Seoul virus

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Seoul virus
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:
Orthohantavirus seoulense
Virus:
Seoul virus
Synonyms [1]
  • Seoul hantavirus
  • Seoul orthohantavirus

Seoul virus (SEOV) is one of the main causes of hemorrhagic fever with renal syndrome (HFRS). Seoul virus is transmitted by the brown rat (Rattus norvegicus) and the black rat (Rattus rattus). In its natural reservoirs, SEOV causes an asymptomatic, persistent infection and is spread through excretions, fighting, and grooming. Humans can become infected by inhaling aerosols that contain rodent saliva, urine, or feces, as well as through bites and scratches. In humans, infection leads to HFRS, an illness characterized by general symptoms such as fever and headache, as well as the appearance of spots on the skin and renal symptoms such as kidney swelling, excess protein in urine, blood in urine, decreased urine production, and kidney failure. The case fatality rate from infection is 1–2%.

Contents

The genome of SEOV is about 12 kilobases (kb) in length and segmented into three negative-sense, single-stranded RNA (-ssRNA) strands. The small strand encodes the viral nucleoprotein, the medium strand encodes the viral spike protein, which attaches to cell receptors for entry into cells, and the long strand encodes the viral RNA-dependent RNA polymerase (RdRp), which replicates and transcribes the genome. Genome segments are encased in nucleoproteins to form ribonucleoprotein (RNP) complexes that are surrounded by a viral envelope that contains spikes emanating from its surface.

SEOV replicates first by binding to the surface of cells with its envelope spikes. Virus particles, called virions, are then taken into the cell by endosomes, where a drop in pH causes the viral envelope to fuse with the endosome, which releases viral RNA into the host cell. RdRp then transcribes the genome for translation by host cell ribosomes and produces copies of the genome for progeny viruses. New virions are assembled at the endoplasmic reticulum and bud from its surface to obtain their viral envelope. Progeny viruses are then transported by a cellular vesicle to the cell membrane, where they leave the cell by exocytosis.

SEOV was first discovered in a brown rat 1980 in Seoul, South Korea. Within a few years of its discovery, it was found in numerous countries and has since been found in Africa, Asia, Europe, and the Americas due to the global distribution of its natural reservoirs. Most cases of SEOV infection occur in China and South Korea. Globally, SEOV accounts for about a quarter of all HFRS cases. SEOV has been found in pet rats, but is not a major public health concern. For laboratory rats, various measures such as culling and screening for SEOV are performed to prevent SEOV infection.

Genome

The genome of Seoul virus is about 12 thousand nucleotides in length [2] and segmented into three negative-sense, single-stranded RNA (-ssRNA) strands. The segments form into circles via non-covalent bonding of the ends of the genome. [3] The small segment, about 1.77 kilobases (kb) in length, [2] encodes the viral nucleoprotein. The medium segment, about 3.65 kb in length. [2] encodes a glycoprotein precursor that is cleaved into the two spike proteins Gn and Gc during virion assembly. The large segment, about 6.53 kb in length, [2] encodes the viral RNA-dependent RNA polymerase (RdRp), which is responsible for transcribing and replicating the genome. The ends of each segment contain untranslated terminal regions (UTRs) that are involved in the replication and transcription of the genome. [4] [5]

Structure

Virions are mostly spherical or pleomorphic in shape and range from 80 to 160 nm in diameter. They contain a lipid envelope covered in spike proteins made of the two viral glycoproteins, Gn and Gc. The spike proteins extend about 10 nm out from the surface and are tetrameric, consisting of four copies each of Gn and Gc with helical symmetry, in which Gn forms the stalk of the spike and Gc the head. Spikes are arranged on the surface in a lattice pattern. Inside the envelope are the three genome segments, which are encased in nucleoproteins to form a ribonucleoprotein (RNP) complex. Attached to each RNP complex is a copy of RdRp. [3] [6] [7]

Life cycle

SEOV primarily infects endothelial cells and macrophages, [4] entering the cells by using β3-integrins as receptors. [6] Virions are taken into a cell via an endosome. Once pH is lowered, the viral envelope fuses with the endosome, which releases viral RNA into the host cell's cytoplasm. The small segment is transcribed by RdRp first, then the medium segment, and lastly the large segment. Once the genome has been transcribed, RdRp snatches caps from host messenger RNA (mRNA) to create viral mRNA that is primed for translation by host ribosomes to produce viral proteins. [6] [8]

