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Este artículo trata sobre la familia de virus que contiene siete géneros. Para obtener información específica sobre la subfamilia que afecta a los humanos, consulte Influenza .
Ortomixoviridae
Fimmu-09-01581-g001.jpg
Diagrama de genoma, ARNm y virión de los virus de la influenza A y B
Clasificación de virus e
(no clasificado):Virus
Reino :Riboviria
Reino:Orthornavirae
Filo:Negarnaviricota
Clase:Instoviricetos
Pedido:Articulavirales
Familia:Ortomixoviridae
Genera

Orthomyxoviridae (ὀρθός, orthós , griego para "recto"; μύξα, mýxa , griego para " moco ") [1] es una familia de virus de ARN de sentido negativo . Incluye siete géneros : Alphainfluenzavirus , Betainfluenzavirus , Deltainfluenzavirus , Gammainfluenzavirus , Isavirus , Thogotovirus y Quaranjavirus . Los primeros cuatro géneros contienen virus que causan influenza en aves (ver también influenza aviar) y mamíferos , incluidos los seres humanos. Los isavirus infectan al salmón ; los togotovirus son arbovirus que infectan a vertebrados e invertebrados (como garrapatas y mosquitos ). [2] [3] [4] Los Quaranjavirus también son arbovirus, que infectan a vertebrados (aves) e invertebrados ( artrópodos ).

Los cuatro géneros de virus de la influenza que infectan a los vertebrados, que se identifican por diferencias antigénicas en su nucleoproteína y proteína de matriz , son los siguientes:

  • El virus de la alfainfluenza infecta a los seres humanos, otros mamíferos y aves, y causa todas las pandemias de gripe
  • Betainfluenzavirus infecta a humanos y focas
  • El virus deltainfluenza infecta a los cerdos y al ganado
  • El gammainfluenzavirus infecta a humanos, cerdos y perros .

Estructura [ editar ]

Estructura del virus de la influenza A

El virión del virus de la influenza es pleomórfico ; la envoltura viral puede presentarse en formas esféricas y filamentosas. En general, la morfología del virus es elipsoidal con partículas de 100 a 120  nm de diámetro o filamentosa con partículas de 80 a 100 nm de diámetro y hasta 20 µm de longitud. [5] Hay aproximadamente 500 proyecciones de superficie en forma de púas distintas en la envoltura, cada una de las cuales se proyecta a 10–14 nm de la superficie con densidades de superficie variables. El pico principal de glucoproteína (HA) está interpuesto de forma irregular por grupos de picos de neuraminidasa (NA), con una proporción de HA a NA de aproximadamente 10 a 1. [6]

La envoltura viral compuesta por una membrana de bicapa lipídica en la que se anclan los picos de glicoproteína encierra las nucleocápsidas ; nucleoproteínas de diferentes clases de tamaño con un bucle en cada extremo; la disposición dentro del virión es incierta. Las proteínas ribonucleares son filamentosas y caen en el rango de 50 a 130 nm de largo y 9 a 15 nm de diámetro con simetría helicoidal.

Genoma [ editar ]

Para obtener un ejemplo en profundidad, consulte la estructura genética del H5N1 .
Genomas del virus de la influenza. Los segmentos se traducen en polimerasa (PB1, PB2 y PA), hemaglutinina (HA), neuramindasa (NA), nucleoproteína (NP), proteína de membrana (M) y proteína no estructural (NS).

Los virus de la familia Orthomyxoviridae contienen de seis a ocho segmentos de ARN monocatenario lineal de sentido negativo. Tienen una longitud total del genoma de 10.000 a 14.600 nucleótidos (nt). [7] El genoma de la influenza A , por ejemplo, tiene ocho piezas de ARN de sentido negativo segmentado (13,5 kilobases en total). [8]

Las proteínas mejor caracterizadas del virus de la influenza son la hemaglutinina y la neuraminidasa , dos glicoproteínas grandes que se encuentran en el exterior de las partículas virales. La hemaglutinina es una lectina que media la unión del virus a las células diana y la entrada del genoma viral en la célula diana. [9] En contraste, la neuraminidasa es una enzima involucrada en la liberación del virus de la progenie de las células infectadas, al escindir los azúcares que se unen a las partículas virales maduras. La hemaglutinina (H) y la neuraminidasa (N) proteínas son dianas clave para los anticuerpos y los fármacos antivirales, [10] [11]y se utilizan para clasificar los diferentes serotipos de virus de influenza A, de ahí el H y N en H5N1 .

