Positive-sense single-stranded RNA virus

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Positive ssRNA Virus
HCV EM picture 2.png
Hepatitis C virus
Virus classification
Group IV ((+)ssRNA)
Orders, Families, and Genera

A positive-sense single-stranded RNA virus (or (+)ssRNA virus) is a virus that uses positive sense, single-stranded RNA as its genetic material. Single stranded RNA viruses are classified as positive or negative depending on the sense or polarity of the RNA. The positive-sense viral RNA genome can serve as messenger RNA and can be translated into protein in the host cell. Positive-sense ssRNA viruses belong to Group IV in the Baltimore classification.[1] Positive-sense RNA viruses account for a large fraction of known viruses, including many pathogens such as the hepatitis C virus, West Nile virus, dengue virus, SARS and MERS coronaviruses, and SARS-CoV-2[2] as well as less clinically serious pathogens such as the rhinoviruses that cause the common cold.[3][4][5]


Positive-sense ssRNA viruses have genetic material that can function both as a genome and as messenger RNA; it can be directly translated into protein in the host cell by host ribosomes.[6] The first proteins to be expressed after infection serve genome replication functions; they recruit the positive-strand viral genome to viral replication complexes (VRCs) formed in association with intracellular membranes. VRCs contain proteins of both viral and host cell origin, and may be associated with the membranes of a variety of organelles, often the rough endoplasmic reticulum, but also including membranes derived from mitochondria, vacuoles, the Golgi apparatus, chloroplasts, peroxisomes, plasma membranes, autophagosomal membranes, and novel cytoplasmic compartments.[3] The replication of the positive-sense ssRNA genome proceeds through double-stranded RNA intermediates, and the purpose of replication in these membranous invaginations may be the avoidance of cellular response to the presence of dsRNA. In many cases subgenomic RNAs are also created during replication.[6] After infection, the entirety of the host cell's translation machinery may be diverted to the production of viral proteins as a result of the very high affinity for ribosomes of the viral genome's internal ribosome entry site (IRES) elements; in some viruses, such as poliovirus and rhinoviruses, normal protein synthesis is further disrupted by viral proteases degrading components required to initiate translation of cellular mRNA.[5]

All positive-sense ssRNA virus genomes encode RNA-dependent RNA polymerase (RdRP), a viral protein that synthesizes RNA from an RNA template. Host cell proteins recruited by positive-sense ssRNA viruses during replication include RNA-binding proteins, chaperone proteins, and membrane remodeling and lipid synthesis proteins, which collectively participate in exploiting the cell's secretory pathway for viral replication.[3]


The genome of a positive-sense ssRNA virus usually contains relatively few genes, usually between three and ten, including an RdRP.[3] Coronaviruses have the largest known RNA genomes, up to 32 kilobases in length, and likely possess replication proofreading mechanisms in the form of a proofreading exoribonuclease, non-structural protein 14, that is otherwise not found in RNA viruses.[7]

Taxonomic distribution[edit]

The (+)ssRNA viruses are classified into 3 orders — the Nidovirales, Picornavirales, and Tymovirales — and 33 families, of which 20 are not assigned to an order. A broad range of hosts can be infected by (+)ssRNA viruses, including bacteria (the Leviviridae), eukaryotic microorganisms, plants, invertebrates, and vertebrates.[8] No examples have been described that infect archaea, whose virome is generally much less well-characterized.[8][9]


Among known (+)ssRNA viruses, only the Leviviridae are bacteriophages (that is, viruses that infect bacteria). Known leviviruses infect enterobacteria. Phage with RNA genomes are relatively rare and poorly understood, with only one other recognized group — a family of double-stranded RNA viruses called the Cystoviridae. However, metagenomics has led to the identification of numerous additional novel examples.[10]


Positive-sense ssRNA viruses are the most common type of plant virus.[11] Members of the (+)ssRNA picornavirus group are also extremely abundant — to the point of "unexpected dominance" — in marine viruses characterized by metagenomics. These viruses likely infect single-celled eukaryotes.[12]

There are eight families of (+)ssRNA viruses that infect vertebrates, of which four are unenveloped (Picornaviridae, Astroviridae, Caliciviridae, and Hepeviridae) and four are enveloped (Flaviviridae, Togaviridae, Arteriviridae, and Coronaviridae). All but the arterivirus family contain at least one human pathogen; arteriviruses are known only as animal pathogens.[5] Many pathogenic (+)ssRNA viruses are arthropod-borne viruses (also called arboviruses) — that is, transmitted by and capable of replicating in biting insects which then transfer the pathogen to animal hosts. Recent metagenomics studies have also identified large numbers of RNA viruses whose host range is specific to insects.[13]

