Orthohantavirus is a genus of single-stranded, enveloped, in the family order. Members of this genus can be called orthohantaviruses or just hantaviruses. They usually cause infection, but does not cause disease in them. Humans can be infected with hantaviruses through contact with rat urine, saliva, or feces. Some strains cause a potentially fatal disease in humans, such as (HFRS), or (HPS), also known as hantavirus cardiopulmonary syndrome (HCP), while others have not been associated with human diseases are known. HPS (HCP) is “rare respiratory disease associated with inhalation of aerosols of rodent feces (urine and feces) contaminated by hantavirus particles.”
Human infection has been almost entirely hantaviruses associated with human contact with rodent droppings; However, in 2005 and 2019, the human-to-human transmission was reported in South America.
Hantavirus is the name for the area where the initial outbreak was observed, and was isolated in 1976 by.
Hemorrhagic fever with renal syndrome (HFRS) is a group of similar clinical disease caused by hantaviruses from the family Hantaviridae species. It is also known as Korean hemorrhagic fever, dengue fever epidemic, and. The species that cause HFRS include ,,,, and. It is found in Europe, Asia, and Africa.
In the hantavirus induced hemorrhagic fever is two to four weeks in humans before symptoms develop. depending on their severity.
Hantavirus pulmonary syndrome (HPS) found in North, Central and South America. It is often fatal lung disease. In the United States, the causative agent is carried by. Prodromal symptoms include flu-like symptoms such as fever, cough ,, headache, and lethargy. It is characterized by a sudden onset of shortness of breath quickly developed lung often fatal despite intervention with mechanical ventilation and powerful diuretic. The mortality rate was 36%.
hantavirus pulmonary syndrome was first recognized during an outbreak in the southwestern United States, 1993. It is 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 of the “Four Corners” stigma of the region. Since it has been identified in the United States. rodent control in and around the home remains the primary prevention strategy.
Hantaviruses is bunya virus. This order is divided into twelve families. Like all members of this Order (except for Arenaviridae), hantaviruses have been made up of three segments of single-stranded RNA, and are classified as negative sense. Other family members Bunyavirales generally -borne virus, but hantaviruses is expected to be transmitted to humans primarily through inhalation aerosol dirt, or rodent bite.
Like other members of the virus Bunyavirales, orthohantaviruses covered with a genome consisting of three, single-stranded RNA segments of negative-sense designated S (small), M (medium), and L (large). S RNA encodes (N) protein. M RNA which encodes a cotranslationally cleaved to generate envelope Gn (formerly G1) and Gc (formerly G2).
L RNA encodes the L protein, which serves as the viral transcriptase / replicase. In RNA genome of hantaviruses thought to complex with the nucleocapsid protein N to form a helix, RNA component which circularizes for sequence complementarity between the 5 ‘and 3’ terminal sequence of the genome segments. 
Like other Bunyavirales, each of the three segments having a 3′-terminal consensus sequence (AUCAUCAUC), which completes the sequence 5′-terminal and distinct from those of four other genera in the family. This sequence appears to form the panhandle structure which seems likely play a role in the replication and facilitated by binding to the viral nucleocapsid protein (N). Large segments is 6530-6550 nucleotides (nt) long, was 3613-3707 nt medium and small length is 1696 to 2083 nt in length. 
There is no known non-structural protein, unlike other genera within this family. At the 5 ‘and 3’ of each segment are short noncoding sequences: noncoding segments in all sequences in the 5 ‘end is 37-51 nt. 3 ‘noncoding region is different: L 38-43 nt segment; M segment nt 168-229; aS segments 370-730 nt d. 3 ‘end of the segment S is conserved between genera indicate a functional role. 
Hantavirus virions are about 120-160 (nm) in diameter. The lipid bilayer of about 5 nm thick and embedded in the surface of the viral protein attached sugar residues. This glycoprotein, known as Gn and Gc, encoded by the M segment of the viral genome. They tend to associate () with one another and have both interior and exterior tail domain that extends to about 6 nm outer envelope surface. 
Inside the envelope is a nucleocapsid. It consists of many copies of the nucleocapsid protein N, which interacts with the three segments of the viral genome to form helical structures. The viral encoded also found in the interior. Massa, virion is greater than 50% protein, 20-30% 2-7% lipids and carbohydrates. The density of the virion 1:18 grams per cubic centimeter. These features are common to all family members Hantaviridae. 
Entry into the host cell is thought to occur with virion attachment to cellular receptors and subsequent. The nucleocapsid is inserted into the cytoplasm by pH-dependent fusion of the virion with. After releasing the nucleocapsid into the cytoplasm, the complex is targeted to the ER-Golgi intermediate compartment (ERGIC) through -associated movement resulting in formation of a virus factory in ERGIC. 
