Influenzavirus C

Virus classification
Group: Group V ((-)ssRNA)
Family: Orthomyxoviridae

Influenza virus A
Influenza virus B
Influenza virus C

Influenza virus C is a genus in the virus family Orthomyxoviridae, which includes those viruses which cause influenza.

The species in this genus is called Influenza C virus. Influenza C viruses are known to infect humans and pigs.[1]

Flu due to the type C species is rare compared to types A or B, but can be severe and can cause local epidemics. Subtype C has 7 RNA segments and encodes 9 proteins, while types A and B have 8 RNA segments and encode at least 10 proteins.

Influenza C virus

Influenza viruses are members of the family Orthomyxoviridae.[2] Influenza viruses A, B and C represent the three antigenic types of influenza viruses.[3] Of the three antigenic types, influenza virus A is the most severe, influenza virus B is less severe but can still cause outbreaks, and influenza virus C is usually only associated with minor symptoms.[4]

Influenza virus A can infect a variety of animals as well as humans and its natural host or reservoir is birds whereas influenza viruses B and C do not have animal reservoirs.[4][5] Influenza virus C is not as easily isolated so less information is known of this type, but studies show that it occurs worldwide.[6]

This virus may be spread from person to person through respiratory droplets or by fomites (non-living material) due to its ability to survive on surfaces for short durations.[4] Influenza viruses have a relatively short incubation period (lapse of time from exposure to pathogen to the appearance of symptoms) of 18–72 hours and infect the epithelial cells of the respiratory tract.[4] Influenza virus C tends to cause mild upper respiratory infections.[7] Cold-like symptoms are associated with the virus including fever (38-40ᵒC), dry cough, rhinorrhea (nasal discharge), headache, muscle pain, and achiness.[4][8] The virus may lead to more severe infections such as bronchitis and pneumonia.[7]

After an individual becomes infected, the immune system develops antibodies against that infectious agent. This is the body’s main source of protection.[4] Most children between five and ten years old have already produced antibodies for influenza virus C.[8] As with all influenza viruses, type C affects individuals of all ages, but is most severe in young children, the elderly and individuals with underlying health problems.[4][9] Young children have less prior exposure and have not developed the antibodies and the elderly have less effective immune systems.[4] Influenza virus infections have one of the highest preventable mortalities in many countries of the world.[9]

Structure and Variation

Influenza viruses, like all viruses in the Orthomyxoviridae family, are enveloped RNA viruses with single stranded genomes.[2] The antigens, matrix protein (M1) and nucleoprotein (NP), are used to determine if an influenza virus is type A, B, or C.[4] The M1 protein is required for virus assembly and NP functions in transcription and replication.[10][11] These viruses also contain proteins on the surface of the cell membrane called glycoproteins. Type A and B have two glycoproteins: hemagglutinin (HA) and neuraminidase (NA). Type C has only one glycoprotein: hemagglutinin-esterase fusion (HEF).[4][12] These glycoproteins allow for attachment and fusion of viral and cellular membranes. Fusion of these membranes allows the viral proteins and genome to be released into the host cell, which then causes the infection.[13] Type C is the only influenza virus to express the enzyme esterase. This enzyme is similar to the enzyme neuraminidase produced by type A and B in that they both function in destroying the host cell receptors.[7] Glycoproteins may undergo mutations (antigenic drift) or reassortment in which a new HA or NA is produced (antigenic shift). Influenza virus C is only capable of antigenic drift whereas type A undergo antigenic shift, as well. When either of these processes occur, the antibodies formed by the immune system no longer protect against these altered glycoproteins. Because of this, viruses continually cause infections.[4]


Influenza virus C is different from type A and B in its growth requirements. Because of this it is not isolated and identified as frequently. Diagnosis is by virus isolation, serology, and other tests.[8] Hemagglutination inhibition (HI) is one method of serology that detects antibodies for diagnostic purposes.[6] Western blot (immunoblot assay) and enzyme-linked immunosorbent assay (ELISA) are two other methods used to detect proteins (or antigens) in serum. In each of these techniques, the antibodies for the protein of interest are added and the presence of the specific protein is indicated by a color change.[14] ELISA was shown to have higher sensitivity to the HEF than the HI test.[5] Because only influenza virus C produces esterase, In Situ Esterase Assays provide a quick and inexpensive method of detecting just type C.[7] If more individuals were tested for influenza virus C as well as the other two types, infections not previously associated with type C may be recognized.[7]


Effective and safe vaccines have been developed for influenza viruses.[15] The Center for Disease Control and Prevention (CDC) and the World Health Organization (WHO) are constantly surveying the wild population of viruses. In doing this, they are able to predict which virus strains might cause the most harm each year during flu season. The strains expected to be most harmful are put into the vaccine for that year's flu vaccine. These vaccines are more commonly known as “flu shots”.[4]

