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Senin, 31 Oktober 2011

Trojan SymbOS/Pbstealer

Disinfection
F-Secure Mobile Anti-Virus is capable to detecting and deleting the Pbstealer.E trojan.
Pbstealer.E tries to remove itself after sending data over Bluetooth. This self-removal doesn’t always work,  but fortunately it can be also removed by uninstalling it with Symbian application manager.
Additional Details
Trojan:SymbOS/Pbstealer.E steals information from a phone (Contacts, Notepad, Calendar, etc) and attempts to forward the stolen data to a random Bluetooth-accessible phone within range.
Payload
Pbstealer.E is distributed in a malicious SIS file that contains Pbstealer.E application file and string resource.
When the SIS file is installed, Pbstealer.E starts automatically and shows the following text:
Compacting your contact(s), step2
Please wait again
until done…
While showing the text, the Pbstealer.E reads all contacts information in the phone contact database, and copies the information to file C:\SYSTEM\MAIL\PHONEBOOK.TXT.
In addition to contacts information, Pbstealer.E also copies the contents of Notepad and Calendar ToDo database files. But, this information is not very readable to receiver as the resulting file contains in the databases is in binary form. If the Notepad and Calendar are empty, it simply fails in execution.
After building the text file, Pbstealer.E searches for the first device it finds over Bluetooth and sends the text file to it. When trying to send the file over Bluetooth, the Pbstealer.E uses repeated connection attempts, so that if user answers no, he will immediately get a second connection request. This technique is similar to the propagation tactic used by Cabir, except that Pbstealer will give up attempts after one minute and exit.
If the user of the target phone accepts the Bluetooth transfer, he will receive a text file that contains information copied from the infected phones contacts database.
Note
Although Pbstealer.E uses Bluetooth for sending phone book data, this data is pure text and cannot infect the receiving device.


Name : Trojan:SymbOS/Pbstealer.E
Category: Malware
Type: Trojan
Platform: SymbOS

SymbOS RommWar

SymbOS.RommWar including trojan virus category. Viruses of this type will put the kind of ‘small program’ to the target phone. The program can then make phone targets malfunction.
The symptoms of dysfunction depending on the version of the ROM software on the phone. Effects caused by rommwar diverse. Start from the hang, the phone restarts itself, to make the power button did not work. However, in some cases, these symptoms did not appear and the phone can run as usual.
Since Cabir, the virus first emerged as a scourge, the next generation of the virus posed a threat that is not less scary. No less than 148 viruses are ready to attack mobile phones with Symbian operating system. Not to mention the threat of viruses for Windows Mobile.
The technology of mobile phone virus is now growing up to be able to jump from PC to mobile platforms. The latest news, mobile Java 2 virus began roaming in cyberspace. More than 80% of mobile phones in circulation is now capable of running java applications. It means that the virus could strike most of the phones, which do not even operating system!
Until now SymbOS.Rommwar has evolved and has four variants, namely:
- RommWar.A
RommWar A will give the effect varies, depending on the version of the ROM software on the phone. The first variant is experiencing hangs and causes the phone to be restarted again. Shortly after the restart, the phone will have to hang back. To do this, utilize the functionality of this Rommwar MIME recognizer
- RommWar.B
This second variant Rommwar will restart the phone by itself and will prevent the phone to boot.
- RommWar.C
Same as version B. This virus will block the phone to light up!
- RommWar.D
This latest variant RommWar effect ranged from mobile phones can not turn on until the power button is not functioning. Interestingly, the installation SymbOS / RommWar sometimes also ‘boarded’ by the installation of Kaspersky Anti-Virus Mobile is not perfect.
RommWar virus is like an extension symbian sis application. His name can change all sorts. During installation, usually Rommwar will display a message such as pictures or later if the installation is complete and when the user opens the file system of phones, you’ll see the files as shown below.
[DRIVE LETTER] \ system \ apps \ klantivirus \ b.dat
[DRIVE LETTER] \ system \ apps \ klantivirus \ engine.exe
[DRIVE LETTER] \ system \ apps \ klantivirus \ Installer.exe
[DRIVE LETTER] \ system \ apps \ klantivirus \ klantivirus.aif
[DRIVE LETTER] \ system \ apps \ klantivirus \ klantivirus.app
[DRIVE LETTER] \ system \ apps \ klantivirus \ klantivirus.rsc
[DRIVE LETTER] \ system \ apps \ klantivirus \ klantivirus_caption.rsc
[DRIVE LETTER] \ system \ apps \ klantivirus \ klimages.mbm
[DRIVE LETTER] \ system \ apps \ klantivirus \ s.mid
[DRIVE LETTER] \ system \ help \ klantivirushelp.hlp
[DRIVE LETTER] \ system \ libs \ klsdll.dll
[DRIVE LETTER] \ system \ libs \ klsdll.idb
c: \ system \ recogs \ kl_antivirus.mdl
[DRIVE LETTER] \ system \ apps \ klantivirus \ startup.app
[DRIVE LETTER] \ system \ apps \ klantivirus \ startup.r02
The two files below are source of the problem. Both of these files are corrupted files that would cause the initiation of cell phones fail when restarting.
[DRIVE LETTER] \ system \ apps \ klantivirus \ startup.app
[DRIVE LETTER] \ system \ apps \ klantivirus \ startup.r02
[DRIVE LETTER] shows the place where the phone is a file system. Usually found in drive C.
Sometimes Rommwar also displays the following message:
“End User Software License Agreement” Kaspersky Antivirus Mobile “2006 License AVDS-Seop-1RIW-7EWD is a registered version by …”
Most anti-virus mobile phone is now able to recognize the latest mobile phone viruses and remove it immediately. Condition, should perform regular virus updates definitionnya. Virus definition for an anti-virus is essential to detect and eliminate the negative effects on the cell phone.
Another preventive measure, regular backuplah important data such as phonebook, reminder, SMS, and others. almost all symbian phones have been providing PC suite CD which can be exploited to create a backup file on your PC.
Handling
If it is still possible, and normal phone, delete the files contained in the above list by using a file manager like FExplorer application.
Then uninstall Rommwarrior through the application manager. If there is an indication hangs when running the application you just installed.
If the damage is already too severe hangs up the phone at all and can not restart, perform the following steps.
- In case of hang, disconnect the phone’s battery until the phone is off. Then plug it back
- Do the hard reset;
a. Press and hold simultaneously three key pieces of the call button (green) + “*” key and the number “3″
b. Press the power button while still holding the three keys
c. Depending on the type of phone, will get the message “formatting” or startup dialog stating that the phone will return to the initial setting
- The phone is now formatted and can be reused
Remember, this step will erase all existing data on the phone, including the phonebook and sms.

Sabtu, 29 Oktober 2011

Virus Family Alphaflexiviridae

Alphaflexiviridae are single-stranded positive sense RNA plant viruses, belonging to the order Tymovirales and thus to group IV of the Baltimore classification of viruses.


The Alphaflexiviridae family include the following genera:

    Genus Allexivirus; type species: Shallot virus X
    Genus Botrexvirus;
    Genus Lolavirus;
    Genus Mandarivirus; type species: Indian citrus ringspot virus
    Genus Potexvirus; type species: Potato virus X
    Genus Sclerodarnavirus;


References

    ICTV Virus Taxonomy 2009
    UniProt Taxonomy

Minggu, 23 Oktober 2011

Family Secoviridae Virus

The Secoviridae are a family of Group IV (positive-sense ssRNA) plant-infecting viruses in the order Picornavirales.
Several plant viruses share features with animal and human viruses of the family Picornaviridae, including a conserved structure of both the virus particle and the viral genome, expressing viral proteins by proteolytic cleavage of large polyproteins and encoding replication proteins with conserved sequence motifs. Members of the family Comoviridae were originally described as the only plant picorna-like viruses. Other plant picorna-like viruses were later discovered and classified in the family Sequiviridae. Sequiviridae and Comoviridae are related to each other in phylogenetic studies and share the common property of encoding specialized proteins to enable their movement in the plant. Recently, it was proposed to regroup plant picorna-like viruses into a single family termed ‘secoviridae’. The proposed family amalgamates the families Comoviridae and Sequiviridae, and incorporates other plant picorna-like viruses currently classified in the genera Sadwavirus and Cheravirus, and the proposed genus ‘Torradovirus’.
Key concepts:

    Many plant viruses are related to the animal and human picornaviridae and to other picorna-like viruses infecting algae and arthropods.
    A recent update in the taxonomy of plant picorna-like viruses has lead to the creation of the family ‘secoviridae’ which amalgamates the families Comoviridae and Sequiviridae as well as the existing genera Cheravirus, Sequivirus and the proposed genus ‘torradovirus’.
    Secoviridae share many common characteristics including having both similar virus particle structures and genomic organizations, and requiring a specialized protein to facilitate their movement within the host plant.
    Secoviridae produce their proteins in the form of large polyproteins that are cleaved at specific sites by a viral proteinase.
    Replication of the viral RNA occurs in large protein complexes in association with intracellular membranes from the host.
    Plant cells infected with secoviridae generally display tubular structures that are composed of the viral movement protein, contain virus-like particles and traverse the cell wall. These tubular structures are probably involved in the movement of the virus from cell to cell.
    Secoviridae can be transmitted through seeds and pollen or with the help of nematode or arthropod vectors and their spread in the field is largely dependent on their mode of transmission.

