Batai virus

Batai virus (BATV) is a RNA virus belonging to order Bunyavirales, genus Orthobunyavirus.

Batai virus
Virus classification
Group V ((−)ssRNA)


Batai virus (BATV) is an enveloped, single-stranded, negative sense RNA genome.[1] It is a member of the genus Orthobunyavirus and belongs to the order Bunyavirales; it was first isolated from Culex mosquitoes in Malaysia in 1955.[2] Evidence from serological surveillance and virus isolation shows that this virus is widely distributed around the world. Similar to other orthobunyaviruses it contributes to both human and animal disease. In humans it has been noted in causing severe fever, and in bovines has been associated with premature birth, birth defects, and increased abortion rates. It is transmitted through mosquito bites, ticks, and biting midges, and occurs from cold to tropical regions of Africa, Asia, and Europe.[2]


The structure of Batai virus (BATV) consists of an enveloped nucleocapsid that is composed of three RNA segments: small (S), medium (M), and large (L). The S segment encodes the nucleocapsid (N) and the non-structural (NSs) proteins. The M segment encodes the virion surface glycoproteins (Gn, Gc) and non-structural proteins (NSm). The L segment encodes for the replicase/ transcriptase L protein. The nonstructural proteins NSm participate in virus assembly and NSs plays a key role in counteracting the host immune response by blocking alpha/beta interferon induction [3] The full-length genome of NM/12 consists of a 947 base pair nucleotide S segment, a 4405 base pair nucleotide M segment, and a 6870 base pair nucelotide L segment. It also contains one open reading frame that encode three proteins of 151, 943, or 1395 amino acids.[2]

Viral enveloped nucleocapsids utilize membrane glycoproteins on their surface to mediate entry into host cells. Averaging of glycoprotein spikes of membrane viruses, such as HIV-1, has been a particularly successful approach for studying their structure.[4] An understanding of the structure is integral for revealing both the molecular basis of virus–host interactions and guiding antiviral and vaccine design development. A software named Jsubtomo enables visualization of the structure of viral glycoprotein spikes to a resolution in the range of 20-40 Å and allows for study of the study of higher order spike-to-spike interactions on the virion membrane.[4]

Extensive research has yet to be performed on the detailed crystalline structure of Batai virus, but research on the closely related Bunyamwera virus has shown a distinct functionality of each of the two nucleocapsid side chains. An N-terminal arm and a C-terminal tail were found to interact with neighboring NP protomers to form a tetrameric ring-shaped organization. Each protomer bound a 10-nucleotide RNA molecule, which was acquired from the expression host, in the positively charged crevice between the N and C lobes.[5] Cryo-electron microscopy has also determined that whilst Bunyamwera virions are pleomorphic in shape, they display a locally ordered lattice of glycoprotein spikes. Each spike protrudes 18 nanometers from the viral membrane and becomes disordered upon introduction to an acidic environment.[6]

Although the exact icosahedral symmetry of a Batai virus viron is yet to be determined, studies using Cryo-electron tomography on related viruses of the Bunyaviridae family have shown that there exists an icosahedral lattice with clear T=12 quasisymmetry.[7] Consequently, this triangulation number would correlate with a viral nuclear capsid exhibiting 720 faces. This study was performed on the Rift Valley Fever Virus (RVFV), which is an arthropod borne disease that is endemic to regions of Africa and Asia, namely the Rift Valley in Kenya from which its name is derived.[8]

Viral Classification and Genome

Batai virus is a member of the genus Orthobunyavirus and a member of the family Bunyaviridae.[9] Batai virus is part of a diverse group of arthropod-borne viruses.[9] Classified via the Baltimore scheme, Batai virus is a negative-sense, single-stranded RNA virus.[9] The orthobunyavirus genome has a characteristic segmented genome, with small, medium, and large (S, M, and L) segments which generally encode the nucleocapsid, envelope protein and the polymerase protein, respectively.[9] The size of the S segment is 943 nucleotides, the size of the M segment is 4440 nucleotides, and the size of the L segment is 6870 nucleotides.[9] In the S segment there are two open reading frames (ORFs), the nucleocapsid and non-structurals which were overlapping.[9] The M segment has a polyprotein precursor in the open reading frame.[9] The L segment encodes for an RNA-dependent RNA polymerase.[9]

Batai virus is geographically spread throughout Asia and Europe. It has been shown that batai viruses from Japan, Malaysia and India share homologies in the genomic sequence more so than when virus strains from Europe and Asia are compared to each other. Reassortment of the genome can have some serious effects. It has been observed that reassortment between the M segment and the S and L segments with another strain of Batai virus (BUNV) can cause an increase in the virulence of Batai virus. Reassortment of the genome within the genus Orthobunyavirus are not uncommon and can lead to an increase in virulence.[2]