La secuencia del genoma tiene secuencias terminales repetidas; repetido en ambos extremos. Terminal se repite en el extremo 5 'de 12 a 13 nucleótidos de longitud. Secuencias de nucleótidos del extremo 3 'idénticas; lo mismo en géneros de la misma familia; la mayoría en ARN (segmentos), o en todas las especies de ARN. Terminal se repite en el extremo 3 'de 9 a 11 nucleótidos de longitud. El ácido nucleico encapsidado es únicamente genómico. Cada virión puede contener copias interferentes defectuosas. En la influenza A (H1N1), PB1-F2 se produce a partir de un marco de lectura alternativo en PB1. Los genes M y NS producen dos genes diferentes mediante un empalme alternativo . [12]

Ciclo de replicación [ editar ]

Infección y replicación del virus de la influenza. Los pasos de este proceso se analizan en el texto.

Por lo general, la influenza se transmite de mamíferos infectados a través del aire al toser o estornudar, creando aerosoles que contienen el virus, y de aves infectadas a través de sus excrementos . La influenza también puede transmitirse por saliva , secreciones nasales , heces y sangre . Las infecciones ocurren por contacto con estos fluidos corporales o con superficies contaminadas. Fuera de un huésped, los virus de la gripe pueden permanecer infecciosos durante aproximadamente una semana a la temperatura del cuerpo humano, más de 30 días a 0 ° C (32 ° F) e indefinidamente a temperaturas muy bajas (como los lagos en el noreste de Siberia ). Se pueden inactivar fácilmente con desinfectantes y detergentes..[13][14][15]

The viruses bind to a cell through interactions between its hemagglutinin glycoprotein and sialic acid sugars on the surfaces of epithelial cells in the lung and throat (Stage 1 in infection figure).[16] The cell imports the virus by endocytosis. In the acidic endosome, part of the hemagglutinin protein fuses the viral envelope with the vacuole's membrane, releasing the viral RNA (vRNA) molecules, accessory proteins and RNA-dependent RNA polymerase into the cytoplasm (Stage 2).[17] These proteins and vRNA form a complex that is transported into the cell nucleus, where the RNA-dependent RNA polymerase begins transcribing complementary positive-sense cRNA (Steps 3a and b).[18] The cRNA is either exported into the cytoplasm and translated (step 4), or remains in the nucleus. Newly synthesised viral proteins are either secreted through the Golgi apparatus onto the cell surface (in the case of neuraminidase and hemagglutinin, step 5b) or transported back into the nucleus to bind vRNA and form new viral genome particles (step 5a). Other viral proteins have multiple actions in the host cell, including degrading cellular mRNA and using the released nucleotides for vRNA synthesis and also inhibiting translation of host-cell mRNAs.[19]

Negative-sense vRNAs that form the genomes of future viruses, RNA-dependent RNA transcriptase, and other viral proteins are assembled into a virion. Hemagglutinin and neuraminidase molecules cluster into a bulge in the cell membrane. The vRNA and viral core proteins leave the nucleus and enter this membrane protrusion (step 6). The mature virus buds off from the cell in a sphere of host phospholipid membrane, acquiring hemagglutinin and neuraminidase with this membrane coat (step 7).[20] As before, the viruses adhere to the cell through hemagglutinin; the mature viruses detach once their neuraminidase has cleaved sialic acid residues from the host cell.[16] After the release of new influenza virus, the host cell dies.

Transcription of mRNAs initiated by viral polymerase using cap snatching

Orthomyxoviridae viruses are one of two RNA viruses that replicate in the nucleus (the other being retroviridae). This is because the machinery of orthomyxo viruses cannot make their own mRNAs. They use cellular RNAs as primers for initiating the viral mRNA synthesis in a process known as cap snatching.[21] Once in the nucleus, the RNA Polymerase Protein PB2 finds a cellular pre-mRNA and binds to its 5′ capped end. Then RNA Polymerase PA cleaves off the cellular mRNA near the 5′ end and uses this capped fragment as a primer for transcribing the rest of the viral RNA genome in viral mRNA.[22] This is due to the need of mRNA to have a 5′ cap in order to be recognized by the cell's ribosome for translation.

Since RNA proofreading enzymes are absent, the RNA-dependent RNA transcriptase makes a single nucleotide insertion error roughly every 10 thousand nucleotides, which is the approximate length of the influenza vRNA. Hence, nearly every newly manufactured influenza virus will contain a mutation in its genome.[23] The separation of the genome into eight separate segments of vRNA allows mixing (reassortment) of the genes if more than one variety of influenza virus has infected the same cell (superinfection). The resulting alteration in the genome segments packaged into viral progeny confers new behavior, sometimes the ability to infect new host species or to overcome protective immunity of host populations to its old genome (in which case it is called an antigenic shift).[10]

Classification[edit]

In a phylogenetic-based taxonomy, the category RNA virus includes the subcategory negative-sense ssRNA virus, which includes the order Articulavirales, and the family Orthomyxoviridae. The genera-associated species and serotypes of Orthomyxoviridae are shown in the following table.