Family Potyviridae Virus

The Picornaviridae family (picornaviruses) causes a wider range of illnesses than most other, if not all, virus families. Infection with various picornaviruses may be asymptomatic or may cause clinical syndromes such as aseptic meningitis (the most common acute viral disease of the CNS), encephalitis, the common cold, febrile rash illnesses (hand-foot-and-mouth disease), conjunctivitis, herpangina, myositis and myocarditis, and hepatitis.

Poliomyelitis, caused by the enteroviral type species, was one of the first recorded infections; an Egyptian tomb carving showed a man with a foot-drop deformity typical of paralytic poliomyelitis.
Characteristics

The term Picornaviridae is derived from pico, which means small (typically, 18-30 nm), and RNA, referring to the single-stranded positive-sense RNA common to all members of the Picornaviridae family. All members of this family, whose RNA molecules range from 7.2-8.5 kilobases (kb) in size, lack a lipid envelope and are therefore resistant to ether, chloroform, and alcohol. However, ionizing radiation, phenol, and formaldehyde readily inactivate picornaviruses.

The viral capsid of picornaviruses consists of a densely packed icosahedral arrangement of 60 protomers. Each protomer consists of 4 polypeptides, etoposide (VP) 1, 2, 3, and 4, which all derive from the cleavage of a larger protein. The capsid-coat protein serves multiple functions, including (1) protecting the viral RNA from degradation by environmental RNAse, (2) determining host and tissue tropism by recognition of cell-specific cell-membrane receptors, (3) penetrating target cells and delivering the viral RNA into the cell cytoplasm, and (4) selecting and packaging viral RNA.

Two genera of Picornaviridae— enterovirus and rhinovirus —have an identical morphology but can be distinguished based on clinical, biophysical, and epidemiological studies. Enteroviruses grow at a wide pH range (ie, 3-10). After initial replication in the oropharynx, enteroviruses survive the acidic environment of the stomach. The small intestine is the major invasion site of enteroviruses, which replicate best at 37°C. Rhinoviruses replicate at a pH of 6-8. After initial replication in the nasal passages, the acidic environment of the stomach destroys rhinoviruses. Rhinoviruses optimally replicate at 33°C and primarily infect the nasal mucosa.[4]
Classification[1, 3, 2]

Enteroviruses have several subgroups: 3 serotypes of polioviruses, 23 serotypes of group A coxsackieviruses, 6 serotypes of group B coxsackieviruses, and at least 31 serotypes of echoviruses. (ECHO virus is a misnomer based on the acronym enteric cytopathic human orphan virus.) Viruses are grouped according to pathogenicity, host range, and serotype, which is based on serum neutralization. Some enteroviruses are not classified further but rather assigned a number, currently 68 to 71. Bovine, equine, simian, porcine, and rodent enteroviruses also exist.

Overall, the family Picornaviridae includes 9 genera. In addition to the major human enteroviral pathogens (poliovirus, enterovirus, coxsackievirus, echovirus), rhinoviruses (approximately 105 serotypes), the human hepatitis A virus (HAV), and several parechoviruses, Picornaviridae contains several other genera of viruses that infect nonhuman vertebrate hosts.

Cardiovirus (type species, encephalomyocarditis virus) is a classic infection in mice, although it has been observed to cause disease in humans.[5] Certain strains of this virus are associated with the development of diabetes in certain strains of mice and are used as a model for virus-associated insulin-requiring diabetes in humans.

Aphthovirus (type species, foot-and-mouth disease virus [FMDV]) creates a major worldwide economic problem, particularly in South America and Australia. FMDV, which has 7 serotypes, is largely controlled by the immunization or slaughter of infected animals. Aphthoviruses are more acid-labile than other picornaviruses.

The other genera include Parechovirus, Erbovirus (equine rhinitis B virus), Kobuvirus (Aichi virus), and Teschovirus (porcine teschovirus). Arthropod-infecting viruses, including Cricket paralysis virus, Drosophila C virus, and Tussock moth virus, are additional unclassified picornaviruses.

Family Picornaviridae Virus

A picornavirus is a virus belonging to the family Picornaviridae. Picornaviruses are non-enveloped, positive-stranded RNA viruses with an icosahedral capsid. The genome RNA is unusual because it has a protein on the 5' end that is used as a primer for transcription by RNA polymerase. The name is derived from pico, meaning small, and RNA, referring to the ribonucleic acid genome, so "picornavirus" literally means small RNA virus.

Picornaviruses are separated into a number of genera and include many important pathogens of humans and animals. The diseases they cause are varied, ranging from acute "common-cold"-like illnesses, to poliomyelitis, to chronic infections in livestock. Additional species not belonging to any of the recognised genera continue to be described.

Taxonomy
Picornaviruses are separated into a number of genera. Contained within the picornavirus family are many organisms of importance as vertebrate and human pathogens, shown in the table below.

Enteroviruses infect the enteric tract, which is reflected in their name. On the other hand, rhinoviruses infect primarily the nose and the throat. Enteroviruses replicate at 37°C, whereas rhinoviruses grow better at 33°C, as this is the lower temperature of the nose. Enteroviruses are stable under acid conditions and thus they are able to survive exposure to gastric acid. In contrast, rhinoviruses are acid-labile (inactivated or destroyed by low pH conditions) and that is the reason why rhinovirus infections are restricted to the nose and throat.

Plant picornaviruses
The plant picornaviruses have a number of properties that are distinct from the animal viruses. They have been classified into the family Secoviridae containing the subfamily Comovirinae (genera Comovirus, Fabavirus and Nepovirus), and genera Sequivirus, Waikavirus, Cheravirus, Sadwavirus and Torradovirus (type species Tomato torrado virus).

Insect picornaviruses
A number of picorna like viruses have been described infecting insects. These include Perina nuda picorna-like virus of the tussock moth, infectious flacherie virus of the silkworm and Sacbrood virus of the honeybee, Plautia stali intestine virus kelp fly virus, Ectropis obliqua picorna-like virus, deformed wing virus, acute bee paralysis virus, Drosophila C virus, Rhopalosiphum padi virus, and Himetobi P virus. Most of these have been placed in a separate family - the Dicistroviridae.

Virology
Picornaviruses are classed under Baltimore's viral classification system as group IV viruses as they contain a single stranded, positive sense RNA genome of between 7.2 and 9.0 kb (kilobases) in length. Like most positive sense RNA genomes, the genetic material alone is infectious; although substantially less virulent than if contained within the viral particle, the RNA can have increased infectivity when transfected into cells.

Structure
The capsid is an arrangement of 60 protomers in a tightly packed Icosahedral structure. Each protometer consists of 4 polypeptides known as VP (viral protein)1, 2, 3 and 4. VP2 and VP4 polypeptides originate from one protomer known as VP0 that is cleaved to give the different capsid components. The Icosahedral is said to have a triangulation number of 3, this means that in the icosahedral structure each of the 60 triangles that make up the capsid are split into 3 little triangles with a subunit on the corner. Depending on the type and degree of dehydration the viral particle is around 27-30 nm in diameter. The viral genome is around 2500 nm in length so we can therefore conclude that it must be tightly packaged within the capsid along with substances such as sodium ions in order to cancel out the negative charges on the RNA caused by the phosphate groups.