Vaccines can use living strains that have been made less harmful or inactive strains. Both forms work by exposing the body to the viral strains within the vaccine. As a result, the immune system develops antibodies providing protection from these strains.[3] Studies show that the vaccines containing less harmful forms of living strains are more effective in providing immunity.[16] It is recommended that all individuals be vaccinated each year, especially health care providers and individuals with chronic illness, in order to prevent infection from influenza viruses.[9][16] Influenza virus vaccines have beneficial implications to an individual’s health.[16]

Because influenza virus A has an animal reservoir that contains all the known subtypes and it can undergo antigenic shift, this type of influenza virus is capable of producing pandemics.[5] Influenza viruses A and B also cause seasonal epidemics every year due to their ability to antigenic shift.[3] Influenza virus C does not have this capability and it is not thought to be a significant concern for human health.[5] Therefore, there are no vaccinations against influenza virus C.[4]


  1. Guo Y.; Jin F.; Wang P.; Wang M.; Zhu J.M. (1983). "Isolation of Influenza C Virus from Pigs and Experimental Infection of Pigs with Influenza C Virus". Journal of General Virology. 64: 177–82. doi:10.1099/0022-1317-64-1-177. PMID 6296296.
  2. 1 2 Pattison, McMullin, Bradbury, Alexander. Poultry Diseases 6th Edition. Elsevier Limited. 2008. P.317. ISBN 978-0-7020-28625.
  3. 1 2 3 “Seasonal Influenza (Flu)” Centers for Disease Control and Prevention. March 22, 2012.
  4. 1 2 3 4 5 6 7 8 9 10 11 12 13 Margaret Hunt. “Microbiology and Immunology On-line” University of South Carolina School of Medicine. 2009.
  5. 1 2 3 4 “Review of latest available evidence on potential transmission of avian influenza (H5H1) through water and sewage and ways to reduce the risks to human health” World Health Organization. 2006. background.pdf
  6. 1 2 Manuguerra JC, Hannoun C, Saenz MDC, Villarand E, Cabezas JA. 1994. “Sero-Epidemiological Survey of Influenza C Virus Infection in Spain” European Journal of Epidemiology. 10(1):91-94.
  7. 1 2 3 4 5 Wagaman PC, Spence HA, and O’Callaghan RJ. 1989. “Detection of Influenza C Virus by Using an In Situ Esterase Assay” Journal of Clinical Microbiology. 1:832-836.
  8. 1 2 3 Matsuzaki Y, Katsushima N, Nagai Y, Shoji M, Itagaki T, Sakamoto M, Kitaoka S, Mizuta K, Nishimura H. 2006. “Clinical Features of Influenza C Virus Infection in Children” The Journal of Infectious Diseases. 193(9):1229-1235.
  9. 1 2 3 Ballada D, Biasio LR, Cascio G, D’Alessandro D, Donatelli I, Fara GM, Pozzi T, Profeta ML, Squarcione S, Ricco D, Todisco T, Vacca F. 1994. “Attitudes and Behavior of Health Care Personnel Regarding Influenza Vaccination” European Journal of Epidemiology. 10(1):63-68.
  10. Ayub A, Avalos RT, Ponimaskin E, and Nayak DP. “Influenza virus assembly: Effect of influenza virus glycoproteins on the membrane association of M1 protein” Journal of Virology. 74(18):8709-8719.
  11. Portela A and Digard P. “The Influenza Virus Nucleoprotein: A Multifunctional RNA-binding Protein Pivotal to Virus Replication” Journal of General Virology. 83(4):723-734.
  12. Gao Q, Brydon EWA, Palese P. 2008. “A Seven-segmented Influenza A Virus Expressing the Influenza C Virus Glycoprotein HEF” Journal of Virology. 82(13):6419-6426.
  13. Weissenhorn W, Dessen A, Calder LJ, Harrison SC, Skehel JJ, Wiley DC. 1999. “Structural Basis for Membrane Fusion by Enveloped Viruses” Molecular Membrane Biology. 1:3-9.
  14. Nelson DL and Cox MM. Principles of Biochemistry 6th Edition. Susan Winslow 2013. P. 179. ISBN 978-1-4292-3414-6.
  15. Belshe RB, Mendelman PM, Treanor J, King J, Gruber WC, Piedra P, Bernstein DI, Hayden FG, Kotloff K, Zangwill K, Iacuzio D, and Wolff M. 1998. “The Efficacy of Live Attenuated, Cold-adapted, Trivalent, Intranasal Influenzavirus Vaccine in Children” New England Journal of Medicine. 338:1405-1412.
  16. 1 2 3 Belshe RB and Gruber WC. 2001. “Safety, Efficacy and Effectiveness of Cold-Adapted, Live, Attenuated, Trivalent, Intranasal Influenza Vaccine in Adults and Children” Philosophical Transactions: Biological Sciences. 356(1416):1947-1951.

Further reading

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