Paramyxoviridae

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Paramyxoviridae
Canine distemper virus (CDV) virion and genome organization
Virus classification e
(unranked): Virus
Realm: Riboviria
Kingdom: Orthornavirae
Phylum: Negarnaviricota
Class: Monjiviricetes
Order: Mononegavirales
Family: Paramyxoviridae
Subfamilies

Paramyxoviridae (from Greek para- “by the side of” and myxa “mucus”) is a family of negative-strand RNA viruses in the order Mononegavirales.[1][2] Vertebrates serve as natural hosts.[3] Diseases associated with this family include measles, mumps, and respiratory tract infections.[4] The family has four subfamilies, 17 genera, and 78 species, three genera of which are unassigned to a subfamily.[5]

Structure

Virions are enveloped and can be spherical or pleomorphic and capable of producing filamentous virions. The diameter is around 150 nm. Genomes are linear, around 15kb in length.[6][1] Fusion proteins and attachment proteins appear as spikes on the virion surface. Matrix proteins inside the envelope stabilise virus structure. The nucleocapsid core is composed of the genomic RNA, nucleocapsid proteins, phosphoproteins and polymerase proteins.[7][8]

Genome

Paramyxovirus genome structure

The genome is nonsegmented, negative-sense RNA, 15–19 kilobases in length, and contains six to 10 genes. Extracistronic (noncoding) regions include:[9][10][11]

  • A 3’ leader sequence, 50 nucleotides in length, which acts as a transcriptional promoter.
  • A 5’ trailer sequence, 50–161 nucleotides long
  • Intergenomic regions between each gene, which are three nucleotides long for morbilliviruses, respiroviruses, and henipaviruses, and variable length for rubulaviruses.

Each gene contains transcription start/stop signals at the beginning and end, which are transcribed as part of the gene.The gene sequence within the genome is conserved across the family due to a phenomenon known as transcriptional polarity in which genes closest to the 3’ end of the genome are transcribed in greater abundance than those towards the 5’ end, this is a result of structure of the genome. After each gene is transcribed, the RNA-dependent RNA polymerase pauses to release the new mRNA when it encounters an intergenic sequence. When the RNA polymerase is paused, a chance exists that it will dissociate from the RNA genome. If it dissociates, it must re-enter the genome at the leader sequence, rather than continuing to transcribe the length of the genome.[9][10][12][13]

Single promoter model was verified when viruses were exposed to UV light, UV radiation can cause dimerization of RNA, which prevents transcription by RNA polymerase. When paramyxovirus genome was exposed to UV light, the level of inhibition of transcription was proportional to the distance from the leader sequence, in other words, the further the gene is from the leader sequence, the greater the chance of RNA dimerization inhibiting RNA polymerase.The virus takes advantage of the single promoter model by having its genes arranged in relative order of protein needed for successful infection.[10][14][15][16]

Viruses in the Paramyxoviridae family are also antigenically stable[17], meaning that the glycoproteins on the viruses are consistent between different strains of the same type, two reasons for this phenomenon are posited:

  • The first is that the genome is nonsegmented, thus cannot undergo genetic reassortment. For this process to occur, segments needed as reassortment happen when segments from different strains are mixed together to create a new strain.hence with no segments, nothing can be mixed with one another, so no antigenic shift occurs.[18][19]
  • The second reason relates to the idea of genetic variation, since RNA-dependent RNA polymerase does not have an error-checking function, many mutations are made when the RNA is processed, these mutations build up and eventually new strains are created. Due to this, one would expect that paramyxoviruses should not be antigenically stable; however, it is. The main hypothesis behind why the viruses are antigenically stable is that each protein and amino acid has an important function. Thus, any mutation would lead to a decrease or total loss of function, which would in turn cause the new virus to be less efficient. These viruses would not be able to survive as long compared to the more virulent strains, and so would die out.Many paramyxovirus genomes follow the "rule of six", the total length of the genome is almost always a multiple of six.[20][14][21]

Proteins

Paramyxoviridae virion is as follows:

Paramyxoviridae virion illustration
  • N – the nucleocapsid protein associates with genomic RNA (one molecule per hexamer) and protects the RNA from nuclease digestion[22]
  • P – the phosphoprotein binds to the N and L proteins and forms part of the RNA polymerase complex. P is the polymerase co-factor.[23]
  • M – the matrix protein assembles between the envelope and the nucleocapsid core, it organizes and maintains virion structure[8]
  • F – the fusion protein projects from the envelope surface as a trimer, and mediates cell entry by inducing fusion between the viral envelope and the cell membrane by class I fusion. One of the defining characteristics of members of the family Paramyxoviridae is the requirement for a neutral pH for fusogenic activity.[24]
  • H/HN/G – the cell attachment proteins span the viral envelope and project from the surface as spikes. They bind to proteins on the surface of target cells to facilitate cell entry. Proteins are designated H for morbilliviruses as they possess haemagglutination activity, observed as an ability to cause red blood cells to clump in laboratory tests. HN attachment proteins occur in respiroviruses, rubulaviruses and avulaviruses. These possess both haemagglutination and neuraminidase activity, which cleaves sialic acid on the cell surface, preventing viral particles from reattaching to previously infected cells. Attachment proteins with neither haemagglutination nor neuraminidase activity are designated G. These occur in henipaviruses.[25][15][26]
  • L – the large protein is the catalytic subunit of RNA-dependent RNA polymerase (RDRP)[27]
  • Accessory proteins – a mechanism known as RNA editing allows multiple proteins to be produced from the P gene. These are not essential for replication but may aid in survival in vitro or may be involved in regulating the switch from mRNA synthesis to antigenome synthesis.[28][29]