Genome
The genome itself is the same sense as mammalian mRNA, being read 5' to 3'. Unlike mammalian mRNA picornaviruses do not have a 5' cap but a virally encoded protein known as VPg. However, like mammalian mRNA, the genome does have a poly(A) tail at the 3' end. There is an un-translated region (UTR) at both ends of the picornavirus genome. The 5' UTR is longer, being around 600-1200 nucleotides (nt) in length, compared to that of the 3' UTR, which is around 50-100 nt. It is thought that the 5' UTR is important in translation and the 3' in negative strand synthesis; however the 5' end may also have a role to play in virulence of the virus. The rest of the genome encodes structural proteins at the 5' end and non-structural proteins at the 3' end in a single polyprotein.

Replication
The viral particle binds to cell surface receptors. This causes a conformational change in the viral capsid proteins, and myristic acid are released. These acids form a pore in the cell membrane through which RNA is injected. Once inside the cell, the RNA un-coats and the (+) strand RNA genome is replicated through a double-stranded RNA intermediate that is formed using viral RDRP (RNA-Dependent RNA polymerase). Translation by host cell ribosomes is not initiated by a 5' G cap as usual, but rather is initiated by an IRES (Internal Ribosome Entry Site). The viral lifecycle is very rapid with the whole process of replication being completed on average within 8 hours. However as little as 30 minutes after initial infection, cell protein synthesis declines to almost zero output – essentially the macromolecular synthesis of cell proteins is “shut off”. Over the next 1–2 hours there is a loss of margination of chromatin and homogeneity in the nucleus, before the viral proteins start to be synthesized and a vacuole appears in the cytoplasm close to the nucleus that gradually starts to spread as the time after infection reaches around 3 hours. After this time the cell plasma membrane becomes permeable, at 4–6 hours the virus particles assemble, and can sometimes be seen in the cytoplasm. At around 8 hours the cell is effectively dead and lyses to release the viral particles.

Experimental data from single step growth-curve-like experiments have allowed scientists to look at the replication of the picornaviruses in great detail. The whole of replication occurs within the host cell cytoplasm and infection can even happen in cells that do not contain a nucleus (known as enucleated cells) and those treated with actinomycin D (this antibiotic would inhibit viral replication if this occurred in the nucleus.)

History
In 1897, foot-and-mouth disease virus (FMDV), the first animal virus, was discovered. FMDV is the prototypic member of the Aphthovirus genus in the Picornaviridae family.[3] The plaque assay was developed using poliovirus. Both RNA dependent RNA polymerase and polyprotein synthesis were discovered by studying poliovirus infected cells.

See also
Dicistroviridae
VPg
Animal viruses

Family Marnaviridae Virus

Marnaviridae is a family of Virus which a single sort is known, Marnavirus . The infected species type to the microscopic alga Heterosigma akashiwo . contains Genome ARN monocatenary positive and therefore Classification of Baltimore is included in Group IV of . virus particles present/display one isometric Cápside with icosahedral symmetry and lack envelope . The length of the genome is of approximately 9000 Nucleotides

An RNA virus is a virus that has RNA (ribonucleic acid) as its genetic material. This nucleic acid is usually single-stranded RNA (ssRNA) but may be double-stranded RNA (dsRNA). The ICTV classifies RNA viruses as those that belong to Group III, Group IV or Group V of the Baltimore classification system of classifying viruses, and does not consider viruses with DNA intermediates as RNA viruses. Notable human diseases caused by RNA viruses include SARS, influenza and hepatitis C. Another term for RNA viruses that explicitly excludes retroviruses is ribovirus.

RNA viruses can be further classified according to the sense or polarity of their RNA into negative-sense and positive-sense, or ambisense RNA viruses. Positive-sense viral RNA is similar to mRNA and thus can be immediately translated by the host cell. Negative-sense viral RNA is complementary to mRNA and thus must be converted to positive-sense RNA by an RNA polymerase before translation. As such, purified RNA of a positive-sense virus can directly cause infection though it may be less infectious than the whole virus particle. Purified RNA of a negative-sense virus is not infectious by itself as it needs to be transcribed into positive-sense RNA, however each virion can be transcribed to several positive-sense RNAs. Ambisense RNA viruses resemble negative-sense RNA viruses, except they also translate genes from the positive strand.

Double-stranded RNA viruses
Further information: Double-stranded RNA viruses
The double-stranded (ds)RNA viruses represent a diverse group of viruses that vary widely in host range (humans, animals, plants, fungi, and bacteria), genome segment number (one to twelve), and virion organization (T-number, capsid layers, or turrets). Members of this group include the rotaviruses, renowned globally as the most common cause of gastroenteritis in young children, and bluetongue virus, an economically important pathogen of cattle and sheep. In recent years, remarkable progress has been made in determining, at atomic and subnanometeric levels, the structures of a number of key viral proteins and of the virion capsids of several dsRNA viruses, highlighting the significant parallels in the structure and replicative processes of many of these viruses.

Mutation rates
RNA viruses generally have very high mutation rates compared to DNA viruses, because viral RNA polymerases lack the proof-reading ability of DNA polymerases] This is one reason why it is difficult to make effective vaccines to prevent diseases caused by RNA viruses. Retroviruses also have a high mutation rate even though their DNA intermediate integrates into the host genome (and is thus subject to host DNA proofreading once integrated), because errors during reverse transcription are embedded into both strands of DNA before integration. Some genes of RNA virus are important to the viral replication cycles and mutations are not tolerated. For example, the region of the hepatitis C virus genome that encodes the core protein is highly conserved, because it contains an RNA structure involved in an internal ribosome entry site.

Replication
Animal RNA viruses are classified into three distinct groups depending on their genome and mode of replication (and the numerical groups based on the older Baltimore classification):

    Double-stranded RNA viruses (Group III) contain from one to a dozen different RNA molecules, each of which codes for one or more viral proteins.
    Positive-sense ssRNA viruses (Group IV) have their genome directly utilized as if it were mRNA, producing a single protein which is modified by host and viral proteins to form the various proteins needed for replication. One of these includes RNA-dependent RNA polymerase, which copies the viral RNA to form a double-stranded replicative form, in turn this directs the formation of new virions.
    Negative-sense ssRNA viruses (Group V) must have their genome copied by an RNA polymerase to form positive-sense RNA. This means that the virus must bring along with it the RNA-dependent RNA polymerase enzyme. The positive-sense RNA molecule then acts as viral mRNA, which is translated into proteins by the host ribosomes. The resultant protein goes on to direct the synthesis of new virions, such as capsid proteins and RNA replicase, which is used to produce new negative-sense RNA molecules.

Retroviruses (Group VI) have a single-stranded RNA genome but are generally not considered RNA viruses because they use DNA intermediates to replicate. Reverse transcriptase, a viral enzyme that comes from the virus itself after it is uncoated, converts the viral RNA into a complementary strand of DNA, which is copied to produce a double stranded molecule of viral DNA. After this DNA is integrated, expression of the encoded genes may lead the formation of new virions.
Classification

Classification of the positive strand RNA viruses is based on the RNA dependent RNA polymerase. Three groups have been recognised:

I. Bymoviruses, comoviruses, nepoviruses, nodaviruses, picornaviruses, potyviruses, sobemoviruses and a subset of luteoviruses (beet western yellows virus and potato leafroll virus) - the picorna like group (Picornavirata).

II. Carmoviruses, dianthoviruses, flaviviruses, pestiviruses, tombusviruses, single-stranded RNA bacteriophages, hepatitis C virus and a subset of luteoviruses (barley yellow dwarf virus) - the flavi like group (Flavivirata).

III. Alphaviruses, carlaviruses, furoviruses, hordeiviruses, potexviruses, rubiviruses, tobraviruses, tricornaviruses, tymoviruses, apple chlorotic leaf spot virus, beet yellows virus and hepatitis E virus - the alpha like group (Rubivirata).

The alpha like groups can be further divided into three clades: the rubi-like, tobamo-like, and tymo-like viruses.

Additional work has identified five groups of positive stranded RNA viruses containing four, three, three, three and one order(s) respectively. These fourteen orders contain 31 virus families (including 17 families of plant viruses) and 48 genera (including 30 genera of plant viruses). This analysis suggests that alphaviruses and flaviviruses can be separated into two families - the Togaviridae and Flaviridae respectively - but suggests that other taxonomic assignments, such as the pestiviruses, hepatitis C virus, rubiviruses, hepatitis E virus and arteriviruses, may be incorrect. The coronaviruses and toroviruses appear to be distinct families in distinct orders and not distinct genera of the same family as currently classified. The luteoviruses appear to be two families rather than one and apple chlorotic leaf spot virus appears not to be a closterovirus but a new genus of the Potexviridae.

