Dobrava-Belgrade virus

Last updated
Orthohantavirus dobravaense
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 dobravaense
Synonyms [1] [2]
  • Dobrava-Belgrade hantavirus
  • Dobrava-Belgrade orthohantavirus
  • Dobrava-Belgrade virus

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.

Contents

DOBV has four genotypes: Dobrava virus, Sochi virus, Kurkino virus, and Saaremaa virus. These genotypes are native to different rodent species and vary in how severe of illness they cause. Dobrava virus, Sochi virus, Kurkino virus, and Saaremaa virus. Dobrava virus is carried by the yellow-necked mouse (Apodemus flavicollis) and has moderate-to-severe symptoms with a case fatality rate of 10–12%. Sochi virus is native to the Black Sea field mouse (Apodemus ponticus) and has moderate-to-severe symptoms and a case fatality rate of at least 6%. Kurkino virus is transmitted by the striped field mouse (Apodemus agrarius) and has mild-to-moderate symptoms with a 0.3–0.9%. Lastly, Saaremaa virus, also transmitted by the striped field mouse, is not associated with disease or mortality.

The genome of DOBV is about 11.8 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.

Dobrava-Belgrade virus 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.

Dobrava-Belgrade virus was first discovered in 1992 after being isolated from the lung tissue of a yellow-necked mouse in Dobrava, Slovenia. At the same time, an identical virus was identified in Belgrade, Serbia, earning the virus the name "Dobrava-Belgrade virus". Within a few years, the virus had been identified throughout Europe and Russia. The virus was implicated in an outbreak of HFRS in Croatia during the Balkan Wars. The main region affected by DOBV is southeastern Europe, but its distribution has been expanding since its hosts extend outside the region.

Genome

The genome of Dobrava-Belgrade virus is about 11.8 thousand nucleotides in length [3] 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. [1] The small segment, about 1.67 kilobases (kb) in length, [3] encodes the viral nucleoprotein. The medium segment, about 3.64 kb in length. [3] 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, [3] 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. [1] [6] [7]

Life cycle

DOBV primarily infects endothelial cells and macrophages. [4] It enters 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

The are four genotypes of DOBV: Dobrava, Kurkino, Saaremaa, and Sochi. [4] [10] The Dobrava genotype causes infection mainly in southeastern Europe in Slovenia, Serbia, Montenegro, Albania, Greece, but also in central Europe in Czechia, Slovakia, and Hungary. The Kurkino genotype exists in Germany, Slovakia, Russia, Hungary, Slovenia, Croatia, and mainland Estonia. The Saaremaa genotype is found on Saaremaa island in Estonia. The Sochi genotype is found in the Black Sea region of eastern Russia. [11]

Evolution

The most common way that hantaviruses evolve is through mutations of individual nucleotides being inserted, deleted, or substituted. Because Dobrava-Belgrade 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. [4] The Saaremaa genotype is likely a reassortment as its M segment is closely related to the M segment of the Kurkino genotype, while its S segment is more closely related to the Dobrava and Sochi genotypes. Reassortment is also observed in the Sochi genotype, which has an S segment that forms a sister clade with the S segment of the Dobrava genotype while its other segments are not closely related to the other genotypes. [10]

Ecology

Apodemus.flavicollis.jpg
The yellow-necked mouse, the natural reservoir of Dobrava virus.
Mysz polna2.jpg
The striped field mouse, the natural reservoir of Kurkino virus and Saaremaa virus.