This factory then facilitates subsequent transcription and translation of viral proteins. Transcription of viral genes must be initiated by the L protein association with the three nucleocapsid species. In addition to transcriptase and replicase functions, L viral proteins also thought to have an endonuclease activity that cut cellular messenger RNA (mRNA) for the primary production of limited use to initiate transcription of the viral mRNA. As a result of this, mRNAs of hantaviruses are limited and nontemplated containing the 5′-terminal extension.
G1 (or Gn) and G2 (Gc) glycoproteins form and then transported from to, where finished. 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. newborn virions are then transported in secretions to and released by. 
The pathogenesis of hantavirus infection is not clear because there is a lack of animal models to describe it (rats and mice seem to get severe disease). While the primary site of viral replication in the body is not known, in HFRS main effect was on blood vessels while in HPS most symptoms associated with lung. In HFRS, there is increased permeability of blood vessels and lower blood pressure due to endothelial dysfunction and the most dramatic visible damage to the kidneys, whereas in HPS, lungs, spleen, and gall bladder are most affected. The initial symptoms of HPS are likely to present similar to the flu (muscle aches, fever and fatigue) and usually appear around 2 to 3 weeks after exposure. the final stage of the disease (approximately 4 to 10 days after symptoms begin), including difficulty breathing, shortness of breath and coughing.
The virus that causes dengue fever Hantavirus has not been shown to transfer from person to person, except. For other species of hantavirus, aerosols of rodent droppings or rodent bites is the only known route of transmission to humans. negative strand RNA viruses are the same, such as dengue fever and can be transmitted through contact with blood and body fluids of infected, and is known to spread to health care workers in hospitals Africa, but did not transfer easily in a modern hospital with proper precautions. Transmission through (inanimate infection) has not been demonstrated in both the hemorrhagic disease or hantavirus pulmonary form.
The findings of alignment significantly between the phylogeny of hantaviruses and phylogeny of reservoir rodents they have led to the theory that the rodent, though infected by a virus, not impaired due to host hantavirus rodent long, despite the findings on in 2008 led to a new hypothesis regarding the evolution of hantavirus.
A variety of hantaviruses have been found to infect several species of rodents, and cases of cross-species transmission () has been recorded. In addition, the degree of substitution by nucleotides of sequence data revealed that clades hantavirus and rodent subfamilies may not deviate at the same time. Furthermore, in 2007 hantaviruses have been found in several species of shrews and moles.
With respect to the inconsistency in the theory of coevolution, proposed in 2009 that the pattern seen in hantaviruses in relation to their reservoirs can be attributed to the preferential host switching directed by geographical proximity and adaptation to a particular host species. Another proposal from 2010 is that the geographic clustering of hantavirus sequence may have been caused by the mechanism of isolation-by-distance. After comparison of hantaviruses are found in a host of orders and proposed in 2011 that hantavirus evolution history is a mixture of both switch hosts and codivergence and that the ancestral shrews or moles, rather than mice, may have been the initial host original ancient hantaviruses.
An analysis in 2014 suggested a common origin for this virus ~ 2000 years ago. Association with specific rodent family seems to have been more recent. Viruses carried by and subfamilies from 500-700 years ago. It later spread to North America ,, and may be brought by their hosts. Subfamily infecting species evolve 500-600 years ago in Central America and later spread to North America. Infecting species evolved in 400 years ago. their ancestors may have been related Neotominae virus from the northern part of South America.
According to the CDC, the best prevention against contracting hantavirus is to eliminate or minimize contact with rodents in the home, workplace, or campsite. As the virus can be transmitted through the saliva of rodents, excretion, and bite, controlling rats and mice in areas frequented by humans is the key to prevention of disease. general prevention can be achieved by removing the nest of rodents, sealing any cracks and holes in the houses where rats or mice can enter, trapping, or put poison or using natural predators like cats at home.
The duration of the hantaviruses remain infectious in the environment varies based on factors such as the rodent’s diet, temperature, humidity, and whether indoors or outdoors. The virus has been shown to remain active for two to three days at normal room temperature, while the ultraviolet rays in sunlight directly killing them within hours. However, rodent droppings or urine indeterminate age should always be treated as infectious.
In 2016, there are no FDA-approved, commercially available hantavirus vaccine. The vaccine, known as Hantavax been studied since 1990. In 2016, the construction was in the stage of phase 3 clinical trials. inactivated vaccine is not considered effective against such European hantaviruses Puumala (PUUV) virus. Killed-virus vaccine was not being pursued because of the dangers associated with mass production under high containment and questions unresolved about the efficiency of the vaccine. A number of laboratories have been working towards a vaccine that would give the virus antigen with either vector DNA or recombinant proteins. In 2016, this recombinant vaccine will not be available in the near future.
No WHO-approved vaccines has gained wide acceptance, but the Korean Army is one of the biggest consumer of hantavirus vaccine, second only to community health centers.
