Henipavirus

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Henipavirus
Colored transmission electron micrograph of a "Hendra henipavirus" virion (ca. 300 nm length)
Colored
transmission electron micrograph
of a Hendra henipavirus virion (ca. 300 nm length)
Virus classification Edit this classification
(unranked): Virus
Realm: Riboviria
Kingdom: Orthornavirae
Phylum:
Negarnaviricota
Class: Monjiviricetes
Order: Mononegavirales
Family: Paramyxoviridae
Subfamily: Orthoparamyxovirinae
Genus: Henipavirus
Species

Henipavirus is a

domestic animals and humans is a cause of concern.[7][8]

In 2009, RNA sequences of three novel viruses in phylogenetic relationship to known henipaviruses were detected in African straw-colored fruit bats (

Eidolon helvum) in Ghana. The finding of these novel henipaviruses outside Australia and Asia indicates that the region of potential endemicity of henipaviruses may be worldwide.[9] These African henipaviruses are slowly being characterised.[10]

Nipah and Hendra henipaviruses are both considered category C (USDA-HHS overlap) select agents.[11]

Structure

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

Henipavirions are

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 (except in the case of MojV-G) is to attach the virus to the surface of a host cell via

syncytia
.

Genome

Nipah virus (NiV) replication cycle

As all mononegaviral genomes, Hendra virus and Nipah virus genomes are non-segmented, single-stranded negative-sense RNA. Both genomes are 18.2 kb in length and contain six genes corresponding to six structural proteins.[17]

In common with other members of the Paramyxoviridae family, the number of nucleotides in the henipavirus genome is a multiple of six, consistent with what is known as the 'rule of six'.[18][19] 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.

Three additional protein products are produced from the henipavirus P gene: V, W, and C. The V and W proteins are generated through an unusual process called

translation. The addition of a single guanosine results in production of V, and the addition of two guanosines residues produces W.[20] The C protein is not produced through RNA editing but instead by leaky scanning of the host cell ribosome during translation of viral mRNA. P, V, and W possess an alternate open reading frame which results in production of C. P, V, W, and C are known to disrupt the host innate antiviral immune response through several different mechanisms.[21] P, V, and W contain STAT1 binding domains, and act as interferon antagonists by sequestering STAT1 in the nucleus and cytoplasm.[22] The C protein controls the early pro-inflammatory response and is also known to promote the viral budding process via a ESCRT-dependent pathway.[23][24]

Life cycle

Cell receptor ephrin-B2, which is located on epithelial cells around smaller arteries, neurons, and smooth muscle cells, is targeted by the viral protein G.[25] Once the protein G binds to ephrin-B2, the viral protein F facilitates fusion with the host cell membrane and releases viral RNA into the host cell cytoplasm.[26] Upon entry, transcription of viral mRNA takes place using the viral RNA as a template. This process is started and stopped by the polymerase complex. Viral proteins are gathering in the cell as transcription occurs until the polymerase complex stops transcription and starts genome replication. Transcription of the viral RNA makes positive sense strands of RNA, which are then used as templates to make more negative sense viral RNA . Genome replication is halted before the viral particles can assemble to make a virion. Once the cell membrane is ready, new virions exit the host cell through budding.[27]

Vaccine

Henipaviruses have high mortality rates in mammalian hosts, both human and animal. Because of this, there is a need for immunization against HeV and NiV. The

phase I clinical trial in November 2022, but results have not yet been published.[31]

The primary mechanism of protection against NiV and HeV induced by vaccination is thought to be neutralizing antibodies.[32] However, a number of preclinical vaccine studies in animal models of disease have identified that the cell-mediated immune response including CD8+ and CD4+ T-cells may play a role in protection.[33]

Causes of emergence

The emergence of henipaviruses parallels the emergence of other

Menangle virus, Marburg virus, COVID 19 and possibly Ebola
viruses 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 that 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, is creating greater overlap of human and flying fox distributions.[34]

Taxonomy

Genus Henipavirus: species and their viruses[35]
Genus Species Virus (Abbreviation)
Henipavirus
Cedar henipavirus
 		Cedar virus (CedV)
Ghanaian bat henipavirus
Kumasi virus
(KV)
Hendra henipavirus
 		Hendra virus (HeV)
Mojiang henipavirus
 		Mòjiāng virus (MojV)[3]
Nipah henipavirus
 		Nipah virus (NiV)
Langya henipavirus
Langya virus (LayV)[6][36]

See also

References

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  5. ^ Cheng, Amy (10 August 2022). "New Langya virus that may have spilled over from animals infects dozens". The Washington Post.
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  28. ^ "Prioritizing diseases for research and development in emergency contexts". www.who.int. Retrieved 29 March 2023.
  29. ^ "Equivac® HeV". www.zoetis.com.au. Retrieved 29 March 2023.
  30. PMID 34358146
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  31. ^ Auro Vaccines LLC (16 November 2022). "A Phase 1 Randomized, Placebo-controlled, Observer-blind Trial to Assess the Safety and Immunogenicity of a Nipah Vaccine, HeV-sG-V (Hendra Virus Soluble Glycoprotein Vaccine), in Healthy Adults". ClinicalTrials.gov. PATH, Coalition for Epidemic Preparedness Innovations, Cincinnati Children's Hospital Medical Center (CCHMC).
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  36. ^ "Zoonotic Langya virus found in China, CDC says - Taipei Times". 9 August 2022.

External links

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