The four genotypes of DOBV have different natural reservoirs. The Dobrava genotype is carried by the yellow-necked mouse (Apodemus flavicollis). The natural reservoir of the Kurkino and Saaremaa genotypes is the striped field mouse (Apodemus agrarius). The Sochi genotype is transmitted by Black Sea field mice (Apodemus ponticus). In southeastern Europe, the yellow-necked mouse is the dominant host of DOBV, and striped field mouse that carry DOBV are also present. In central and eastern Europe, the stripe field mouse is the dominant DOBV host, while in central Europe DOBV-infected yellow-necked mice are also present. [11]

In its rodent hosts, DOBV causes a persistent and asymptomatic infection. [12] Rodent-to-rodent transmission occurs through contact with bodily fluids and through fighting and grooming. [6] Transmission to humans occurs mainly through the inhalation of aerosols that contain rat saliva, urine, or feces. [5] [13] Transmission can also occur through consumption of contaminated food, bites, and scratches. [4] [13]

Disease

Dobrava-Belgrade 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. [14] 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] A common complication of DOBV infection is acute respiratory distress syndrome (ARDS). [9] In more mild cases, the different phases of illness may be hard to distinguish, [15] or some phases may be absent, while in more severe cases, the phases may overlap. [5]

Disease severity depends on genotype: infection with the Dobrava genotype has moderate-to-severe symptoms with case fatality rate of 10–12%; Sochi virus infection has moderate-to-severe symptoms with a case fatality rate of more than 6%; the Kurkino genotype causes mild-to-moderate HFRS with a case fatality rate of 0.3–0.9%, and the Saaremaa genotype appears to cause a mainly subclinical infection with no mortality. The reason for the disparity in the course of disease by genotype is unknown. [11] DOBV infection is the most common cause of HFRS in southern Europe. The Balkans are the main region affected, but the distribution of DOBV has been spreading since the distribution of its host extends beyond the region. [9]

DOBV 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] [16] [17] [18] About 10% of cases require mechanical ventilation due to the development of ARDS. [9] The main way to prevent infection is to avoid or minimize contact with rodents. [4] Repeated infections of hantaviruses have not been observed, so recovering from infection likely grants life-long immunity. [13] [19]

Classification

Dobrava-Belgrade virus is classified as the species Orthohantavirus dobravaense in the genus Orthohantavirus, which is in the family Hantaviridae , the family that all hantaviruses belong to. The species includes the four genotypes of DOBV. The Ano/Poroia/Afl9/1999 isolate of Dobrava virus is the exemplar virus of the species. This taxonomy is shown hereafter: [1] [2] [20]

History

The Dobrava virus was first isolated in the 1992 [4] from the lung tissue of a yellow-necked mouse captured in Dobrava, Slovenia. [9] [15] At the same time, Belgrade virus was isolated from someone who had severe HFRS. The two viruses were found to be identical, so the virus received the name Dobrava-Belgrade virus. Within a few years, DOBV had been identified throughout Europe and Russia. In 1997, the Saaremaa genotype was discovered in Estonia in striped field mice. [11]

An epidemic of HFRS occurred in 1995 in Croatia during the Balkan Wars among soldiers who lived in poor conditions such as wooden huts in forests. This exposed them to rodents that carried the virus. In addition to DOBV, Puumala virus was also responsible for the 1995 epidemic. [21] Dobrava-Belgrade virus was accepted as a species by the International Committee on Taxonomy of Viruses in 1995 and has undergone a series of changes to its species name, first changing to Dobrava-Belgrade hantavirus, then Dobrava-Belgrade orthohantavirus, and most recently to the current Orthohantavirus dobravaense. [2]

Related Research Articles

<i>Orthohantavirus</i> Genus of viruses

Orthohantavirus is a genus of viruses that includes all hantaviruses that cause disease in humans. Orthohantaviruses, hereafter referred to as hantaviruses, are naturally found primarily in rodents. In general, each hantavirus is carried by one rodent species and each rodent that carries a hantavirus carries one hantavirus species. Hantaviruses in their natural reservoirs usually cause an asymptomatic, persistent infection. In humans, however, hantaviruses cause two diseases: hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS). HFRS is mainly caused by hantaviruses in Africa, Asia, and Europe, called Old World hantaviruses, and HPS is usually caused by hantaviruses in the Americas, called New World hantaviruses.

<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%.