Ribavirin may be a cure for HPS and HFRS but its effectiveness is still unknown, still, perhaps spontaneous recovery with supportive therapy. People with suspected hantavirus infections can be treated at the hospital, was given oxygen support and mechanical ventilation to help them breathe during the phase of acute lung with severe respiratory distress. Immunotherapy, human neutralizing antibody during the acute phase of hantavirus, only been studied in mice, hamsters, and mice. There were no reports of controlled clinical trials.
hantavirus infection have been reported from all continents except Australia. The area is mainly affected by hemorrhagic fever with renal syndrome included, which, (Hantaan, Puumala and Seoul viruses), and the north and west (and Dobrava virus). The area with the highest incidence of hantavirus pulmonary syndrome including ,,, which ,, and.
In 2010, a new hantavirus, isolated in Africa that cause hemorrhagic fever with renal syndrome.
In Hong Kong, and, hemorrhagic fever with renal syndrome caused by Hantaan, Puumala and Seoul viruses.
In March 2020, a man of tested positive for hantavirus. He died while traveling to work on a chartered bus. According to reports, about 32 other people have been tested for the virus.
In 2005, no human infection was reported in Australia, although the mouse antibodies carry.
In Europe two hantaviruses – Puumala and Dobrava-Belgrade virus – known to cause hemorrhagic fever with renal syndrome. Puumala usually causes mild general illness, which usually presents with fever, headache, gastrointestinal symptoms, impaired kidney function and blurred vision. Dobrava infection are similar, except that they often also have a hemorrhagic complications.
Puumala done by the host rodent, (Clethrionomys glareolus), and is present in most of Europe, except for the Mediterranean region. There are four known Dobrava virus genotypes, each performed by a different rodent species. Dobrava genotype was found in (Apodemus flavicollis); Saaremaa and Kurkino genotype at (Apodemus agrarius), and genotype of Sochi (Apodemus Ponticus).
In 2017 alone, the Robert Koch Institute (RKI) in Germany receive 1,713 notifications of hantavirus infection.
The main cause of illness in Canada is Sin Nombre virus infected deer mice. Between 1989 and 2014, there were a total of 109 confirmed cases, with an estimated mortality rate of 29%. Viruses exist in national deer mice, but the cases are concentrated in western Canada (British Columbia, Alberta, Saskatchewan and Manitoba) with only one case in eastern Canada. In Canada, “[a] ll cases occur in rural areas and around 70% of the cases have been linked to domestic and agricultural activities.”
In the US, minor cases of HPS including ,,, and possible.
In January 2017, 728 cases of hantavirus have been reported in the United States cumulatively since 1995, in 36 countries, excluding cases with exposure considered outside the United States. More than 96% of cases occur in western countries. Top 10 countries with the number of reported cases (which is slightly different from the count ordered by state exposure to the original) is (109), (104), (78), (61), (50), (45), (43), ( 38), (21) and (21); 36% of the total reported cases have resulted in death.
In Mexico, the rats have been found to carry hantaviruses included (Megadontomys thomasi), which Neotoma picta, (Peromyscus beatae), (Reithrodontomys megalotis) and (Reithrodontomys sumichrasti).
Agent of HPS found in the included (also called Oran, Castelo de Sonhos – Portuguese for “Castle of Dreams”, Lechiguanas, Juquitiba, Araraquara, and Bermejo viruses, among many other synonymous), which is only hantavirus that has shown interpersonal form of transmission, and, a very close relative of the Rio Mamore virus was previously known.
Rodents that have been shown to carry hantaviruses, including and.
hantaviruses is a relatively newly discovered genus of viruses. Outbreaks among American and Korean soldiers during the (1950-1953) caused by hantavirus infection. More than 3000 soldiers became ill with symptoms including, general bleeding, and shock. It has a mortality rate of 10%. Hantavirus is named for the region. This outbreak triggers 25-year search for the etiologic agent. Ho-Wang Lee, a virologist South Korea, and colleagues Hantaan virus isolated in 1976 from the lungs of striped field mice.
At the end of the mysterious struck the country in 1485 before. Noting that the symptoms overlap with hantavirus pulmonary syndrome (see), some scientists have theorized that the virus may be the cause of the disease. hypothesis criticized for sweating sickness recorded as being transmitted from human to human, while the unknown hantaviruses spread this way. limited transmission through contact with human-to-human since it has been shown in hantavirus outbreaks in Argentina.
In 1993, an outbreak of hantavirus pulmonary syndrome occurred in the region in the southwestern United States. The virus causing the disease was found only a weeks later and called Sin Nombre virus (SNV), or in “sin nombre virus,” which means “nameless virus”. the host was first identified as a deer () by, a professor at the.
On March 24, 2020, a man who died in a bus tested positive for hantavirus.
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