For replication of the genome, a complementary positive-sense strand is produced by RdRp. Copies of the genome are made from this complementary strand. Progeny RNA strands are then encapsidated by nucleoproteins. [4] During replication, the glycoprotein is cleaved in the endoplasmic reticulum by the host signal peptidase during translation. This produces Gn at the N-terminus and Gc at the C-terminus of the protein. [6] Spike proteins are expressed on the surface of the endoplasmic reticulum. Viral RNPs are transported to the endoplasmic reticulum where they bud from the surface, thereby obtaining their envelope. Progeny viruses are then transported by a cellular vesicle to the cell membrane, where they leave the cell via exocytosis. [8] [9]

Diversity

Six lineages of SEOV have been described based on the medium genome segment, number lineages 1–6. Lineages 1, 2, 3, and 5 have been isolated in China and lineage 6 in the UK and Brazil. Lineage 4 is more widespread, having been isolated from China, South Korea, Japan, Singapore, Vietnam, and the USA. [4]

Evolution

The most common way that hantaviruses evolve is through mutations of individual nucleotides being inserted, deleted, or substituted. Because Seoul virus has a segmented genome, it is possible for recombination and reassortment of segments to occur, whereby segments from different lineages mix in a single host cell and produce hybrid progeny. For Seoul virus, this has been observed in the S and M segments in the wild. [4]

Ecology

Rattus norvegicus - Brown rat 02.jpg
The brown rat, a natural reservoir of Seoul virus.
Roofrat Hagenbeck 02.jpg
The black rat, a natural reservoir of Seoul virus.

Seoul virus is transmitted by murid brown rats (Rattus norvegicus) and black rats (Rattus rattus). [10] These rats are distributed globally and consequently spread Seoul virus throughout the world. [4] [11] Most cases of HFRS caused by Seoul virus, however, occur in China and South Korea. [12] Pet rats have sometimes been infected and caused HFRS, but this has not been a major public health concern. Strict screening for SEOV, traceability of lab rats, and extermination of infected lab rats have been implemented to ensure that SEOV does not spread in lab rats. [13]

In its rodent hosts, SEOV causes a persistent and mainly asymptomatic infection. Rodent-to-rodent transmission occurs through contact with bodily fluids and through fighting and grooming. [6] [14] Transmission to humans occurs mainly through the inhalation of aerosols that contain rat saliva, urine, or feces. [5] [15] Transmission can also occur through consumption of contaminated food, bites, and scratches. [4] [15] Infections with Seoul virus usually occur in urban settings such as in one's home. [15] While HFRS is primarily associated with the Old World, HFRS caused by SEOV does occasionally occur in the Americas. In one incident in 2016–2017, there was an outbreak of HFRS caused by SEOV in the USA. Seoul virus had spread amongst pet rats, which exposed their owners to the virus. [13]

Disease

Seoul virus infection can cause hemorrhagic fever with renal syndrome (HFRS). Symptoms usually occur 12–16 days after exposure and come in five phases: fever, hypotension, low urine production, high urine production, then recovery. [16] The disease is hallmarked by acute kidney disease with kidney swelling, excess protein in urine, and blood in urine. Early symptoms include fever, headache, lower back pain, nausea, vomiting, diarrhea, bloody stool, and the appearance of spots on the skin. During the hypotensive phase, there is a sudden lowering of blood pressure and shock due to microvascular leakage. Low urine production then occurs as a result of renal failure. As renal function recovers, urine production increases. [4] [9] The case fatality rate from SEOV infection is 1–2%. [11] In addition to standard HFRS symptoms, SEOV infection may cause hepatitis. In more mild cases, the different phases of illness may be hard to distinguish, [17] or some phases may be absent, while in more severe cases, the phases may overlap. [5]

Seoul virus mainly circulates it China and South Korea but is found worldwide due to the global distribution of its hosts. It is responsible for approximately 25% of all HFRS cases in the world. [4] Infections are most common in spring. [18] SEOV infection is diagnosed based on observation of symptoms and testing for hantavirus nucleic acid, proteins, or hantavirus-specific antibodies. Treatment is supportive in nature and includes intravenous hydration, electrolyte therapy, platelet transfusions, and, in cases of kidney injury or failure, intermittent dialysis and continuous renal replacement therapy. [4] [12] [19] [20] Avoiding or minimizing contact with rodents is key to prevent infection. In China and South Korea, bivalent vaccines for Seoul virus and Hantaan virus are available for use. [4] Repeated infections of hantaviruses have not been observed, so recovering from infection likely grants life-long immunity. [15] [21]

Classification

Seoul virus is classified into the species Orthohantavirus seoulense in the genus Orthohantavirus, which is in the family Hantaviridae , the family that all hantaviruses belong to. Other members of Orthohantavirus seoulense include the Gōu virus. The 80-39 isolate of Seoul virus is the exemplar virus of the species. This taxonomy is shown hereafter: [1] [3] [10]

