Hutchinson, Edward C.

Trends in Microbiology

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Trends in Microbiology | Microbe of the MonthInfluenza Virus
Edward C. Hutchinson1,*
1MRC-University of Glasgow Centre for Virus Research, 464 Bearsden Road, Glasgow G61 1QH, UKKEY FACTS:
Virus with an unusual ability to adapt to
new vertebrate host species.
Negative-sense RNA genome, 12–
14 kb, in eight (IAV, IBV) or seven (ICV,
IDV) segments.
IAV, IBV, and ICV are highly
transmissible human respiratory
pathogens.
Global distribution. In temperate
climates, peaks in winter months.
Adaptation of new IAV strains to
humans causes pandemics.
Diverse IAV strains circulate in
waterfowl, often as asymptomatic
gastrointestinal infections.
DISEASE FACTS:
An acute infection. In humans, viral
shedding begins after around 1 day
and peaks before the onset of
symptoms.
Typical symptoms include sudden
onset of fever, muscle pain, headachesRNP NP Polymerase
subunit
HA NA M1 M2 NS1 NEP Viral receptor
(5) TranslaƟon
Golgi
mRNA
(4) TranscripƟon
vRNA
cRNA
(6) ReplicaƟon
of vRNA (-ve) via
a cRNA (+ve)
intermediate
(3) UncoaƟng and
membrane fusion
(2) Endocytosis
(1) AƩachment
to sialic acid
Influenza virions
(7) Virion budding
and release
Key:
This infographic briefly summarises the natural history, replication cycle, and pathogenesis of influenza viruses,
the cause of seasonal influenza and of influenza pandemics. and exhaustion, peaking 2–3 days after
infection and resolving within 1–2
weeks.
Serious illness occurs in a minority of
cases, often due to secondary bacterial
infections or exacerbation of
cardiovascular and respiratory illness.
At-risk groups include infants, older
adults, pregnant women, and the
immunocompromised.
The large total number of cases meansInfluenza viruses infect many vertebrates, with Influenza A, B and C viruses (IAV, IBV, and ICV) infecting humans.
High mutation rates allow the evasion of immunity. IAV from different host species can ‘reassort’ their segmented
genomes, producing pandemic strains that are antigenically novel but otherwise well adapted to humans.
The ‘Great Influenza’ pandemic of 1918 remains the worst outbreak of infectious disease in history. There is
concern that highly pathogenic avian influenza viruses of the H5 and H7 subtypes may evolve to cause similar
pandemics.
In humans, influenza viruses infect the respiratory epithelium. The haemagglutinin (HA) proteins of IAV and IBV, or
the haemagglutinin-esterase-fusion (HEF) proteins of ICV, bind sialic acid, causing endocytosis. Unusually
among RNA viruses, the viral genome replicates in the nucleus. New viruses assemble at the cell surface and are
released by the receptor-cleaving neuraminidase (NA) proteins of IAV and IBV or the ICV HEF protein.that seasonal influenza, mainly caused
by IAV and IBV, typically kills 290 000–
650 000 a year globally.
IAV pandemics can be more serious.
The ‘Great Influenza’ of 1918 killed
around 1 in 30 of the global population
in 18 months.
IAV also causes serious illness in
poultry.
Seasonal influenza vaccines are
available but must be regularly
updated.
NA inhibitors can be used for
treatment.
*Correspondence:H1N1 H1N1 H1N1H2N2
H3N2
1918 1957 1977 2009
1968
Reassortment
“anƟgenic shiŌ”
MutaƟons
“anƟgenic driŌ”
Weaker immunity:
seasonal epidemics
No immunity:
pandemics
ExisƟng immunity:
IAV pandemics
introduce new
seasonal strainsTrends in Microbiology, SeptembTAXONOMY AND CLASSIFICATION:
ORDER: Unassigned
FAMILY: Orthomyxoviridae
GENERA (SPECIES): Alphainfluenzavirus (Influenza A virus),
Betainfluenzavirus (Influenza B virus), Gammainfluenzavirus
(Influenza C virus) and Deltainfluenzavirus (Influenza D virus)
can all infect mammals. Distinct influenza viruses of fish
and amphibians have been reported
SUBTYPES AND LINEAGES: based on the major surface
antigens, there are 18 HA (H1–H18) and 11 NA (N1–N11)
subtypes of Influenza A virus and two recent lineages,
‘Victoria’ and ‘Yamagata,’ of Influenza B virus
GENOME: segmented, negative-sense RNA
STRUCTURE: enveloped, pleomorphic (ranging from
spheres to extremely long filaments) with a helical capsidedward.hutchinson@glasgow.ac.uk
(E.C. Hutchinson).er 2018, Vol. 26, No. 9 © 2018 The Author. Published by Elsevier Ltd. This
is an open access article under the CC BY license
(http://creativecommons.org/licenses/by/4.0/).
https://doi.org/10.1016/j.tim.2018.05.013 809
Trends in Microbiology | Microbe of the Month
Acknowledgments
E.C.H. is funded by an MRC Career Development Award (MR/N008618/1).
Literature
1. Carrat, F. et al. (2008) Time lines of infection and disease in human influenza: a review of volunteer challenge studies. Am. J. Epidemiol. 167, 775–785
2. Iuliano, A.D. et al. (2018) Estimates of global seasonal influenza-associated respiratory mortality: a modelling study. Lancet 391, 1285–1300
3. Hirve, S. et al. (2016) Influenza seasonality in the tropics and subtropics – when to vaccinate? PLoS One 11, e0153003
4. Shi, M. et al. (2018) The evolutionary history of vertebrate RNA viruses. Nature 556, 197–202
5. Taubenberger, J.K. and Morens, D.M. (2006) 1918 Influenza: the mother of all pandemics. Emerg. Infect. Dis. 12, 15–22
6. Webster, R.G. et al. (1992) Evolution and ecology of influenza A viruses. Microbiol. Rev. 56, 152–179
7. Krammer, F. and Palese, P. (2015) Advances in the development of influenza virus vaccines. Nat. Rev. Drug Discov. 14, 167–182
8. Farrukee, R. and Hurt, A.C. (2017) Antiviral drugs for the treatment and prevention of influenza. Curr. Treatm. Options Infect. Dis. 9, 318–332
9. Eisfeld, A.J. et al. (2015) At the centre: influenza A virus ribonucleoproteins. Nat. Rev. Microbiol. 13, 28–41810 Trends in Microbiology, September 2018, Vol. 26, No. 9 © 2018 The Author. Published by Elsevier Ltd. This
is an open access article under the CC BY license
(http://creativecommons.org/licenses/by/4.0/).
https://doi.org/10.1016/j.tim.2018.05.013