Life cycle

Replication of the canine distemper virus (CDV) cycle.

Viral replication is cytoplasmic. Entry into the host cell is achieved by viral attachment to host cell. Replication and transcription follow the negative-stranded RNA virus models.[30] Translation takes place by leaky scanning, ribosomal shunting, and RNA termination-reinitiation. The virus exits the host cell by budding. Human, vertebrates, and birds serve as the natural hosts. Transmission route is airborne particles.[1]

The Paramyxoviridae are able to undergo mRNA editing, which produces different proteins from the same mRNA transcript by slipping back one base to read off in a different open reading frame (ORF) due to the presence of secondary structures such as pseudoknots. Paramyxoviridae also undergo transcriptional stuttering to produce the poly (A) tail at the end of mRNA transcripts by repeatedly moving back one nucleotide at a time at the end of the RNA template.[31][32]

Taxonomy

Phylogenetic tree of paramyxoviruses[33]

Family: Paramyxoviridae[5]

Subfamily: Avulavirinae, which contains three genera and 22 species
Subfamily: Metaparamyxovirinae, which contains one genus and one species
Subfamily: Orthoparamyxovirinae, which contains eight genera and 34 species
Subfamily: Rubulavirinae, which contains two genera and 18 species
Unassigned genera:
Cynoglossusvirus
Hoplichthysvirus
Scoliodonvirus

Pathogenic paramyxoviruses

TEM image revealed the ultrastructural appearance of a measles virus particle, a Paramyxoviridae family member, and a member of the genus, Morbillivirus.

A number of important human diseases are caused by paramyxoviruses. These include mumps, as well as measles, which caused around 733,000 deaths in 2000.[34]

The human parainfluenza viruses (HPIV) are the second most common causes of respiratory tract disease in infants and children. There are four types of HPIVs, known as HPIV-1, HPIV-2, HPIV-3 and HPIV-4. HPIV-1 and HPIV-2 may cause cold-like symptoms, along with croup in children. HPIV-3 is associated with bronchiolitis, bronchitis, and pneumonia. HPIV-4 is less common than the other types, and is known to cause mild to severe respiratory tract illnesses.[35]

Measles

Measles is a highly contagious infectious disease caused by measles virus.[36][37]

Symptoms usually develop 10–12 days after exposure to an infected person and last 7–10 days.[38][39] Initial symptoms typically include fever, often greater than 40 °C (104 °F), cough, runny nose, and inflamed eyes.[36][40] Small white spots known as Koplik's spots may form inside the mouth two or three days after the start of symptoms.[40] A red, flat rash which usually starts on the face and then spreads to the rest of the body typically begins three to five days after the start of symptoms.[40]

Mumps

TEM micrograph of a mumps virus particle

Mumps is a viral disease caused by the mumps virus.[41] Initial signs and symptoms often include fever, muscle pain, headache, poor appetite, and feeling generally unwell.[42] This is then usually followed by painful swelling of one or both parotid salivary glands.[43][42]

Human parainfluenza viruses

It is estimated that there are 5 million children with lower respiratory infections (LRI) each year in the United States alone.[44] HPIV-1, HPIV-2 and HPIV-3 have been linked with up to a third of these infections.[45] Upper respiratory infections (URI) are also important in the context of HPIV, however, they are caused to a lesser extent by the virus.[46]

Other animals

Paramyxoviruses are also responsible for a range of diseases in other animal species, for example canine distemper virus (dogs), phocine distemper virus (seals), Newcastle disease virus (birds), and rinderpest virus (cattle). [47][48][49][50]

Some paramyxoviruses, such as the henipaviruses, are zoonotic pathogens, occurring naturally in an animal host, but also able to infect humans.[51]

Hendra virus (HeV) and Nipah virus (NiV) in the genus Henipavirus have emerged in humans and livestock in Australia and Southeast Asia. Both viruses are contagious, highly virulent, and capable of infecting a number of mammalian species and causing potentially fatal disease. Due to the lack of a licensed vaccine or antiviral therapies, HeV and NiV are designated as Biosafety level (BSL) 4 agents. The genomic structure of both viruses is that of a typical paramyxovirus.[52]