History

The Seoul virus was first isolated in 1980 in South Korea in a brown rat captured in an apartment building in Seoul. This made it the second hantavirus to be discovered after Hantaan virus (HTNV). Initially, no strict distinction was made between Seoul virus and Hantaan virus since SEOV infection caused similar but milder symptoms, so early cases of SEOV infection were often labeled as being "HTNV-like" and these cases of HFRS were often called "Rattus-type HFRS". [13] Within just a few years of its discovery, SEOV had been identified in numerous other countries and has since been found throughout the world in five continents: Africa, [22] Asia, Europe, North America, and South America. [13]

From the 1960s to the 1980s, there were a series of HFRS outbreaks in laboratory workers that worked with lab rats, which were thought to be free of rodent viruses. These outbreaks, determined to have been caused by SEOV, were important in understanding the then-novel disease, which was given its official name by the World Health Organization. [13] Seoul virus was accepted as a species by the International Committee on Taxonomy of Viruses in 1987 and has undergone a series of changes to its species name, first changing to Seoul hantavirus, then Seoul orthohantavirus, and most recently to the current Orthohantavirus seoulense. Both the species name and SEOV are named after Seoul, the city where the virus was first discovered. [1]

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.

<span class="mw-page-title-main">Sedoreoviridae</span> Family of viruses

Sedoreoviridae is a family of double-stranded RNA viruses. Member viruses have a wide host range, including vertebrates, invertebrates, plants, protists and fungi. They lack lipid envelopes and package their segmented genome within multi-layered capsids. Lack of a lipid envelope has allowed three-dimensional structures of these large complex viruses to be obtained, revealing a structural and likely evolutionary relationship to the cystovirus family of bacteriophage. There are currently 97 species in this family, divided among 15 genera in two subfamilies. Reoviruses can affect the gastrointestinal system and respiratory tract. The name "reo-" is an acronym for "respiratory enteric orphan" viruses. The term "orphan virus" refers to the fact that some of these viruses have been observed not associated with any known disease. Even though viruses in the family Reoviridae have more recently been identified with various diseases, the original name is still used.

<span class="mw-page-title-main">Sin Nombre virus</span> Prototypical agent of hantavirus cardiopulmonary syndrome

Sin Nombre virus (SNV) is the most common cause of hantavirus pulmonary syndrome (HPS) in North America. Sin Nombre virus is transmitted mainly by the eastern deer mouse. In its natural reservoir, SNV causes an asymptomatic, persistent infection and is spread through excretions, fighting, and grooming. Humans can become infected by inhaling aerosols that contain rodent saliva, urine, or feces, as well as through bites and scratches. In humans, infection leads to HPS, an illness characterized by an early phase of mild and moderate symptoms such as fever, headache, and fatigue, followed by sudden respiratory failure. The case fatality rate from infection is high, at 30–50%.

<span class="mw-page-title-main">Rabies virus</span> Species of virus

Rabies virus, scientific name Rabies lyssavirus, is a neurotropic virus that causes rabies in animals, including humans. It can cause violence, hydrophobia, and fever. Rabies transmission can also occur through the saliva of animals and less commonly through contact with human saliva. Rabies lyssavirus, like many rhabdoviruses, has an extremely wide host range. In the wild it has been found infecting many mammalian species, while in the laboratory it has been found that birds can be infected, as well as cell cultures from mammals, birds, reptiles and insects. Rabies is reported in more than 150 countries and on all continents except Antarctica. The main burden of disease is reported in Asia and Africa, but some cases have been reported also in Europe in the past 10 years, especially in returning travellers.

<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.

<span class="mw-page-title-main">H5N1 genetic structure</span> Genetic structure of Influenza A virus

The genetic structure of H5N1, a highly pathogenic avian influenza virus, is characterized by a segmented RNA genome consisting of eight gene segments that encode for various viral proteins essential for replication, host adaptation, and immune evasion.

Andes virus (ANDV) is the most common cause of hantavirus pulmonary syndrome (HPS) in South America. Andes virus is transmitted mainly by the long-tailed pygmy rice rat. In its natural reservoir, ANDV causes an asymptomatic, persistent infection and is spread through excretions, fighting, and grooming. Humans can become infected by inhaling aerosols that contain rodent saliva, urine, or feces, as well as through bites and scratches. In humans, infection leads to HPS, an illness characterized by an early phase of mild and moderate symptoms such as fever, headache, and fatigue, followed by sudden respiratory failure. The case fatality rate from infection is high, at about 40%.

Puumala virus (PUUV) is the main cause of hemorrhagic fever with renal syndrome (HFRS) in Europe and Russia. Puumala virus is transmitted by the bank vole. In its natural reservoir, PUUV causes a persistent infection with few symptoms and is spread through excretions, fighting, and grooming. Humans can become infected by inhaling aerosols that contain rodent saliva, urine, or feces, as well as through bites and scratches. In humans, infection is usually asymptomatic but can lead to a mild form of HFRS often called nephropathia epidemica (NE). Symptoms include fever and headache, impaired vision, as well as the appearance of spots on the skin and renal symptoms such as kidney swelling, excess protein in urine, blood in urine, decreased urine production, and kidney failure. The case fatality rate from infection is less than 1%.