Influenza virus

Edward C. Hutchinson

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Influenza Virus

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Trends in Microbiology | Microbe of the MonthInﬂuenza VirusEdward C. Hutchinson1,*1MRC-University of Glasgow Centre for Virus Research, 464 Bearsden Road, Glasgow G61 1QH, UKKEY FACTS:Virus with an unusual ability to adapt tonew vertebrate host species.Negative-sense RNA genome, 12–14 kb, in eight (IAV, IBV) or seven (ICV,IDV) segments.IAV, IBV, and ICV are highlytransmissible human respiratorypathogens.Global distribution. In temperateclimates, peaks in winter months.Adaptation of new IAV strains tohumans causes pandemics.Diverse IAV strains circulate inwaterfowl, often as asymptomaticgastrointestinal infections.DISEASE FACTS:An acute infection. In humans, viralshedding begins after around 1 dayand peaks before the onset ofsymptoms.Typical symptoms include suddenonset of fever, muscle pain, headachesRNP NP PolymerasesubunitHA NA M1 M2 NS1 NEP Viral receptor(5) TranslaƟonGolgimRNA(4) TranscripƟonvRNAcRNA(6) ReplicaƟonof vRNA (-ve) viaa cRNA (+ve)intermediate(3) UncoaƟng andmembrane fusion(2) Endocytosis(1) AƩachmentto sialic acidInfluenza virions(7) Virion buddingand releaseKey:This infographic brieﬂy summarises the natural history, replication cycle, and pathogenesis of inﬂuenza viruses,the cause of seasonal inﬂuenza and of inﬂuenza pandemics. and exhaustion, peaking 2–3 days afterinfection and resolving within 1–2weeks.Serious illness occurs in a minority ofcases, often due to secondary bacterialinfections or exacerbation ofcardiovascular and respiratory illness.At-risk groups include infants, olderadults, pregnant women, and theimmunocompromised.The large total number of cases meansInﬂuenza viruses infect many vertebrates, with Inﬂuenza A, B and C viruses (IAV, IBV, and ICV) infecting humans.High mutation rates allow the evasion of immunity. IAV from different host species can ‘reassort’ their segmentedgenomes, producing pandemic strains that are antigenically novel but otherwise well adapted to humans.The ‘Great Inﬂuenza’ pandemic of 1918 remains the worst outbreak of infectious disease in history. There isconcern that highly pathogenic avian inﬂuenza viruses of the H5 and H7 subtypes may evolve to cause similarpandemics.In humans, inﬂuenza viruses infect the respiratory epithelium. The haemagglutinin (HA) proteins of IAV and IBV, orthe haemagglutinin-esterase-fusion (HEF) proteins of ICV, bind sialic acid, causing endocytosis. Unusuallyamong RNA viruses, the viral genome replicates in the nucleus. New viruses assemble at the cell surface and arereleased by the receptor-cleaving neuraminidase (NA) proteins of IAV and IBV or the ICV HEF protein.that seasonal inﬂuenza, mainly causedby IAV and IBV, typically kills 290 000–650 000 a year globally.IAV pandemics can be more serious.The ‘Great Inﬂuenza’ of 1918 killedaround 1 in 30 of the global populationin 18 months.IAV also causes serious illness inpoultry.Seasonal inﬂuenza vaccines areavailable but must be regularlyupdated.NA inhibitors can be used fortreatment.