Replication of Batai Virus

It is well known that the geographical distribution of Batai virus (BATV) includes the regions of Europe, Asia and Africa. The most common vertebrate affected by BATV are domestic pigs, horses, ruminants and wild birds, which have been known to be the primary mammalian hosts. The transmission cycle of BATV occurs in agricultural ecosystems via Anopheles, Culex and Ochlerotatus species mosquitoes in a typical vertebrate–mosquito cycle.[9]

While limited research has been conducted on the viral cycle of the Batai virus, comparable studies with the close relative Bunyamwera virus has shown that viral infection begins in the salivary glands of mosquitos.[10] At the onset of replication the virus particles coalesce into vacuole membranes lining the cytoplasm of the infected cells.[11] Entry into the cell is facilitated by the viral enveloped nucleocapsid, which contains glycoproteins G1 and G2. Encoded by the M RNA segment they are involved in attachment to the host cell through unidentified receptors on the surface and elicit neutralizing antibodies. Transcription of BATV is said to be similar to that of influenza in that mRNA synthesis is primed by cap-containing oligonucleotides that are generated by a certain viral-endonuclease, functioning to cleave the host cell mRNA. These resulting primers are then incorporated into the viral mRNA.[12] BATV will also encode for two non-structural proteins, NSm on the M segment and NSs on the S segment. During the process it is believed that NSm actively participates in assembly of the virus. These newly assembled viral particles will mature over a period of time inside of the hosts cell in the membranes of the Golgi apparatus before being released.[11]

However, while able to replicate in both vertebrate and invertebrate species, in mosquito cells no cell death is observed and persistent infection is established. Whereas in mammalian cells infection is typically categorized as lytic and eventually leads to cell death. This stems from the viruses ability to form clear lytic plaques in cells of vertebrate species but not in those derived from insects.[13] It has been demonstrated in previous studies that in mammalian cells, the NSs protein will induce a shut-off of host protein synthesis which will lead to the death of the host cell. It has also been shown to counteract the host cell antiviral response.[14] This would establish it as the main virulence factor as it acts during the transcriptional phase by inhibiting RNA polymerase II–mediated transcription. Meanwhile, the mosquito cells neither host cell transcription nor translation are inhibited by this fact. It would seem the difference in the behavior of the NSs protein could be one of the factors responsible for the different outcomes of infection attributed to the Batai virus in mammalian and mosquito cells. Some have theorized that a release method that does not rupture the cell membrane could explain why viral replication does not kill mosquito cells and persistence is maintained.[13] Similar NSs proteins of the Rift Valley fever phlebovirus have quite a distinct size and amino acid sequence, but they play a similar role in mammalian cells in overcoming the innate immune responses that are a consequence of the global shut-down of the cells transcription mechanisms. Similar NSs proteins of the Rift Valley fever phlebovirus have quite a distinct size and amino acid sequence, but they play a similar role in mammalian cells in overcoming the innate immune responses that are a consequence of the global shut-down of the cells transcription mechanisms.[15]

Associated Diseases

Batai virus (BATV) is a member of the family Bunyaviridae.[2] Associated viruses include Crimean-Congo hemorrhagic fever, Bunyamwera orthobunyavirus, and severe fever with thrombocytopenia syndrome.[16]

Crimean-Congo hemorrhagic fever is one of the viruses that is associated with Batai virus, as it is in the same family Bunyaviridae. This occurs in the same areas throughout the world including Africa, Asia, Europe. It mainly infects farmworkers in these regions of the world, and is a tick-borne illness. Infection results in high fever, chills, severe headache, dizziness, back, and abdominal pains. Other symptoms that have been noted include nausea, vomiting, diarrhea, and cardiovascular and neuropsychiatric changes. If severe symptoms may include hemorrhages in the skin, causing lesions or bruising. It has a 30% fatality rate.[17]

A closely associated disease is the Bunyamwera virus, which is of the same family and genus as the Batai virus (BATV); it is known to cause Bunyamwera fever. This particular virus is spread by mosquitos biting infected mice and then biting humans.[18]

Batai virus (BATV) is also associated with severe fever with thrombocytopenia syndrome (SFTS). This was a recently discovered in China in 2011 and is transmitted either directly to humans through ticks, or to house pets as an intermediate host and then on to humans. Symptoms are characterized by fever, vomiting, diarrhea, thrombocytopenia and leukopenia. SFTS virus has a 6-30% fatality rate.[19]


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Adria virus

Adria virus (ADRV), named after the Adriatic Sea, is a phlebovirus transmitted by sandflies that can cause a febrile illness in people. It has been found in sandfly populations in Albania and northern Greece.

Amur virus

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.

