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Henipavirus

2007 Schools Wikipedia Selection. Related subjects: Organisms

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   Henipaviruses
      Virus classification

   Group:  Group V ( (-)ssRNA)
   Order:  Mononegavirales
   Family: Paramyxoviridae
   Genus:  Henipavirus
             Species

   Hendravirus
   Nipahvirus

   Henipavirus is a genus of the family Paramyxoviridae, order
   Mononegavirales containing two members, Hendravirus and Nipahvirus. The
   henipaviruses are naturally harboured by Pteropid fruit bats (flying
   foxes) and are characterised by a large genome, a wide host range and
   their recent emergence as zoonotic pathogens capable of causing illness
   and death in domestic animals and humans.

Virus structure

   Structure of henipaviruses
   Enlarge
   Structure of henipaviruses
   The henipavirus genome (3’ to 5’ orientation) and products of the P
   gene
   The henipavirus genome (3’ to 5’ orientation) and products of the P
   gene

   Henipaviruses are pleomorphic (variably shaped), ranging in size from
   40 to 600 nm in diameter . They possess a lipid membrane overlying a
   shell of viral matrix protein. At the core is a single helical strand
   of genomic RNA tightly bound to N (nucleocapsid) protein and associated
   with the L (large) and P (phosphoprotein) proteins which provide RNA
   polymerase activity during replication.

   Embedded within the lipid membrane are spikes of F (fusion) protein
   trimers and G (attachment) protein tetramers. The function of the G
   protein is to attach the virus to the surface of a host cell via ephrin
   B2, a highly conserved protein present in many mammals . The F protein
   fuses the viral membrane with the host cell membrane, releasing the
   virion contents into the cell. It also causes infected cells to fuse
   with neighbouring cells to form large, multinucleated syncytia.

Genome structure

   As with all viruses in the Mononegavirales order, the Hendra virus and
   Nipah virus genomes are non-segmented, single-stranded negative-sense
   RNA. Both genomes are 18.2 kb in size and contain six genes
   corresponding to six structural proteins .

   In common with other members of the Paramyxovirinae subfamily, the
   number of nucleotides in the henipavirus genome is a multiple of six,
   known as the 'rule of six'. Deviation from the rule of six, through
   mutation or incomplete genome synthesis, leads to inefficient viral
   replication, probably due to structural constraints imposed by the
   binding between the RNA and the N protein.

   Henipaviruses employ an unusual process called RNA editing to generate
   mulitple proteins from a single gene. The process involves the
   insertion of extra guanosine residues into the P gene mRNA prior to
   translation. The number of residues added determines whether the P, V
   or W proteins are synthesised. The functions of the V and W proteins
   are unknown, but they may be involved in disrupting host antiviral
   mechanisms.

Hendra virus

Emergence

   Hendra virus (originally Equine morbillivirus) was discovered in
   September 1994 when it caused the deaths of thirteen horses, and a
   trainer at a training complex in Hendra, a suburb of Brisbane in
   Queensland, Australia.

   The index case, a mare, was housed with 23 other horses after falling
   ill and died two days later. Subsequently, 19 of the remaining horses
   succumbed with 12 dying. Both the trainer and a stable hand were
   involved in nursing the index case and both fell ill within one week of
   the horse’s death with an influenza-like illness. The stable hand
   recovered while the trainer died of respiratory and renal failure. The
   source of virus was most likely frothy nasal discharge from the index
   case.

   A second outbreak occurred in August 1994 (chronologically preceding
   the first outbreak) in Mackay 1000km north of Brisbane resulting in the
   deaths of two horses and their owner . The owner assisted in autopsies
   of the horses and within three weeks was admitted to hospital suffering
   from meningitis. He recovered, but 14 months later developed neurologic
   signs and died. This outbreak was diagnosed retrospectively by the
   presence of Hendra virus in the brain of the patient.

   A survey of wildlife in the outbreak areas was conducted and identified
   pteropid fruit bats as the most likely source of Hendra virus with a
   seroprevalence of 47%. All of the other 46 species sampled were
   negative. Virus isolations from the reproductive tract and urine of
   wild bats indicated that transmission to horses may have occurred via
   exposure to bat urine or birthing fluids .

Outbreaks

   Four more incidents, in Cairns in January 1999 and October 2004, in
   Townsville in December 2004 and on the Sunshine Coast in June 2006 each
   resulted in the death of one horse. A vet involved in autopsy of the
   horse from the 2004 Townsville incident developed a Hendra-related
   illness soon after and recovered.

   The distribution of black and spectacled flying foxes covers Townsville
   and Cairns, and the timing of incidents indicates a seasonal pattern of
   outbreaks possibly related to the seasonality of fruit bat birthing. As
   there is no evidence of transmission to humans directly from bats, it
   is thought that human infection only occurs via an intermediate host.

Pathology

   Flying foxes are unaffected by Hendra virus infection. Symptoms of
   Hendra virus infection of humans may be respiratory, including
   haemorrhage and oedema of the lungs, or encephalitic resulting in
   meningitis. In horses, infection usually causes pulmonary oedema and
   congestion.

Nipah virus

Emergence

   Pteropus vampyrus (Malayan flying fox), one of the natural reservoirs
   of Nipah virus
   Enlarge
   Pteropus vampyrus (Malayan flying fox), one of the natural reservoirs
   of Nipah virus

   Nipah virus was identified in 1999 when it caused an outbreak of
   neurological and respiratory disease on pig farms in peninsular
   Malaysia, resulting in 105 human deaths and the culling of one million
   pigs . In Singapore, 11 cases including one death occurred in abattoir
   workers exposed to pigs imported from the affected Malaysian farms.