*Correspondence:H1N1 H1N1 H1N1H2N2H3N21918 1957 1977 20091968Reassortment“anƟgenic shiŌ”MutaƟons“anƟgenic driŌ”Weaker immunity:seasonal epidemicsNo immunity:pandemicsExisƟng immunity:IAV pandemicsintroduce newseasonal strainsTrends in Microbiology, Month TAXONOMY AND CLASSIFICATION:ORDER: UnassignedFAMILY: OrthomyxoviridaeGENERA (SPECIES): Alphainﬂuenzavirus (Inﬂuenza A virus),Betainﬂuenzavirus (Inﬂuenza B virus), Gammainﬂuenzavirus(Inﬂuenza C virus) and Deltainﬂuenzavirus (Inﬂuenza D virus)can all infect mammals. Distinct inﬂuenza viruses of ﬁshand amphibians have been reportedSUBTYPES AND LINEAGES: based on the major surfaceantigens, there are 18 HA (H1–H18) and 11 NA (N1–N11)subtypes of Inﬂuenza A virus and two recent lineages,‘Victoria’ and ‘Yamagata,’ of Inﬂuenza B virusGENOME: segmented, negative-sense RNASTRUCTURE: enveloped, pleomorphic (ranging fromspheres to extremely long ﬁlaments) with a helical capsidedward.hutchinson@glasgow.ac.uk(E.C. Hutchinson).Year, Vol. xx, No. yy © 2018 The Author. Published by Elsevier Ltd. Thisis an open access article under the CC BY license(http://creativecommons.org/licenses/by/4.0/).https://doi.org/10.1016/j.tim.2018.05.013 1Trends in Microbiology | Microbe of the MonthAcknowledgmentsE.C.H. is funded by an MRC Career Development Award (MR/N008618/1).Literature1. Carrat, F. et al. (2008) Time lines of infection and disease in human inﬂuenza: a review of volunteer challenge studies. Am. J. Epidemiol. 167, 775–7852. Iuliano, A.D. et al. (2018) Estimates of global seasonal inﬂuenza-associated respiratory mortality: a modelling study. Lancet 391, 1285–13003. Hirve, S. et al. (2016) Inﬂuenza seasonality in the tropics and subtropics – when to vaccinate? PLoS One 11, e01530034. Shi, M. et al. (2018) The evolutionary history of vertebrate RNA viruses. Nature 556, 197–2025. Taubenberger, J.K. and Morens, D.M. (2006) 1918 Inﬂuenza: the mother of all pandemics. Emerg. Infect. Dis. 12, 15–226. Webster, R.G. et al. (1992) Evolution and ecology of inﬂuenza A viruses. Microbiol. Rev. 56, 152–1797. Krammer, F. and Palese, P. (2015) Advances in the development of inﬂuenza virus vaccines. Nat. Rev. Drug Discov. 14, 167–1828. Farrukee, R. and Hurt, A.C. (2017) Antiviral drugs for the treatment and prevention of inﬂuenza. Curr. Treatm. Options Infect. Dis. 9, 318–3329. Eisfeld, A.J. et al. (2015) At the centre: inﬂuenza A virus ribonucleoproteins. Nat. Rev. Microbiol. 13, 28–412 Trends in Microbiology, Month Year, Vol. xx, No. yy © 2018 The Author. Published by Elsevier Ltd. Thisis an open access article under the CC BY license(http://creativecommons.org/licenses/by/4.0/).https://doi.org/10.1016/j.tim.2018.05.013

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