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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%.
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 , 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 in 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 , but is not a major public health concern. For , various measures such as culling and screening for SEOV are performed to prevent SEOV infection.
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. 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. 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.
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. Transmission to humans occurs mainly through the inhalation of aerosols that contain rat saliva, urine, or feces. Transmission can also occur through consumption of contaminated food, bites, and scratches. Infections with Seoul virus usually occur in urban settings such as in one's home. 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.
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. Infections are most common in spring. 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. 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. Repeated infections of hantaviruses have not been observed, so recovering from infection likely grants life-long immunity.
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. 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.
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