Arbovirus encephalitis

Arbovirus encephalitis refers to encephalitis that is caused by arbovirus infection.There are many types of arboviral encephalitides found in the United States.Examples include:

California encephalitis

Japanese encephalitis

St. Louis encephalitis

Tick-borne encephalitis

West Nile fever

Murray Valley encephalitis

Bhanja virus

The Bhanja virus is a tick-borne Phlebovirus first discovered in a tick (Haemaphysalis intermedia) taken from a paralyzed goat in Bhanjanagar, India in 1954. Bhanja virus in humans was first documented in 1974 when Charles Calisher was working with the virus in a lab and contracted it himself. His experience with the virus was mild and included symptoms of mild aching in muscles and joints, moderate headache, slight photophobia. The Bhanja virus is a member of the Bhanja virus serocomplex and is a member of the Bunyavirales order.

Brazilian hemorrhagic fever

Brazilian hemorrhagic fever (BzHF) is an infectious disease caused by the Sabiá virus, an arenavirus. The Sabiá virus is one of the arenaviruses from South America to cause hemorrhagic fever. It shares a common progenitor with the Junin virus, Machupo virus, Tacaribe virus, and Guanarito virus. It is an enveloped RNA virus and is highly infectious and lethal. Very little is known about this disease, but it is thought to be transmitted by the excreta of rodents.There have only been three documented infections of the Sabiá virus, only one of which occurred naturally and the other two cases occurred in the clinical setting. The only naturally occurring case was in 1990, when a female agricultural engineer who was staying in the neighborhood of Jardim Sabiá near São Paulo, Brazil contracted the disease. She presented with hemorrhagic fever and died. Her autopsy showed liver necrosis. A virologist who was studying the woman's disease contracted the virus but survived. Ribavirin was not given in these first two cases. Four years later, in 1994, a researcher was exposed to the virus in a level 3 biohazard facility at Yale University when a centrifuge bottle cracked, leaked, and released aerosolized virus particle. He was successfully treated with ribavirin.Ribavirin is thought to be effective in treating the illness, similar to other arenaviruses. Compared to the patients who did not receive ribavirin, the patient who was treated with it had a shorter and less severe clinical course. Symptomatic control such as fluids to address dehydration and bleeding may also be required.The Sabiá virus is a biosafety Level 4 pathogen.This virus has also been implicated as a means for bioterrorism, as it can be spread through aerosols.

Bunyamwera orthobunyavirus

Bunyamwera orthobunyavirus (BUNV) is a negative-sense, single-stranded enveloped RNA virus. It is the type species of the Orthobunyavirus genus, in the Bunyavirales order.

Bunyamwera orthobunyavirus can infect both humans and Aedes aegypti (yellow fever mosquito).It is named for Bunyamwera, a town in western Uganda, where the type species was isolated in 1943. Reassortant viruses derived from Bunyamwera orthobunyavirus, such as Ngari virus, which has been associated with large outbreaks of viral haemorrhagic fever in Kenya and Somalia.

Chandipura vesiculovirus

Chandipura vesiculovirus (CHPV) is a member of the Rhabdoviridae family that is associated with an encephalitic illness in humans. It was first identified in 1965 after isolation from the blood of two patients from Chandipura village in Maharashtra state, India and has been associated with a number of otherwise unexplained outbreaks of encephalitic illness in central India. The most recent occurred in Andhra Pradesh and Maharashtra in June–August 2003 with 329 children affected and 183 deaths.

Further sporadic cases and deaths in children were observed in Gujarat state in 2004.Chandipura vesiculovirus has been isolated from sandflies in India and West Africa and is probably spread through its bite. The presence of the virus in Africa indicates a wide distribution although no human cases have been observed outside India.

The significance of Chandipura vesiculovirus as a human pathogen is unresolved due to doubts over its role in the 2003 and 2004 outbreaks.


Flaviviridae is a family of viruses. Humans and other mammals serve as natural hosts. They are primarily spread through arthropod vectors (mainly ticks and mosquitoes). The family gets its name from the yellow fever virus, the type virus of Flaviviridae; flavus is Latin for "yellow", and Yellow fever in turn was named because of its propensity to cause jaundice in victims. There are currently over 100 species in this family, divided among four genera. Diseases associated with this family include: hepatitis (hepaciviruses), hemorrhagic syndromes, fatal mucosal disease (pestiviruses), hemorrhagic fever, encephalitis, and the birth defect microcephaly (flaviviruses).

Hantaan orthohantavirus

Hantaan orthohantavirus (HTNV) is an enveloped, single-stranded, negative-sense RNA virus species of Old World Orthohantavirus. It is the causative agent of Korean Hemorrhagic Fever in humans. It is named for the Hantan River in South Korea, and in turn lends the name to its genus Orthohantavirus and family Hantaviridae.