This analysis also suggests that the dsRNA viruses are not closely related to each other but instead belong to four additional classes - Birnaviridae, Cystoviridae, Partitiviridae and Reoviridae - and one additional order (Totiviridae) of one of the classes of positive ssRNA viruses in the same subphylum as the positive strand RNA viruses.

These proposals were based on an analysis of the RNA polymerases and are still under consideration. To date they have not been broadly accepted because of doubts over the suitability of a single gene to determine the taxonomy of the clade.

Virus Family Iflaviridae

General Description
This genus (the sole member of the family Iflaviridae, contains viruses of invertebrates that belong in the picornavirus "superfamily", and which share a number of features, both of virion structure and genomic organisation, of members of the families Picornaviridae and Dicistroviridae but which form a distinct group in phylogenetic analyses. It is named from the type member, Infectious flacherie virus.

Morphology
Virions isometric (icosahedral), not enveloped 30 nm in diameter.

Genome
Monopartite, linear, positive sense single-stranded RNA of 8.5-10 kb. There is a genome-linked protein (VPg) at the 5'-terminus and a 3'-polyA tail.

Genus Genomic Organization
The RNA encodes a single polyprotein of 330-350 kDa that is subsequently processed into the functional products. The 3 (or sometimes 4) coat proteins are encoded near the N-terminus.

Type Member Genomic Organization
The RNA encodes a single polyprotein of 346 kDa that is subsequently processed into the functional products. The 3 coat proteins are encoded near the N-terminus and the non-structural proteins contain the recognised motifs for the RNA helicase, cysteine protease and the RNA polymerase.

Family Dicistroviridae Virus

The Dicistroviridae are a family of Group IV (positive-sense ssRNA) insect-infecting viruses. Some of the insects commonly infected by dicistroviruses include aphids, leafhoppers, flies, bees, ants, silkworms.

Taxonomy
Although many dicistroviruses were initially placed in the Picornaviridae they have since been reclassified into their own family. The name (Dicistro) is derived from the characteristic di-cistronic arrangement of the genome.

This family is a member of the 'picornavirus-like superfamily' (Comoviridae, Iflavirus, Picornaviridae, Potyviridae and Sequiviridae). Within this superfamily the gene order is the gene order of the non-structural proteins Hel(helicase)-Pro(protease)-RdRp(polymerase). The Dicistroviridae can be distinguished from the members of the taxa by the location of the their genome's organisation: the structural proteins are located at the 3' end rather than the 5' end (as found in Iflavirus, Picornaviridae and Sequiviridae) and by having 2 genomic segments rather than a single one (as in the Comoviridae).

This family has been divided into two genera and a number of as yet unclassified species.

    Genus Cripavirus:
        Aphid lethal paralysis virus
        Black queen cell virus
        Cricket paralysis virus (type species)
        Drosophila C virus
        Himetobi P virus
        Homalodisca coagulata virus-1
        Plautia stali intestine virus
        Rhopalosiphum padi virus
        Triatoma virus

    Genus: Aparavirus
        Acute bee paralysis virus (type species)
        Israeli acute paralysis virus
        Kashmir bee virus
        Solenopsis invicta virus 1
        Taura syndrome virus

Other species:

    Cloudy wing virus
    Blackberry virus Z
    Acheta domesticus virus
    Ervivirus
    Mud crab dicistrovirus
The Dicistroviridae are a family of Group IV (positive-sense ssRNA) insect-infecting viruses. Some of the insects commonly infected by dicistroviruses include aphids, leafhoppers, flies, bees, ants, silkworms.

Notable species

    Aphid lethal paralysis virus
    Black queen cell virus – a Western honey bee virus
    Bombyx mori infectious flacherie virus (BmIFV) – a silkworm virus
    Cricket paralysis virus
    Drosophila C virus
    Himetobi P virus
    Plautia stali intestine virus
    Rhopalosiphum padi virus
    Taura syndrome virus
    Triatoma virus
    Homalodisca coagulata virus 1 (HoCV-1) – a sharpshooter virus
    Solenopsis invicta virus 1 (SINV-1) – a Red imported fire ant virus


RNA structural elements
Many of the Dicistroviridae genomes contains structured RNA elements. For example, the Cripaviruses have an internal ribosome entry site, which mimics a Met-tRNA and is used in the initiation of translation

Family Roniviridae Virus

Coronaviridae is a family of virus of the order Nidovirales. The name is derived from their rod like shape - rod like nidoviridae.

Virology
The viruses in this family are enveloped, bacilliform-shaped, ~150-200 nanometers (nm) in length and 40-60 nm in diameter. The envelope has surface projections. These surface projections are prominent, distinctive peplomers surrounded by a prominent fringe. The nucleocapsid is elongated and has a helical symmetry with a diameter of 20-30 nm.

The genome is non segmented, linear,positive sense single stranded RNA 26 kilobases in length. It is capped, and polyadenylated.

The genome encodes 6 open reading frames (ORF). The 5' and largest OFRs (OFR1a and ORF 1b) encode the RNA polymerase and other non structurla proteins. OFR 1a is encoded by the genomic RNA. ORF 1b is encoded by a frameshift within OFR 1a and the sequence 3' of ORF 1b. The structural proteins (N, Gp116, Gp64 and ORF 4) are transcribed as sub genomic RNAs.

Proein encoded with the genome include a cysteine protease, RNA-dependent RNA polymerase, helicase and metal ion binding domains, nucleoprotein, and S glycoproteins.

This family is grouped with the Coronaviridae and Arteriviridae to form the order Nidovirales. All members of the order have enveloped particles containing a single species of single-stranded RNA that encodes for a number of proteins by means of a series of nested (Latin Nido = nest) subgenomic RNAs. Members of the family Roniviridae infect crustaceans and are distinguished by their bacilliform particles (hence the name rod-shaped nidovirus). Members of the family Arteriviridae have spherical virions 45-60nm in diameter, while those of the family Coronaviridae are more than 100nm, and all infect mammals.

Morphology
Virions enveloped and bacilliform, 150-200 nm x 40-60 nm.

Genome
Monopartite positive sense single-stranded RNA of size about 26kb and with a 3'-polyA tail. Two large, overlapping ORFs at the 5'-end of the genome encode the major non-structural proteins and are expressed as a fusion protein by ribosomal frameshift. Downstream are about 4 other genes, encoding structural proteins, and these are expressed from a 3'-coterminal nested set of subgenomic RNAs.

Genera in the Family
There is currently only one genus:

Okavirus

Sabtu, 22 Oktober 2011

Family Coronaviridae Virus

Coronaviruses are species in the genera of virus belonging to the subfamily Coronavirinae in the family Coronaviridae.
Coronaviruses are enveloped viruses with a positive-sense single-stranded RNA genome and a helical symmetry. The genomic size of coronaviruses ranges from approximately 16 to 31 kilobases, extraordinarily large for an RNA virus. The name "coronavirus" is derived from the Greek κορώνα, meaning crown, as the virus envelope appears under electron microscopy (E.M.) to be crowned by a characteristic ring of small bulbous structures. This morphology is actually formed by the viral spike (S) peplomers, which are proteins that populate the surface of the virus and determine host tropism. Coronaviruses are grouped in the order Nidovirales, named for the Latin nidus, meaning nest, as all viruses in this order produce a 3' co-terminal nested set of subgenomic mRNA's during infection.

Proteins that contribute to the overall structure of all coronaviruses are the spike (S), envelope (E), membrane (M) and nucleocapsid (N). In the specific case of SARS (see below), a defined receptor-binding domain on S mediates the attachment of the virus to its cellular receptor, angiotensin-converting enzyme 2 (ACE2). Members of the group 2 coronaviruses also have a shorter spike-like protein called hemagglutinin esterase (HE) encoded in their genome, but for some reason this protein is not always brought to expression (produced) in the cell.

