asia, and Africa. The species that cause HFRS include Hantaan orthohantavirus, Dobrava-Belgrade orthohantavirus, Saaremaa virus, Seoul orthohantavirus, Puumala orthohantavirus and other orthohantaviruses. Of these species, Hantaan River virus and Dobrava-Belgrade virus cause the most severe form of the syndrome and have the highest morbidity rates. When caused by the Puumala virus, it is also called nephropathia epidemica. This infection is known as sorkfeber in Swedish, myyräkuume in Finnish, and musepest in Norwegian.

<span class="mw-page-title-main">Hantavirus pulmonary syndrome</span> Viral pulmonary disease of humans

Hantavirus pulmonary syndrome (HPS) is one of two potentially fatal syndromes of zoonotic origin caused by species of hantavirus. These include Black Creek Canal virus (BCCV), New York orthohantavirus (NYV), Monongahela virus (MGLV), Sin Nombre orthohantavirus (SNV), and certain other members of hantavirus genera that are native to the United States and Canada.

Dobrava-Belgrade orthohantavirus (DOBV), also known as Dobrava virus, is an enveloped, single-stranded, negative-sense RNA virus species of Old World Orthohantavirus. It is one of several species of Hantavirus that is the causative agent of severe Hantavirus hemorrhagic fever with renal syndrome. It was first isolated in 1985 from a yellow-necked mouse found in the village of Dobrava, southeastern Slovenia. It was subsequently isolated in striped field mice in Russia and other parts of Eastern Europe. It has also been found in Germany but the reservoir host there is unknown.

Saaremaa virus is a single-stranded, negative-sense, RNA virus Orthohantavirus that causes a milder form of Hantavirus hemorrhagic fever with renal syndrome. It is a member virus of Dobrava-Belgrade orthohantavirus. It was first isolated from a striped field mouse in Slovakia.

Monongahela virus (MGLV) is a single-stranded, negative-sense Orthohantavirus virus of zoonotic origin that causes hantavirus pulmonary syndrome.

Limestone Canyon virus (LSC) is a single-stranded, negative-sense RNA zoonotic Orthohantavirus that is genetically similar to Sin Nombre orthohantavirus which causes Hantavirus pulmonary syndrome (HPS) in humans. HPS causing hantaviruses are found only in the United States and South America.

Imjin thottimvirus(MJNV) is a single-stranded, enveloped, negative-sense RNA virus of the orthohantavirus genus in the Bunyavirales order. It is a newly identified hantavirus isolated from the lung tissues of Ussuri white-toothed shrews of the species Crocidura lasiura (order Soricomorpha, family Soricidae, subfamily Crocidurinae) captured near the demilitarized zone in the Republic of Korea during 2004 and 2005.

El Moro Canyon orthohantavirus is a single-stranded, negative sense RNA virus of the genus Orthohantavirus. It is a causative agent of Hantavirus pulmonary syndrome.

Rockport virus (RKPV) is a single-stranded, enveloped, negative-sense RNA orthohantavirus.

Asama orthohantavirus(ASAV), also called Asama virus, is a single-stranded, enveloped, segmented negative-sense RNA hantavirus. The hantavirus was isolated in Japan from Japanese shrew mole. Hantaviruses harbored by shrews are genetically closer to ASAV than to hantaviruses harbored by rodents. Host-switching may be evident in the future due to the viruses closeness to soricine shrew-borne hantaviruses. The detection of the ASAV was the first hantavirus found to be hosted by members of the family Talpidae, which includes shrew moles. Thoughts on hantavirus evolutionary history has expanded due to the discovery of ASAV.

Oxbow virus(OXBV) is a single-stranded, enveloped, negative-sense RNA orthohantavirus.

Blue River virus (BRV) is a single-stranded, negative sense RNA virus of New World hantavirus isolated from a white-footed mouse near the Blue River in Jackson County, Missouri in 1995. Its genome is similar to Sin Nombre orthohantavirus (SNV) but varies in the S1 and S2 segments. Like Sin Nombre orthohantavirus, Blue River virus causes Hantavirus pulmonary syndrome (HPS) in humans.

References

  1. Ye C, Prescott J, Nofchissey R, Goade D, Hjelle B (March 2004). "Neutralizing antibodies and Sin Nombre virus RNA after recovery from hantavirus cardiopulmonary syndrome". Emerging Infect. Dis. 10 (3): 478–82. doi:10.3201/eid1003.020821. PMC   3322788 . PMID   15109416.
  2. Van Hook, Charles J. (November 2018). "Hantavirus Pulmonary Syndrome—The 25th Anniversary of the Four Corners Outbreak". Emerging Infectious Diseases. 24 (11): 2056–2060. doi:10.3201/eid2411.180381. PMC   6199996 .
  3. "Navajos Decry Muerto Canyon Hantavirus Site". Los Angeles Times. April 24, 1994. Retrieved 3 July 2019.
  4. Strauss, Ellen G.; Strauss, James H. (2002). Viruses and human disease . Boston: Academic Press. p.  161. ISBN   978-0-12-673050-0.
  5. "Hantaviruses, with emphasis on Four Corners Hantavirus". Bvs.insp.mx. Archived from the original on 2013-04-20. Retrieved 2016-11-17.
  6. Lehmer EM, Clay CA, Pearce-Duvet J, St Jeor S, Dearing MD (March 2008). "Differential regulation of pathogens: the role of habitat disturbance in predicting prevalence of Sin Nombre virus". Oecologia. 155 (3): 429–39. Bibcode:2008Oecol.155..429L. doi:10.1007/s00442-007-0922-9. PMID   18064494. S2CID   19495085.
  7. Warner, Bryce (2019-12-02). "Development and Characterization of a Sin Nombre Virus Transmission Model in Peromyscus maniculatus". Viruses. 11 (2): 183. doi: 10.3390/v11020183 . PMC   6409794 . PMID   30795592.
  8. Parvate, Amar (2019-09-16). "Diverse Morphology and Structural Features of Old and New World Hantaviruses". Viruses. 11 (9): 862. doi: 10.3390/v11090862 . PMC   6783877 . PMID   31527500.