Kemerovo tickborne viral fever

Kemerovo tickborne viral fever is an aparalytic febrile illness accompanied by meningism following tick-bite. The causative agent is a zoonotic Orbivirus first described in 1963 in western Siberia by Mikhail Chumakov and coworkers. The virus has some 23 serotypes, and can occur in coinfections with other Orbiviruses and tick-transmitted encephalitis viruses, complicating the course of illness. Rodents and birds are the primary vertebrate hosts of the virus; Ixodes persulcatus ticks are a vector of the virus. Kemerovo and related viruses may be translocated distances in the environment by migratory birds.

Lagos bat lyssavirus

Lagos bat lyssavirus, formerly Lagos bat virus (LBV) is a Lyssavirus of southern and central Africa that causes a rabies-like illness in mammals. It was first isolated from a fruit bat (Eidolon helvum) from Lagos Island, Nigeria in 1956. Brain samples from the bat showed poor cross-reactivity to rabies antibodies but the virus was found to be closely related to the rabies virus. This was the first discovery of a rabies-related virus. Until this time, rabies was thought to have a single causal agent.

Lagos bat lyssavirus has been isolated from wild and domestic mammals in southern Africa including bats, cats and one dog. One isolate was detected in France in 1999 when a fruit bat (Rousettus egypticus), which had been displaying signs of aggression, died. The bat had been imported from Africa.No human cases of Lagos bat lyssavirus infection have been documented.

Langat virus

Langat virus (LGTV) is a virus of the genus Flavivirus. The virus was first isolated in Malaysia in 1956 from a hard tick of the Ixodes genus. This virus is antigenically related to Omsk hemorrhagic fever virus, Kyasanur forest disease virus, Alkhurma virus, Louping ill virus and other viruses of the tick-borne encephalitis virus (TBEV) complex. The Langat virus does not pose a significant epidemiological threat in comparison with TBEV. There are no known cases of human diseases associated with LGTV. The Malaysian strain (LGT strain TP21, also known as the Yelantsev virus) is naturally attenuated and induces neutralizing antibodies to tick-borne encephalitis virus (TBEV) and protection against other TBEV complex viruses in animals.

Pappataci fever

Pappataci fever (also known as Phlebotomus fever and, somewhat confusingly, sandfly fever and three-day fever) is a vector-borne febrile arboviral infection caused by three serotypes of Phlebovirus. It occurs in subtropical regions of the Eastern Hemisphere. The name, pappataci fever, comes from the Italian word for sandfly, it is the union of the word "pappa" (food) and taci (silent) which distinguishes these insects from blood-feeding mosquitoes, which produce a typical noise while flying.

Ross River fever

Ross River fever is a mosquito-borne infectious disease caused by infection with the Ross River virus. The illness is typically characterised by an influenza-like illness and polyarthritis. The virus is endemic to mainland Australia and Tasmania, the island of New Guinea, Fiji, Samoa, the Cook Islands, New Caledonia and several other islands in the South Pacific.

Sandfly fever Naples phlebovirus

Sandfly fever Naples phlebovirus (SFNV) is an antigenic species of genus Phlebovirus within the family Phenuiviridae of the order Bunyavirales. It is an enveloped RNA virus with a tripartite genome e Uukuniemi (UUK) serogroup. The Sandfly group's natural reservoir are sandflies, while the natural reservoir for Uukuniemi is ticks. The SFNV serogroup consists of two main serocomplexes associated with disease in humans, the Naples and Sicilian serocomplexes. Sandfly fever induces myalgia, fever, and elevated liver enzymes in humans. It is difficult to diagnose outside endemic areas.


Tanapox (a virus from the genus Yatapoxvirus), was first seen among individuals in the flood plain of the Tana River in Kenya during two epidemics (1957 and 1962) of acute febrile illness accompanied by localized skin lesions.

Tete virus

Tete virus is a Bunyavirus found originally in Tete Province, Mozambique. It is a disease of animals and humans. Two forms, Bahig and Matruh viruses, were isolated from bird ticks including Hyalomma marginatum, but elsewhere mosquitoes and biting midges have been implicated as vectors.

Tick-borne encephalitis virus

Tick-borne encephalitis virus (TBEV) is the virus associated with tick-borne encephalitis.

Yaba monkey tumor virus

The Yaba monkey tumor virus is a type of poxvirus. The first case of the virus was obtained from a colony of rhesus monkeys in Yaba, Lagos, Nigeria. The virus caused the formation of tumors on the bodies of the monkeys. From these tumors the virus was isolated and determined to be its own species of virus. It is a species of the Yatapoxvirus genus and is closely related to the tanapox. The virus gets its name from the suburb of Yaba, Lagos.


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