Diseases of coronavirus
Coronaviruses primarily infect the upper respiratory and gastrointestinal tract of mammals and birds. Four to five different currently known strains of coronaviruses infect humans. The most publicized human coronavirus, SARS-CoV which causes SARS, has a unique pathogenesis because it causes both upper and lower respiratory tract infections and can also cause gastroenteritis. Coronaviruses are believed to cause a significant percentage of all common colds in human adults. Coronaviruses cause colds in humans primarily in the winter and early spring seasons. The significance and economic impact of coronaviruses as causative agents of the common cold are hard to assess because, unlike rhinoviruses (another common cold virus), human coronaviruses are difficult to grow in the laboratory.

Coronaviruses also cause a range of diseases in farm animals and domesticated pets, some of which can be serious and are a threat to the farming industry. Economically significant coronaviruses of farm animals include porcine coronavirus (transmissible gastroenteritis coronavirus, TGE) and bovine coronavirus, which both result in diarrhea in young animals. Feline Coronavirus: 2 forms, Feline enteric coronavirus is a pathogen of minor clinical significance, but spontaneous mutation of this virus can result in feline infectious peritonitis (FIP), a disease associated with high mortality. There are two types of canine coronavirus (CCoV), one that causes mild gastrointestinal disease and one that has been found to cause respiratory disease. Mouse hepatitis virus (MHV) is a coronavirus that causes an epidemic murine illness with high mortality, especially among colonies of laboratory mice. Prior to the discovery of SARS-CoV, MHV had been the best-studied coronavirus both in vivo and in vitro as well as at the molecular level. Some strains of MHV cause a progressive demyelinating encephalitis in mice which has been used as a murine model for multiple sclerosis. Significant research efforts have been focused on elucidating the viral pathogenesis of these animal coronaviruses, especially by virologists interested in veterinary and zoonotic diseases.

Replication
The infection cycle of coronavirus
Replication of Coronavirus begins with entry to the cell takes place in the cytoplasm in a membrane-protected microenvironment, upon entry to the cell the virus particle is uncoated and the RNA genome is deposited into the cytoplasm. The Coronavirus genome has a 5’ methylated cap and a 3’polyadenylated-A tail to make it look as much like the host RNA as possible. This also allows the RNA to attach to ribosomes for translation. Coronaviruses also have a protein known as a replicase encoded in its genome which allows the RNA viral genome to be transcribed into new RNA copies using the host cells machinery. The replicase is the first protein to be made as once the gene encoding the replicase is translated the translation is stopped by a stop codon. This is known as a nested transcript, where the transcript only encodes one gene- it is monocistronic. The RNA genome is replicated and a long polyprotein is formed, where all of the proteins are attached. Coronaviruses have a non-structural protein called a protease which is able to separate the proteins in the chain. This is a form of genetic economy for the virus allowing it to encode the most amounts of genes in a small amount of nucleotides.

Coronavirus transcription involves a discontinuous RNA synthesis (template switch) during the extension of a negative copy of the subgenomic mRNAs. Basepairing during transcription is a requirement. Coronavirus N protein is required for coronavirus RNA synthesis, and has RNA chaperone activity that may be involved in template switch. Both viral and cellular proteins are required for replication and transcription. Coronaviruses initiate translation by cap-dependent and cap-independent mechanisms. Cell macromolecular synthesis may be controlled after Coronavirus infection by locating some virus proteins in the host cell nucleus. Infection by different coronaviruses cause in the host alteration in the transcription and translation patterns, in the cell cycle, the cytoskeleton, apoptosis and coagulation pathways, inflammation, and immune and stress responses.

Severe acute respiratory syndrome
Main article: Severe acute respiratory syndrome
In 2003, following the outbreak of Severe acute respiratory syndrome (SARS) which had begun the prior year in Asia, and secondary cases elsewhere in the world, the World Health Organization issued a press release stating that a novel coronavirus identified by a number of laboratories was the causative agent for SARS. The virus was officially named the SARS coronavirus (SARS-CoV).

The SARS epidemic resulted in over 8000 infections, about 10% of which resulted in death. X-ray crystallography studies performed at the Advanced Light Source of Lawrence Berkeley National Laboratory have begun to give hope of a vaccine against the disease "since [the spike protein] appears to be recognized by the immune system of the host."

Recent discoveries of novel human coronaviruses
Following the high-profile publicity of SARS outbreaks, there has been a renewed interest in coronaviruses in the field of virology. For many years, scientists knew only about the existence of two human coronaviruses (HCoV-229E and HCoV-OC43). The discovery of SARS-CoV added another human coronavirus to the list. By the end of 2004, three independent research labs reported the discovery of a fourth human coronavirus. It has been named NL63, NL or the New Haven coronavirus by the different research groups. The naming of this fourth coronavirus is still a controversial issue, because the three labs are still battling over who actually discovered the virus first and hence earns the right to name the virus. Early in 2005, a research team at the University of Hong Kong reported finding a fifth human coronavirus in two pneumonia patients, and subsequently named it HKU1.

Species
Genus: Alphacoronavirus; type species: Alphacoronavirus 1
        Species: Alphacoronavirus 1, Human coronavirus 229E, Human coronavirus NL63, Miniopterus Bat coronavirus 1, Miniopterus Bat coronavirus HKU8, Porcine epidemic diarrhea virus, Rhinolophus Bat coronavirus HKU2, Scotophilus Bat coronavirus 512
    Genus Betacoronavirus; type species: Murine coronavirus
        Species: Betacoronavirus 1, Human coronavirus HKU1, Murine coronavirus, Pipistrellus Bat coronavirus HKU5, Rousettus Bat coronavirus HKU9, Severe acute respiratory syndrome-related coronavirus, Tylonycteris Bat coronavirus HKU4
    Genus Gammacoronavirus; type species: Avian coronavirus
        Species: Avian coronavirus, Beluga whale coronavirus SW1

In April 2008, the following proposals were ratified by the ICTV:

    2005.260V.04 To create the following species in the genus Coronavirus in the family Coronaviridae, named Goose coronavirus, Pigeon coronavirus, Duck coronavirus.
    2006.009V.04 To create a species in the genus Coronavirus in the family Coronaviridae, named Human coronavirus NL63.
    2006.010V.04 To create a species in the genus Coronavirus in the family Coronaviridae, named Human coronavirus HKU1.
    2006.011V.04 To create a species in the genus Coronavirus in the family Coronaviridae, named Equine coronavirus.

In July 2009, the following proposals were ratified by the ICTV:

    2008.085-122V.A.v3.Coronaviridae
    2008.085V Create a new subfamily in the family Coronaviridae, order Nidovirales
    2008.086V Name the new subfamily Coronavirinae
    2008.087V Create a new genus in the proposed subfamily Coronavirinae
    2008.088V Name the new genus Alphacoronavirus
    2008.089V Assign three existing species (Human coronavirus 229E, Human coronavirus NL63, Porcine epidemic diarrhea virus) and five new species proposed in 2008.091-095V.01 to the proposed new genus Alphacoronavirus
    2008.090V Designate proposed species Alphacoronavirus 1 as type species of the genus Alphacoronavirus
    2008.091V Create new species named Alphacoronavirus 1 in the new genus
    2008.092V Create new species named Rhinolophus bat coronavirus HKU2 in the new genus
    2008.093V Create new species named Scotophilus bat coronavirus 512 in the new genus
    2008.094V Create new species named Miniopterus bat coronavirus 1 in the new genus
    2008.095V Create new species named Miniopterus bat coronavirus HKU8 in the new genus
    2008.096V Create a new genus in the proposed subfamily Coronavirinae
    2008.097V Name the new genus Betacoronavirus
    2008.098V Assign the existing species Human coronavirus HKU1 and six new species proposed in
    2008.100-105V.01 to the proposed genus Betacoronavirus
    2008.099V Designate proposed species Murine coronavirus as type species of the genus Betacoronavirus
    2008.108V Assign the two species proposed in 2008.110,111V.01 to the new genus
    2008.109V Designate proposed species Avian coronavirus as type species of the new genus
    2008.110V Create species named Avian coronavirus in the new genus
    2008.111V Create species named Beluga whale coronavirus SW1 in the new genus
    2008.112V Create a new subfamily in the family Coronaviridae, order Nidovirales
    2008.113V Name the new subfamily Torovirinae
    2008.114V Create a new genus in the subfamily Torovirinae
    2008.115V Name the new genus Bafinivirus
    2008.116V Assign the species White breamVirus (proposed in 2008.118V.01) to the new genus
    2008.117V Designate species White bream virus as type species in the new genus
    2008.118V Create species named White bream virus in the new genus
    2008.119V Remove the genus Torovirus from the family Coronaviridae
    2008.120V Reassign the genus Torovirus to the subfamily Torovirinae
    2008.121V.U Remove (abolish) 18 species (Human enteric coronavirus, Human coronavirus OC43, Bovine coronavirus, Porcine hemagglutinating encephalomyelitis virus, Equine coronavirus, Murine hepatitis virus, Puffinosis coronavirus, Rat coronavirus, Transmissible gastroenteritis virus, Canine coronavirus, Feline coronavirus, Infectious bronchitis virus, Duck coronavirus, Goose coronavirus, Pheasant coronavirus, Pigeon coronavirus, Turkey coronavirus, Severe acute respiratory syndrome coronavirus) from the genus Coronavirus
    2008.122V.U Reassign species Human coronavirus 229E, Human coronavirus NL63 and Porcine epidemic diarrhea virus to the new genus Alphacoronavirus and Human coronavirus HKU1 to the new genus Betacoronavirus