Bayou orthohantavirus (BAYV) is a species of Orthohantavirus comprising enveloped and spherical viruses. It was first identified in 1993 in Louisiana and later confirmed by other investigators. BAYV was recognized as a distinct form of hantavirus disease, now known as hantavirus pulmonary syndrome (HPS). It now represents the second most common hantavirus in the United States behind the Sin Nombre orthohantavirus[]. In 1996, the marsh rice rat, which is seen in marshes in the southeast and mountain streams in the northeast, was identified as the natural reservoir of the virus. Due to the virus being first identified in Louisiana, this indicated the virus to be widespread throughout the Southeastern United States. This hantavirus disease is known as a severe and sometimes fatal respiratory disease, and HPS has a case-rate fatality of almost 50%.

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.

Dobrava-Belgrade virus (DOBV) is the main cause of hemorrhagic fever with renal syndrome (HFRS) in southern Europe. In its natural reservoirs, DOBV causes a persistent, asymptomatic infection and is spread through excretions, fighting, and grooming. Humans can become infected by inhaling aerosols that contain rodent saliva, urine, or feces, as well as through bites and scratches. In humans, infection causes such as fever and headache, as well as the appearance of spots on the skin and renal symptoms such as kidney swelling, excess protein in urine, blood in urine, decreased urine production, and kidney failure. Acute respiratory distress syndrome occurs in about 10% of cases.

Soochong virus (SOOV) is a zoonotic negative sense single-stranded RNA virus. It may be a member of the genus Orthohantavirus, but it has not be definitively classified as a species and may only be a strain. It is one of four rodent-borne Hantaviruses found in the Republic of Korea. It is the etiologic agent for Hantavirus hemorrhagic fever with renal syndrome (HFRS). The other species responsible for HFRS in Korea are Seoul virus, Haantan virus, and Muju virus.

Muju virus(MUV) is a zoonotic negative-sense single-stranded RNA virus of the genus Orthohantavirus. It is a member virus of Puumala orthohantavirus. It is one of four rodent-borne Hantaviruses found in the Republic of Korea. It is the etiologic agent for Hantavirus hemorrhagic fever with renal syndrome (HFRS). The other species responsible for HFRS in Korea are Seoul orthohantavirus, Hantaan orthohantavirus, and Soochong virus.

Hantaan virus (HTNV) is the main cause of hemorrhagic fever with renal syndrome (HFRS) in East Asia. Hantaan virus is transmitted by the striped field mouse In its natural reservoir, HTNV causes a persistent, asymptomatic infection and is spread through excretions, fighting, and grooming. Humans can become infected by inhaling aerosols that contain rodent saliva, urine, or feces, as well as through bites and scratches. In humans, infection causes such as fever and headache, as well as the appearance of spots on the skin, hepatitis, and renal symptoms such as kidney swelling, excess protein in urine, blood in urine, decreased urine production, and kidney failure. Rarely, HTNV infection affects the pituitary gland and can cause empty sella syndrome. The case fatality rate from infection is up to 6.3%.

Nova virus is a single-stranded, negative-sense, enveloped RNA virus with a trisegmented genome. It belongs to one of the most divergent lineages of the hantavirus group, which consists of zoonotic viruses belonging to the family Bunyaviridae. As of now, no human cases of infection have been reported.

Thailand virus (THAIV) is a single-stranded, enveloped, negative-sense RNA orthohantavirus.

Serang virus(SERV) is a single-stranded, negative-sense, enveloped, novel RNA orthohantavirus.

Gou virus (GOUV) is a single-stranded, negative-sense, enveloped novel RNA orthohantavirus. It is one of the known hantaviruses responsible for hantavirus hemorrhagic fever with renal syndrome in humans.

<span class="mw-page-title-main">Negative-strand RNA virus</span> Phylum of viruses

Negative-strand RNA viruses are a group of related viruses that have negative-sense, single-stranded genomes made of ribonucleic acid (RNA). They have genomes that act as complementary strands from which messenger RNA (mRNA) is synthesized by the viral enzyme RNA-dependent RNA polymerase (RdRp). During replication of the viral genome, RdRp synthesizes a positive-sense antigenome that it uses as a template to create genomic negative-sense RNA. Negative-strand RNA viruses also share a number of other characteristics: most contain a viral envelope that surrounds the capsid, which encases the viral genome, −ssRNA virus genomes are usually linear, and it is common for their genome to be segmented.

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