Henipavirus, a genus of the Paramyxoviridae family, contains two members: Hendravirus and Nipahvirus. Pteropid fruit bats are natural harborers of the henipaviruses. They are characterized by a large genome, a wide host range, and their zoonotic pathogens.
They viruses are pleomorphic and range in shape from 40 to 600 nm in diameter. They have a lipid membrane overlying a shell of viral matrix protein. The core has a single helical strand of genomic RNA tightly bound to N protein and associated with the L and P proteins which provide RNA polymerase activity during replication.
Within the lipid membrane are spikes of F protein trimers and G protein tetramers. The F protein causes infected cells to fuse with neighboring cells to form large, multinucleated syncytia. Henipaviruses us a process called RNA editing to generate multiple proteins from a single gene.
In September of 1994, Hendra virus was discovered when it caused the deaths of fourteen horses and a trainer in Hendra. The initial case was a mare housed with 23 other horses which was ill and died two days later. Nineteen of the other horses succumbed with 13 dying. The stable hand was also infected but recovered.
In 1994 a second outbreak occurred in Mackay resulting in the deaths of two horses and their owner. A survey in the area of the outbreaks identified pteropid fruit bats as the source of the Hendra virus. Virus isolations show that the horses may have been infected via exposure to urine of wild bats.
Since 1994 there have been thirteen outbreaks of Hendra virus all involved the infection of horses. Timing of the outbreaks indicates a seasonal pattern possibly related to the seasonality of fruit bat birthing. There is no evidence of transmission from humans to bats directly.
Hendra virus does not infect flying foxes. Symptoms in humans may be respiratory, including hemorrhage and edema of the lungs, or encephalitic resulting in meningitis. In horses infection causes pulmonary edema and congestion.
Nipah virus was found in 1999 when an outbreak of neurological and respiratory disease on pig farms in peninsular Malaysia resulting in 105 human deaths and the deaths of millions of pigs. The Centers for Disease Control and prevention have categorized the Nipah virus as a Category C agent. The name “Nipah” is from the place, Kampung Nipah, where the virus was first isolated.
It was originally mistaken for Japanese encephalitis until it was noted that victims had been vaccinated against JE. Symptoms of the outbreak in Malaysia were primarily encephalitic in humans and respiratory in pigs. Later outbreaks caused respiratory illness in humans which increased the likelihood of human-to-human transmission.
Pteropid fruit bats were also confirmed as the primary reservoir for Nipah virus. The transmission of Nipah to pigs is thought to be due to an increasing overlap between bat habitats and piggeries in peninsular Malaysia. Since 2001 eleven cases of Nipah have been documented in Bangladesh. Humans will present the infection in the form of fever, headache, drowsiness, cough, abdominal pain, nausea, vomiting, problems swallowing, and blurred vision. Around a quarter of those infected will have seizures.
In animals the virus causes porcine respiratory and neurological syndrome known as barking pig syndrome or one mile cough.