Family Retroviridae Virus

Description and Significance

Retroviruses are viruses that are remarkable for their use of reverse transcription of viral RNA into DNA during replication. Members of this family include Human immunodeficiency virus (the virus that causes AIDS), feline leukemia, and several cancer-causing viruses. Retroviruses were discovered in 1908 by Vilhelm Ellermann and Oluf Bang. The first sixty years of study of retroviruses focused exclusively on animal infection and disease. In the 1960s and 1970s, study focused on the viral replication cycle and pathogenic effects at the cellular level. Current study of retroviruses focuses on the diverse pathogenic effects of these viruses at the cellular and molecular levels. Retroviruses were the first viruses to be modified for gene therapy, and continue to be used in the majority of gene therapy clinical trials.

Genome Structure
The genome of retroviridae is dimeric, unsegmented and contains a single molecule of linear. The genome is -RT and a positive-sense, single-stranded RNA. Minor species of non-genomic nucleic acid are also found in virions. The encapsidated nucleic acid is mainly of genomic origin but virions may also contain nucleic acid of host origin, including host RNA and fragments of host DNA believed to be incidental inclusions. The complete genome of one monomer is 7000-11000 nucleotides long. The 5'-end of the genome has a methylated nucleotide cap with a cap sequence type 1 m7G5ppp5'GmpNp. The 3'-terminus of each monomer has a poly (A) tract and the terminus has a tRNA-like structure.

Virion Structure of a Retroviridae
The virions of a retroviridae consist of an envelope, a nucleocapsid and a nucleoid. The virus capsid is enveloped. The virions are spherical to pleomorphic and measure 80-100 nm in diameter. The surface projections are small or distinctive glycoprotein spikes that cover the surface evenly. The projections are densely dispersed and 8 nm long. The nucleoid is concentric or eccentric while the core is spherical.

Reproduction Cycle of a Retroviridae in a Host Cell

Retrovirus virions enter host cells through interaction between a virally-encoded envelope protein and a cellular receptor. Viral RNA is transcribed into a DNA copy by the enzyme reverse transcriptase which is present in the virion. The viral DNA copy is integrated into, and becomes a permanent part of, the host genome. This integrated DNA is referred to as a provirus. The host cell's transcriptional and translational machinery expresses the viral genes. The host RNA polymerase II transcribes the provirus to create new viral RNA, which is then transported out of the nucleus by other cellular processes. A fraction of these new RNAs are spliced to allow expression of some genes, while others are left as full-length RNAs. Viral proteins are synthesized by the host cell's translational machinery. Virions are assembled and bud from the host cell.

This reproduction cycle applies to all of the members of Retroviridae except for spumaviruses. Spumaviruses complete reverse transcription in the virus-producing cells rather than infected target cells, and the infectious virus contains a DNA genome.

Viral Ecology & Pathology
Retroviruses cause a wide variety of malignancies, immunodeficiencies, and neurological disorders affecting a wide variety of species. According to Coffin et al., "Some of these disorders have significant agricultural impact, crippling farm animals during their most productive years, whereas others have a devastating medical and economic impact on humans. Still others, particularly many of the retrovirus-induced malignancies of rodents, were found originally in laboratory settings and provide excellent model systems for probing the biological and molecular mechanisms of carcinogenesis."

Vaccines
The failure of 'classical' vaccines to induce protection to the most important of all retroviruses, HIV, has led to the development of a huge variety of 'molecular vaccines', i.e. vaccines produced using modern molecular biological techniques. Such vaccines range from simple plasmid DNA coding for the genes of choice, through recombinant viruses carrying such genes to engineered bacteria designed to deliver HIV genes to the mucosal immune system. Evaluation of such vaccines in animal models has resulted in sporadic successes and many failures and the few human clinical trials have been, at best, negative. However, the relative success of molecular vaccines in combating other retroviral infections and the continuing refinement of HIV/SIV vaccines showing some efficacy suggests that a molecular AIDS vaccine may be achievable.

Jumat, 21 Oktober 2011

Family Totiviridae Virus

The Totiviridae are a family of viruses. They are non enveloped, icosahedral viruses. The viron is composed of a single capsid protein and are ~40 nanometers in diameter. The capsid has a T=2 symmetry.

The genome is composed of a linear double stranded RNA molecule of 4.6-6.7 kilobases. It contains 2 overlapping open reading frames (ORF) - gag and pol - which respectively encode the capid protein and the RNA dependent RNA polymerase. Some totiviruses contain a third small potential ORF.

The family Totiviridae comprises viruses with nonsegmented dsRNA genomes and isometric virions. A new genus, Victorivirus, has been approved for this family, named from the specific epithet of Helminthosporium victoriae, host of the type species, Helminthosporium victoriae virus 190S. Distinguishing characteristics of the 11 viruses so far assigned to this genus include infection of filamentous fungi, an apparently coupled termination-reinitiation mechanism for translating the RNA-dependent RNA polymerase as a separate product from the upstream capsid protein, and sequence-based phylogenetic grouping in a distinct clade from other family members.

A dsRNA virus with a genome of 3.5 kb was isolated from field and greenhouse-grown tomato plants of different cultivars and geographic locations in North America. Cloning and sequencing of the viral genome showed the presence of two partially overlapping open reading frames (ORFs), and a genomic organization resembling members of the family Totiviridae that comprises fungal and protozoan viruses, but not plant viruses. The 5'-proximal ORF codes for a 377 amino acid-long protein of unknown function, whereas the product of ORF2 contains typical motifs of an RNA-dependant RNA-polymerase and is likely expressed by a +1 ribosomal frame shift. Despite the similarity in the genome organization with members of the family Totiviridae, this virus shared very limited sequence homology with known totiviruses or with other viruses. Repeated attempts to detect the presence of an endophytic fungus as the possible host of the virus failed, supporting its phytoviral nature. The virus was efficiently transmitted by seed but not mechanically and/or by grafting. Phylogenetic analyses revealed that this virus, for which the name Southern tomato virus (STV) is proposed, belongs to a partitivirus-like lineage and represents a species of a new taxon of plant viruses.

Family Reoviridae Virus

Reoviridae is a family of viruses that can affect the gastrointestinal system (such as Rotavirus) and respiratory tract. Viruses in the family Reoviridae have genomes consisting of segmented, double-stranded RNA (dsRNA). The name "Reoviridae" is derived from respiratory enteric orphan viruses. The term "orphan virus" means that a virus that is not associated with any known disease. Even though viruses in the Reoviridae family have more recently been identified with various diseases, the original name is still used.

Reovirus infection occurs often in humans, but most cases are mild or subclinical. The virus can be readily detected in feces, and may also be recovered from pharyngeal or nasal secretions, urine, cerebrospinal fluid, and blood. Despite the ease of finding Reovirus in clinical specimens, their role in human disease or treatment is still uncertain.

Some viruses of this family infect plants. For example, Phytoreovirus and Oryzavirus.

Structure
Reoviruses are non-enveloped and have an icosahedral capsid (T-13) composed of an outer and inner protein shell. The genomes of viruses in Reoviridae contain 10-12 segments which are grouped into three categories corresponding to their size: L (large), M (medium) and S (small). Segments range from ~ 3.9 kbp – 1kbp and each segment encodes 1-3 proteins. Reoviridae proteins are denoted by the Greek character corresponding to the segment it was translated from (the L segment encodes for λ proteins, the M segment encodes for μ proteins and the S segment encodes for σ proteins).