<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">Yellow-necked mouse</span> Species of mammal

The yellow-necked mouse, also called yellow-necked field mouse, yellow-necked wood mouse, and South China field mouse, is closely related to the wood mouse, with which it was long confused. It was only recognised as a separate species in 1894. It differs in its band of yellow fur around the neck and in having slightly larger ears and usually being slightly larger overall. Around 100 mm in length, it can climb trees and sometimes overwinters in houses. It is found mostly in mountainous areas of southern Europe, but extends north into parts of Scandinavia and Britain. It facilitates the spread of tick-borne encephalitis to humans and is a reservoir species for the Dobrava virus, a hantavirus that is responsible for causing haemorrhagic fever with renal syndrome.

<span class="mw-page-title-main">BK virus</span> Member of the polyomavirus family

The BK virus, also known as Human polyomavirus 1, is a member of the polyomavirus family. Past infection with the BK virus is widespread, but significant consequences of infection are uncommon, with the exception of the immunocompromised and the immunosuppressed. BK virus is an abbreviation of the name of the first patient, from whom the virus was isolated in 1971. This patient - a male - was then 39 years old, who had developed constriction of the ureter after a renal transplant.

Seoul virus (SEOV) is one of the main causes of hemorrhagic fever with renal syndrome (HFRS). Seoul virus is transmitted by the brown rat and the black rat. 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%.

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%.

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.

Bayou virus (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 virus. 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%.

Amur virus (AMRV) 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 has been identified as a causative agent of hemorrhagic fever with renal syndrome.

<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 disease that occurred in the Four Corners region of the US states in Arizona, Colorado, and New Mexico. The outbreak marked the discovery of hantaviruses in the Western Hemisphere that could cause disease and revealed the existence of a novel type of disease caused by hantaviruses: hantavirus pulmonary syndrome (HPS). Hantaviruses that cause disease in humans are native to rodents and, prior to the outbreak, were known to exist in Asia and Europe, but previously were only associated with a different disease called hemorrhagic fever with renal syndrome (HFRS).

Sangassou virus(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.

Hantavirus hemorrhagic fever with renal syndrome (HFRS) is a hemorrhagic fever caused by hantaviruses. Symptoms occur usually occur 12–16 days after exposure to the virus and come in five distinct phases: febrile, hypotensive, low urine production (oliguric), high urine production (diuretic), and recovery. Early symptoms include headache, lower back pain, nausea, vomiting, diarrhea, bloody stool, the appearance of spots on the skin, bleeding in the respiratory tract, and renal symptoms such as kidney swelling, excess protein in urine, and blood in urine. During the hypotensive phase, blood pressure lowers due to microvascular leakage. Renal failure then causes the diuretic phase, before recovering and increasing urine production as disease progression improves. The severity of symptoms varies depending on which virus causes HFRS and ranges from a mild illness to severe. The case fatality rate likewise varies by virus, at less than 1% up to 15%.

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

Hantavirus pulmonary syndrome (HPS), also called hantavirus cardiopulmonary syndrome (HCPS), is a severe respiratory disease caused by hantaviruses. The main features of illness are microvascular leakage and acute respiratory distress syndrome. Symptoms occur anywhere from 1 to 8 weeks after exposure to the virus and come in three distinct phases. First, there is prodromal phase with flu-like symptoms such as fever, headache, muscle, shortness of breath, as well as low platelet count. Second, there is cardiopulmonary phase during which people experience elevated or irregular heart rate, cardiogenic shock, and pulmonary capillary leakage, which can lead to respiratory failure, low blood pressure, and buildup of fluid in the lungs and chest cavity. The final phase is recovery, which typically takes months, but difficulties with breathing can persist for up to two years. The disease has a case fatality rate of 30–60%.

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.

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.

Hantavirus vaccine is a vaccine that protects in humans against hantavirus infections causing hantavirus hemorrhagic fever with renal syndrome (HFRS) or hantavirus pulmonary syndrome (HPS). The vaccine is considered important as acute hantavirus infections are responsible for significant morbidity and mortality worldwide. It is estimated that about 1.5 million cases and 46,000 deaths occurred in China from 1950 to 2007. The number of cases is estimated at 32,000 in Finland from 2005 to 2010 and 90,000 in Russia from 1996 to 2006.

<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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