   Symptoms of infection from the Malaysian outbreak were primarily
   encephalitic in humans and respiratory in pigs. Later outbreaks have
   caused respiratory illness in humans, increasing the likelihood of
   human-to-human transmission and indicating the existence of more
   dangerous strains of the virus.

   Based on seroprevalence data and virus isolations, the primary
   reservoir for Nipah virus was identified as Pteropid fruit bats
   including Pteropus vampyrus (Malayan flying fox) and Pteropus
   hypomelanus (Island flying fox), both of which occur in Malaysia.

   The transmission of Nipah virus from flying foxes to pigs is thought to
   be due to an increasing overlap between bat habitats and piggeries in
   peninsular Malaysia. At the index farm, fruit orchards were in close
   proximity to the piggery, allowing the spillage of urine, faeces and
   partially eaten fruit onto the pigs . Retrospective studies demonstrate
   that viral spillover into pigs may have been occurring in Malaysia
   since 1996 without detection . During 1998, viral spread was aided by
   the transfer of infected pigs to other farms where new outbreaks
   occurred.

Outbreaks

   Six more outbreaks of Nipah virus have occurred since 1998, one in
   India and five in Bangladesh. All outbreak sites lie within the range
   of Pteropus species (Pteropus giganteus). As with Hendra virus, the
   timing of the outbreaks indicates a seasonal effect.
   Locations of henipavirus outbreaks (red stars–Hendra virus; blue
   stars–Nipah virus) and distribution of henipavirus flying fox
   reservoirs (red shading–Hendra virus ; blue shading–Nipah virus)
   Enlarge
   Locations of henipavirus outbreaks (red stars–Hendra virus; blue
   stars–Nipah virus) and distribution of henipavirus flying fox
   reservoirs (red shading–Hendra virus ; blue shading–Nipah virus)
     * 2001 January 31 – February 23, Siliguri, India: 66 cases with a 74%
       mortality rate . 75% of patients were either hospital staff or had
       visited one of the other patients in hospital, indicating
       person-to-person transmission.

     * 2001 April – May, Meherpur district, Bangladesh: 13 cases with nine
       fatalities (69% mortality) .

     * 2003 January, Naogaon district, Bangladesh: 12 cases with eight
       fatalities (67% mortality) .

     * 2004 January – February, Manikganj and Rajbari provinces,
       Bangladesh: 42 cases with 14 fatalities (33% mortality).

     * 2004 19 February – 16 April, Faridpur district, Bangladesh: 36
       cases with 27 fatalities (75% mortality). Epidemiological evidence
       strongly suggests that this outbreak involved person-to-person
       transmission of Nipah virus, which had not previously been
       confirmed . 92% of cases involved close contact with at least one
       other person infected with Nipah virus. Two cases involved a single
       short exposure to an ill patient, including a rickshaw driver who
       transported a patient to hospital. In addition, at least six cases
       involved acute respiratory distress syndrome which has not been
       reported previously for Nipah virus illness in humans. This symptom
       is likely to have assisted human-to-human transmission through
       large droplet dispersal.

     * 2005 January, Tangail district, Bangladesh: 32 cases with 12
       fatalities (38% mortality). The virus was probably contracted from
       drinking date palm juice contaminated by fruit bat droppings or
       saliva .

   Eleven isolated cases of Nipah virus encephalitis have also been
   documented in Bangladesh since 2001.

   Nipah virus has been isolated from Lyle's flying fox (Pteropus lylei)
   in Cambodia and viral RNA found in urine and saliva from P. lylei and
   Horsfield's roundleaf bat (Hipposideros larvartus) from Thailand . The
   Cambodian strain shows 98% identity with the virus causing the 1998
   outbreak. No infection of humans or other species have been observed in
   Cambodia or Thailand.

Pathology

   In humans, the infection presents as fever, headache and drowsiness.
   Cough, abdominal pain, nausea, vomiting, weakness, problems with
   swallowing and blurred vision are relatively common. About a quarter of
   the patients have seizures and about 60% become comatose and might need
   mechanical ventilation. In patients with severe disease, their
   conscious state may deteriorate and they may develop severe
   hypertension, fast heart rate, and very high temperature.

   Nipah virus is also known to cause relapse encephalitis. In the initial
   Malaysian outbreak, a patient presented with relapse encephalitis some
   53 months after his initial infection. There is no definitive treatment
   for Nipah encephalitis, apart from supportive measures, such as
   mechanical ventilation and prevention of secondary infection.
   Ribavirin, an antiviral drug, was tested in the Malaysian outbreak and
   the results were encouraging, though further studies are still needed.

   In animals, especially in pigs, the virus causes porcine respiratory
   and neurologic syndrome also known as barking pig syndrome or one mile
   cough.

Causes of Emergence

   The emergence of henipaviruses parallels the emergence of other
   zoonotic viruses in recent decades. SARS coronavirus, Australian bat
   lyssavirus, Menangle virus and probably Ebola virus and Marburg virus
   are also harboured by bats and are capable of infecting a variety of
   other species. The emergence of each of these viruses has been linked
   to an increase in contact between bats and humans, sometimes involving
   an intermediate domestic animal host. The increased contact is driven
   both by human encroachment into the bats’ territory (in the case of
   Nipah, specifically pigpens in said territory) and by movement of bats
   towards human populations due to changes in food distribution and loss
   of habitat.

   There is evidence of habitat loss for flying foxes both in South Asia
   and Australia (particularly along the east coast) as well as
   encroachment of human dwellings and agriculture into the remaining
   habitats, creating greater overlap of human and flying fox
   distributions.
   Retrieved from " http://en.wikipedia.org/wiki/Henipavirus"
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   with only minor checks and changes (see www.wikipedia.org for details
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