Since these viruses have dsRNA genomes, replication occurs exclusively in the cytoplasm and the virus encodes several proteins which are needed for replication and conversion of the dsRNA genome into (+)-RNAs. The virus can enter the host cell via a receptor on the cell surface. The receptor is not known but is thought to include sialic acid and junctional adhesion molecules (JAMs). The virus is partially uncoated by proteases in the endolysosome, where the capsid is partially digested to allow further cell entry. The core particle then enters the cytoplasm by a yet unknown process where the genome is transcribed conservatively causing an excess of (+) sense strands, which are used as mRNA templates to synthesize (-) sense strands. Viral particles begin to assemble in the cytoplasm 6–7 hours after infection.

Genera and type species
Fifteen genera of Reoviridae exist and are divided based on the presence of a "turret" protein on the inner capsid.

As of July 2009, ratified by the ICTV, there are two subfamilies; Sedoreovirinae & Spinareovirinae in the family Reoviridae.

"The name Spinareovirinae will be used to identify the subfamily containing the spiked or turreted viruses and is derived from ‘reovirus’ and the Latin word ‘spina’ as a prefix, which means spike, denoting the presence of spikes or turrets on the surface of the core particles. The term ‘spiked’ is an alternative to ‘turreted’, that was used in early research to describe the structure of the particle, particularly with the cypoviruses. The name Sedoreovirinae will be used to identify the subfamily containing the non-turreted virus genera and is derived from ‘reovirus’ and the Latin word ‘sedo’, which means smooth, denoting the absence of spikes or turrets from the core particles of these viruses, which have a relatively smooth morphology."

The subfamily Sedoreovirinae contains 6 genera:

    Cardoreovirus
    Mimoreovirus
    Orbivirus
    Phytoreovirus
    Rotavirus
    Seadornavirus

The subfamily Spinareovirinae contains 9 genera:

    Aquareovirus
    Coltivirus
    Cypovirus
    Dinovernavirus
    Fijivirus
    Idnoreovirus
    Mycoreovirus
    Orthoreovirus
    Oryzavirus

Therapeutic applications
The reovirus has been demonstrated to have oncolytic (cancer-killing) properties and has encouraged the development of reovirus-based therapies for cancer treatment.

Reolysin is a formulation of reovirus that is currently in clinical trials for the treatment of various cancers.

Family Picobirnaviridae Virus

Picobirnavirus is a genus of dsRNA virus, which infect certain mammals. It may be implicated in gastroenteritis in animals and humans. The viruses have only been isolated from mammals to date.

The virons have a diameter of 35-40 nanometers with a triangulation number (T) = 1, 3 or 4.

The genome is a bipartate and double stranded RNA. The length of the two parts of the genome are 1.7 kilobases (kb) and 2.5 kb. The capsid protein gene is encoded by the second open reading frame of the larger genomic segment.

Picobirnaviruses (PBVs) are small, non-enveloped viruses with a bisegmented double-stranded RNA genome. Their pathogenic potential, ecology, and evolutionary features are largely unexplored. Here, we describe the molecular analysis of porcine PBVs identified in the intestinal content of dead pigs. Six of 13 positive samples were cloned and then subjected to single-strand conformation polymorphism analysis and nucleotide sequencing. All clones belonged to genogroup I PBVs and almost all clones clustered on separate branches from human strains. A single strain shared a notably close genetic relationship with a Hungarian human PBV strain (89.9 nt and 96.4 % aa identity). Genetic diversity was also observed among strains identified in mixed infections. Single point mutations and deleterious mutations within highly related strains suggested that PBVs exist as quasispecies in the swine alimentary tract. Clones with complete sequence identities originating from different animals suggested effective animal-to-animal transmission of the virus. Our findings indicate that infection with genogroup I PBVs is common in pigs.

Nucleotide and amino acid sequence identity data among selected human and porcine PBVs are available with the online version of this paper.

Picobirnaviruses (PBVs) belong to the newly proposed virus family, Picobirnaviridae /asp/iPublicMessageBoardMain.asp?Topic=5&MID=0&click=Vertebrate). They have a small, non-enveloped virion and a bisegmented double-stranded (ds) RNA genome; the large genome segment is 2.2–2.7 kbp long and encodes the putative capsid protein, while the small genome segment is 1.2–1.9 kbp long and encodes the viral RNA-dependent RNA polymerase (RdRp) (Chandra, 1997; Rosen, 2003). Based on the sequences of the RdRp gene, human PBVs are classified into genogroups I and II. The sequence similarity along a short nucleic acid fragment of the RdRp gene within and between the two genogroups ranges from 49 to 97 % and 28 to 37 %, respectively (Bányai et al., 2003; Rosen et al., 2000).

Laboratory diagnosis of PBV infections is mainly based on appearance of the two dsRNA genome segments in polyacrylamide gel separations. In spite of the relative insensitivity of this method, PBVs could be identified from faecal specimens of a variety of mammals and birds due to large amounts of virus occasionally shed through the faeces (Browning et al., 1991; Buzinaro et al., 2003; Chasey, 1990; Gallimore et al., 1993; Haga et al., 1999; Ludert et al., 1995; Masachessi et al., 2007; Pereira et al., 1988a; Wang et al., 2007). The development of virus-specific primers for RT-PCR amplification (Rosen et al., 2000) has been a milestone in the laboratory diagnosis of PBVs; however, thus far it has not been determined whether PBVs are pathogenic or innocuous agents of the intestine. A recent metagenomic analysis of faecally shed RNA viruses identified PBVs as a mixture of different strains in individuals without symptoms of gastroenteritis (Zhang et al., 2006). PBVs have also been detected in patients with gastroenteritis. PBVs have been frequently detected as co-infections together with rotaviruses, caliciviruses and astroviruses (Bányai et al., 2003; Bhattacharya et al., 2006a, b, 2007; Rosen et al., 2000). In addition, the higher detection rates of PBVs in immuncompromised patients without the detection of conventional enteric pathogens (Giordano et al., 1998, 1999; Gonzalez et al., 1998; Grohmann et al., 1993; Martinez et al., 2003) suggest that PBV might be an opportunistic pathogen.

The limited available information does not clearly establish an impact of PBVs on human health. Further, the lack of comprehensive sequence data does not allow establishment of firm epidemiological linkage between cases (Bányai et al., 2003; Rosen et al., 2000), or assessment of the potential existence of risk groups in the human population. It is also unclear whether the epidemiology of PBVs is influenced by host-species restriction or whether animals may act as reservoirs of infection for humans. Accordingly, gathering information on the genetic diversity of animal PBVs is critical to generate a more precise picture of the ecology of PBVs in humans. In this paper, a survey of porcine PBVs was carried out in order to obtain information on the genetic relationships between human and animal PBVs.

The intestinal contents of weaned pigs from various regions of Hungary were collected in 2005 as part of an ongoing programme aimed at investigating the zoonotic potential of known and recently emerging enteric viruses. Samples were sent with a diagnostic request by local veterinary practitioners to the Division of Pathology (Clinic for Large Animals, Faculty of Veterinary Science, Szent István University, Üllő, Hungary), where the gross pathological and bacteriological examinations were performed. A subset of samples was sent for virological examinations to the Regional Laboratory of Virology, Baranya County Institute of State Public Health Service (Pécs, Hungary).

Virological investigations included the following steps. Total RNA was extracted by use of TRIzol reagent (Invitrogen) from 150 μl 10–20 % suspension of faecal specimens (prepared in Tris/HCl, pH 7.2) following the manufacturer's recommendation. The RNA was resuspended in 60 μl DEPC-treated sterile distilled water (Bio 101 Systems) and frozen at –80 °C until analysis. First, 20 μl RNA was loaded onto a polyacrylamide gel and stained with silver nitrate to detect rotaviruses in the samples. However, only PBVs were detected by this method in 2 of 20 samples (designated C10 and E4). Of interest, sample E4 displayed four dsRNA segments in the gel with a size range consistent with that of PBVs (data not shown). To confirm these results, RT-PCR amplification was performed using the primers and the algorithm described previously (Bányai et al., 2003; Rosen et al., 2000). PCR products ∼200 bp in length were obtained in a total of 13 (out of 20; 65 %) samples. The uniform amplicon size suggested that all strains might belong to genogroup I PBVs (Bányai et al., 2003; Rosen et al., 2000).