See also[edit]


  1. ^ Baltimore, D (1971). "Expression of animal virus genomes". Bacteriological Reviews. 35 (3): 235–241. PMC 378387. PMID 4329869.
  2. ^ Lu, Roujian; Zhao, Xiang; Li, Juan; Niu, Peihua; Yang, Bo; Wu, Honglong; Wang, Wenling; Song, Hao; Huang, Baoying; Zhu, Na; Bi, Yuhai; Ma, Xuejun; Zhan, Faxian; Wang, Liang; Hu, Tao; Zhou, Hong; Hu, Zhenhong; Zhou, Weimin; Zhao, Li; Chen, Jing; Meng, Yao; Wang, Ji; Lin, Yang; Yuan, Jianying; Xie, Zhihao; Ma, Jinmin; Liu, William J; Wang, Dayan; Xu, Wenbo; Holmes, Edward C; Gao, George F; Wu, Guizhen; Chen, Weijun; Shi, Weifeng; Tan, Wenjie (January 2020). "Genomic characterisation and epidemiology of 2019 novel coronavirus: implications for virus origins and receptor binding". The Lancet. doi:10.1016/S0140-6736(20)30251-8.
  3. ^ a b c d Nagy, Peter D.; Pogany, Judit (19 December 2011). "The dependence of viral RNA replication on co-opted host factors". Nature Reviews Microbiology. 10 (2): 137–149. doi:10.1038/nrmicro2692. PMID 22183253.
  4. ^ Ahlquist, P.; Noueiry, A. O.; Lee, W.-M.; Kushner, D. B.; Dye, B. T. (1 August 2003). "Host Factors in Positive-Strand RNA Virus Genome Replication". Journal of Virology. 77 (15): 8181–6. doi:10.1128/JVI.77.15.8181-8186.2003. PMC 165243. PMID 12857886.
  5. ^ a b c Modrow, Susanne; Falke, Dietrich; Truyen, Uwe; Schätzl, Hermann (2013). "Viruses with Single-Stranded, Positive-Sense RNA Genomes". Molecular virology. Berlin, Heidelberg: Springer Berlin Heidelberg. pp. 185–349. doi:10.1007/978-3-642-20718-1_14. ISBN 978-3-642-20718-1.
  6. ^ a b "Positive stranded RNA virus replication". ViralZone. Retrieved 8 September 2016.
  7. ^ Smith, Everett Clinton; Denison, Mark R.; Racaniello, Vincent (5 December 2013). "Coronaviruses as DNA Wannabes: A New Model for the Regulation of RNA Virus Replication Fidelity". PLoS Pathogens. 9 (12): e1003760. doi:10.1371/journal.ppat.1003760. PMC 3857799. PMID 24348241.
  8. ^ a b "Positive Strand RNA Viruses". ViralZone. Retrieved 10 September 2016.
  9. ^ Koonin, Eugene V; Dolja, Valerian V (October 2013). "A virocentric perspective on the evolution of life". Current Opinion in Virology. 3 (5): 546–557. doi:10.1016/j.coviro.2013.06.008. PMC 4326007. PMID 23850169.
  10. ^ Krishnamurthy, Siddharth R.; Janowski, Andrew B.; Zhao, Guoyan; Barouch, Dan; Wang, David; Sugden, Bill (24 March 2016). "Hyperexpansion of RNA Bacteriophage Diversity". PLOS Biology. 14 (3): e1002409. doi:10.1371/journal.pbio.1002409. PMC 4807089. PMID 27010970.
  11. ^ Saxena, Pooja; Lomonossoff, George P. (4 August 2014). "Virus Infection Cycle Events Coupled to RNA Replication". Annual Review of Phytopathology. 52 (1): 197–212. doi:10.1146/annurev-phyto-102313-050205. PMID 24906127.
  12. ^ Kristensen, David M.; Mushegian, Arcady R.; Dolja, Valerian V.; Koonin, Eugene V. (January 2010). "New dimensions of the virus world discovered through metagenomics". Trends in Microbiology. 18 (1): 11–19. doi:10.1016/j.tim.2009.11.003. PMC 3293453. PMID 19942437.
  13. ^ Vasilakis, Nikos; Tesh, Robert B (December 2015). "Insect-specific viruses and their potential impact on arbovirus transmission". Current Opinion in Virology. 15: 69–74. doi:10.1016/j.coviro.2015.08.007. PMC 4688193. PMID 26322695.