Diversity and evolution

Seal

In the past few decades, paramyxoviruses have been discovered from terrestrial, volant and aquatic animals, demonstrating a vast host range and great viral genetic diversity.[53]

As molecular technology advances and viral surveillance programs are implemented, the discovery of new viruses in this group is increasing.The evolution of paramyxoviruses is still debated, as McCarthy et al., indicates "the evolution of paramyxoviruses is still poorly understood". Using pneumoviruses as an outgroup, paramyxoviruses can be divided into two clades: one consisting of avulaviruses and rubulaviruses and one consisting of respiroviruses, henipaviruses, and morbilliviruses. Within the second clade the respiroviruses appear to be the basal group. The respirovirus-henipavirus-morbillivirus clade may be basal to the avulavirus-rubulavirus clade.[54][4][55][56]

See also

References

  1. ↑ 1.0 1.1 1.2 "Viral Zone". ExPASy. Archived from the original on 29 April 2017. Retrieved 15 June 2015.
  2. ↑ "Paramyxoviridae - Paramyxoviridae - Negative-sense RNA Viruses - ICTV". talk.ictvonline.org. Archived from the original on 2022-07-11. Retrieved 2020-12-14.
  3. ↑ Fields virology. Fields, Bernard N., Knipe, David M. (David Mahan), 1950-, Howley, Peter M. (6th ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. 2013. p. 883. ISBN 9781451105636. OCLC 825740706.{{cite book}}: CS1 maint: others (link)
  4. ↑ 4.0 4.1 Samal, SK, ed. (2011). The Biology of Paramyxoviruses. Caister Academic Press. ISBN 978-1-904455-85-1.
  5. ↑ 5.0 5.1 "Virus Taxonomy: 2020 Release". International Committee on Taxonomy of Viruses (ICTV). March 2021. Archived from the original on 20 March 2020. Retrieved 18 May 2021.
  6. ↑ Rima, B; Balkema-Buschmann, A; Dundon, WG; Duprex, WP; Easton, A; Fouchier, R; Kurath, G; Lamb, R; Lee, B; Rota, P; Wang, L; ICTV Report Consortium (December 2019). "ICTV Virus Taxonomy Profile: Paramyxoviridae". The Journal of General Virology. 100 (12): 1593–1594. doi:10.1099/jgv.0.001328. PMC 7273325. PMID 31609197.
  7. ↑ Morrison, Trudy G. (1 January 1998). "Paramyxoviruses, Infection and Immunity". Encyclopedia of Immunology (Second Edition). Elsevier. pp. 1909–1916. ISBN 978-0-12-226765-9. Retrieved 20 March 2023.
  8. ↑ 8.0 8.1 Cox, Robert M; Plemper, Richard K (2017). "Structure and Organization of Paramyxovirus Particles". Current opinion in virology. 24: 105–114. doi:10.1016/j.coviro.2017.05.004. ISSN 1879-6257. Archived from the original on 26 March 2023. Retrieved 26 March 2023.
  9. ↑ 9.0 9.1 Mishra, Pushpendra Mani; Verma, Navneet Chandra; Rao, Chethana; Uversky, Vladimir N.; Nandi, Chayan Kanti (1 January 2020). "Chapter One - Intrinsically disordered proteins of viruses: Involvement in the mechanism of cell regulation and pathogenesis". Progress in Molecular Biology and Translational Science. Academic Press. pp. 1–78. Archived from the original on 11 October 2022. Retrieved 20 March 2023.
  10. ↑ 10.0 10.1 10.2 Noton, Sarah L.; Fearns, Rachel (May 2015). "Initiation and regulation of paramyxovirus transcription and replication". Virology. 479–480: 545–554. doi:10.1016/j.virol.2015.01.014. ISSN 1096-0341. Archived from the original on 21 October 2022. Retrieved 22 March 2023.
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  14. ↑ 14.0 14.1 Knipe, David Mahan; Howley, Peter M. (2007). Fields' Virology. Lippincott Williams & Wilkins. p. 1451. ISBN 978-0-7817-6060-7. Archived from the original on 24 March 2023. Retrieved 24 March 2023.
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  54. ↑ McCarthy AJ, Goodman SJ (January 2010). "Reassessing conflicting evolutionary histories of the Paramyxoviridae and the origins of respiroviruses with Bayesian multigene phylogenies". Infect. Genet. Evol. 10 (1): 97–107. doi:10.1016/j.meegid.2009.11.002. PMID 19900582.
  55. ↑ Larsen, Brendan B.; Gryseels, Sophie; Otto, Hans W.; Worobey, Michael (9 February 2022). "Evolution and Diversity of Bat and Rodent Paramyxoviruses from North America". Journal of Virology. 96 (3): e0109821. doi:10.1128/JVI.01098-21. ISSN 1098-5514. Archived from the original on 11 November 2022. Retrieved 27 March 2023.
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External links

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