For a subset of samples detailed diagnostic findings were available, revealing various scenarios of lesions in the organs and concomitant bacterial infections, that likely accounted for the death of the animals (Table 1⇓). Most importantly, in none of the PBV-positive animals was infection by PBV associated with peculiar clinical signs or pathology. Various health conditions associated with PBV infections have been reported by others (e.g. Cascio et al., 1996; Gallimore et al., 1995; Ludert & Liprandi, 1993; Wang et al., 2007; Zhang et al., 2006). In pigs, one study indicated that PBVs occur more frequently in diarrhoeic animals (Gatti et al., 1989), while another study reported that PBVs were detected at similar proportions in diarrhoeic and healthy animals (Ludert et al., 1991). Experimental infection of gnotobiotic animals would be required to acquire more conclusive data on the pathogenicity of porcine PBVs in piglets.
View this table:

   Pathological diagnosis or gross lesion(s) and the bacteriological findings of PBV-positive pigs

+, Positive; –, negative.

To evaluate the relationships of Hungarian porcine PBV strains with other PBVs, nine samples were selected for sequencing on the basis of PCR product quantity and epidemiological context. The Big Dye cycle sequencing kit (version 1.1; Applied Biosystems) was utilized with the same primers used for PCR. Dye-labelled products were run and analysed on an ABI Prism 310 sequence analyser (Applied Biosystems). Visual inspection of the sequence chromatograms of all nine selected strains suggested the co-existence of heterogeneous amplicon populations. Therefore, six gel-purified amplicons were cloned into pGEM-T vector (Promega) and amplified in competent cells (Escherichia coli strain JM109). Depending on the clone numbers, 16–31 clones per sample were screened for PBV using the virus-specific primer pair, B25 and B43.

Positive plasmid clones were subjected to single-strand conformation polymorphism (SSCP) analysis in order to estimate the heterogeneity of the amplicon population and to select clones for further nucleotide sequencing. Briefly, 1 μl amplicon without purification was added to 18 μl molecular grade formamide (Sigma) and 1 μl 6× Blue/Orange loading dye (Promega). This mixture was heat denatured (97 °C, 5 min) and immediately placed on an ice slurry. The denatured amplicons (10 μl) were loaded on a pre-cooled polyacrylamide gel and were separated at 230 V, 50 mA for ∼100 min. Bands were visualized by silver-staining. Band patterns were categorized (Fig. 1⇓) and ≥1 clone representing each pattern was selected for nucleotide sequencing. Overall, between 4 and 10 plasmid clones obtained from the six selected amplicons were sequenced. Despite the optimized cloning procedure four clones were found to contain a mixture of DNA sequences and therefore they were not analysed further.

SSCP patterns and relative abundance of selected clones of six porcine picobirnavirus strains. 1, Sample identity; 2, no. clones subjected to SSCP; 3, SSCP patterns; 4, no. clones with the indicated SSCP pattern; 5, example clone. Clone names on the right hand side are identical to those given in the phylogenetic tree. The patterns of five additional clones are not shown because subsequent nucleotide sequence analysis revealed that four of them were mixed amplicon populations (in four cases) and one clone gave only faint bands in the gel (however, this latter clone yielded sufficient signal in the sequencing reaction). Asterisks indicate electrophoretic mobility of bands equivalent to ∼200 bp (*) and ∼400–500 bp (**). The molecular mass marker is not shown on the figure.

The resulting nucleotide sequences were edited and aligned with the GeneDoc software (Nicholas et al., 1997). The alignment included 43 porcine PBV sequences determined in this study and 17 human PBV sequences downloaded from GenBank, including the partial RdRp genes of three Hungarian, four Argentinean, one Thai, one Chinese strain, one gene sequence from India and seven gene sequences from the USA. Sixteen of these human strains belonged to genogroup I, while genogroup II was represented by a single strain. The Multalin free-ware (Corpet, 1988) was used to align longer gene sequences available in the DNA database. Phylogenetic analysis was performed by the neighbour-joining method with the p-distance model using the mega2 program (Kumar et al., 2001). A bootstrap resampling analysis of 500 replicates was performed.

Along with a short nucleic acid fragment of the RdRp gene (168 bp), the nucleotide sequence identity between any of the porcine PBV clones and those of human genogroup I strains ranged from 50.6 (e.g. E2-14 vs 745-ARG-95) to 89.9 % (E4-14 vs 1-HUN-01), while the range of similarity among porcine strains was between 54.5 (C10-5 vs D4-3) and 100 % (e.g. D4-5 vs D6-10). In these comparisons the nucleotide sequence identity values fell within the same ranges as seen among human genogroup I PBV strains (e.g. 49.4 % between 104-FL-97 and 745-ARG-95, and 97.6 % between 207-FL-97 and Hy005102). See details in the similarity matrix of human and porcine PBVs (Supplementary Table S1 available in JGV Online).

In the phylogenetic tree several clades supported with high (>90 %) bootstrap values could be distinguished (Fig. 2⇓). In a few cases complete and almost-complete sequence identities were identified among clones derived from distinct animals, suggesting that PBV strains can be easily transmitted from one host to another. All but one of the clones clustered on branches distinct from human strains. A single clone (designated E4-14) was most closely related to a Hungarian human PBV strain (89.9 nt identity and 96.4 % aa identity). Interestingly, the extent of sequence variation along the 168 nt fragment of RdRp correlates with the overall sequence variation of the entire RdRp gene for those two strains (1-CHN-97 and Hy005102, 61.9 % for the short fragment and 62.1 % for the full-length gene; data not shown) for which currently the complete RdRp gene sequence is available (Rosen et al., 2000; Wakuda et al., 2005). A taxonomic scheme based on partial RdRp sequences that are amplified with the broadly reactive primer set would be beneficial for future epidemiological studies on PBV, analogous to the genotyping systems used for other non-cultivatable small RNA viruses.

Phylogenetic relationship of porcine (po) and human (hu) genogroup I picobirnaviruses based on nucleotide sequence. In most instances, human and porcine strains separate into distinct genetic clades. In a single case, however, we identified close genetic relatedness between two heterologous strains (E4-14 and 1-HUN-01). Bootstrap values above 90 % are indicated. Bar, 0.05 substitutions per nucleotide.

The extent of sequence heterogeneity within an isolate has not yet been thoroughly studied for PBVs, although re-analysis of sequences from a metagenomic investigation of RNA viruses shed in the faeces revealed a heterogeneous population of PBVs in healthy individuals (data not shown; Zhang et al., 2006). A notable result of our study was the detection of mixed infections by different PBV strains in pigs. Furthermore, a remarkable genetic variability was observed within the RNA of the same PBV strain, likely accounted for by continuous accumulation of point mutations. A variety of these substitutions were nonsense mutations. We also identified a single point mutation in one clone (D6-1) that resulted in an in-frame stop codon within the RdRp gene. In another clone (C10-5) a deleterious mutation of three residues resulted in the removal of an amino acid but was not accompanied with the termination of translation within this short gene fragment (data not shown). Mutations altering the open reading frame may be tolerated in the presence of non-mutated copies of the virus genome, and able to compensate such deleterious mutations (Yoon et al., 2006). A preliminary investigation into whether the PBVs exist as a quasispecies was initiated, and data suggesting that the virus may exist as a quasispecies were obtained (unpublished results) but, for PBVs, these data and how the data were generated need to be studied in much more detail for reliable conclusions to be made.

PBVs are regarded as enteric viruses because all cases reported thus far have been associated with virus shed in the faeces and some data suggest that they may be associated with diarrhoea under certain conditions (Giordano et al., 1998, 1999; Grohmann et al., 1993; Pereira et al., 1988b). In this study we demonstrated the spread of a PBV isolate in the affected community (in a swine herd in this case), the co-infection of affected animals with several unrelated PBV strains, the possible quasispecies nature of this small dsRNA virus, and provided some evidence for a wider host-range for certain genetic clades of genogroup I PBVs. Although most porcine genogroup I PBV strains seem to form separate genetic clades from human isolates, the question whether host-species mechanisms exist requires additional gene sequences from these species to be analysed. Finally, our findings suggest the possibility that certain porcine and human PBVs shared crossing points in their evolution. Repeated exposures of humans to heterologous, but genetically related and rapidly evolving viruses shed in large amounts from domestic animals might be an occupational health risk that needs attention and thorough investigation in the future.