Orthomyxovirus Genera, Species, and Serotypes
GenusSpecies (* indicates type species)Serotypes or SubtypesHosts
AlphainfluenzavirusInfluenza A virus*H1N1, H1N2, H2N2, H3N1, H3N2, H3N8, H5N1, H5N2, H5N3, H5N8, H5N9, H7N1, H7N2, H7N3, H7N4, H7N7, H7N9, H9N2, H10N7Human, pig, bird, horse, bat
BetainfluenzavirusInfluenza B virus*Victoria, Yamagata[24]Human, seal
DeltainfluenzavirusInfluenza D virus*Pig, cattle
GammainfluenzavirusInfluenza C virus*Human, pig, dog
IsavirusInfectious salmon anemia virus*Atlantic salmon
ThogotovirusThogotovirus*Tick, mosquito, mammal (including human)
Dhori virusBatken virus, Bourbon virus, Jos virus
Quaranjavirus[25]
Quaranfil virus,* Johnston Atoll virus

Types[edit]

There are four genera of influenza virus, each containing only a single species, or type. Influenza A and C infect a variety of species (including humans), while influenza B almost exclusively infects humans, and influenza D infects cattle and pigs.[26][27][28]

Influenza A[edit]

Main article: Influenza A virus
Diagram of influenza nomenclature

Influenza A viruses are further classified, based on the viral surface proteins hemagglutinin (HA or H) and neuraminidase (NA or N). Sixteen H subtypes (or serotypes) and nine N subtypes of influenza A virus have been identified.

Further variation exists; thus, specific influenza strain isolates are identified by a standard nomenclature specifying virus type, geographical location where first isolated, sequential number of isolation, year of isolation, and HA and NA subtype.[29][30]

Examples of the nomenclature are:

  1. A/Brisbane/59/2007 (H1N1)
  2. A/Moscow/10/99 (H3N2).

The type A viruses are the most virulent human pathogens among the three influenza types and cause the most severe disease. The serotypes that have been confirmed in humans, ordered by the number of known human pandemic deaths, are:

  • H1N1 caused "Spanish flu" in 1918 and "Swine flu" in 2009.[31]
  • H2N2 caused "Asian Flu".
  • H3N2 caused "Hong Kong Flu".
  • H5N1, "avian" or "bird flu".[32]
  • H7N7 has unusual zoonotic potential.[33]
  • H1N2 infects pigs and humans.[34]
  • H9N2, H7N2, H7N3, H10N7.
Known flu pandemics[10][35][36]
Name of pandemicDateDeathsCase fatality rateSubtype involvedPandemic Severity Index
1889–1890 flu pandemic
(Asiatic or Russian Flu)[37]		1889–18901 million0.15%Possibly H3N8
or H2N2		N/A
1918 flu pandemic
(Spanish flu)[38]		1918–192020 to 100 million2%H1N15
Asian Flu1957–19581 to 1.5 million0.13%H2N22
Hong Kong Flu1968–19690.75 to 1 million<0.1%H3N22
Russian flu1977–1978No accurate countN/AH1N1N/A
2009 flu pandemic[39][40]2009–2010105,700–395,600[41]0.03%H1N1N/A

Influenza B[edit]

Main article: Influenza B virus
Host range of influenza viruses

Influenza B virus is almost exclusively a human pathogen, and is less common than influenza A. The only other animal known to be susceptible to influenza B infection is the seal.[42] This type of influenza mutates at a rate 2–3 times lower than type A[43] and consequently is less genetically diverse, with only one influenza B serotype.[26] As a result of this lack of antigenic diversity, a degree of immunity to influenza B is usually acquired at an early age. However, influenza B mutates enough that lasting immunity is not possible.[44] This reduced rate of antigenic change, combined with its limited host range (inhibiting cross species antigenic shift), ensures that pandemics of influenza B do not occur.[45]

Influenza C[edit]

Main article: Influenza C virus

The influenza C virus infects humans and pigs, and can cause severe illness and local epidemics.[46] However, influenza C is less common than the other types and usually causes mild disease in children.[47][48]

Influenza D[edit]

Main article: Influenza D virus

This is a genus that was classified in 2016, the members of which were first isolated in 2011.[49] This genus appears to be most closely related to Influenza C, from which it diverged several hundred years ago.[50] There are at least two extant strains of this genus.[51] The main hosts appear to be cattle, but the virus has been known to infect pigs as well.

Viability and disinfection[edit]

Mammalian influenza viruses tend to be labile, but can survive several hours in mucus.[52] Avian influenza virus can survive for 100 days in distilled water at room temperature, and 200 days at 17 °C (63 °F). The avian virus is inactivated more quickly in manure, but can survive for up to 2 weeks in feces on cages. Avian influenza viruses can survive indefinitely when frozen.[52] Influenza viruses are susceptible to bleach, 70% ethanol, aldehydes, oxidizing agents, and quaternary ammonium compounds. They are inactivated by heat of 133 °F (56 °C) for minimum of 60 minutes, as well as by low pH <2.[52]

Vaccination and prophylaxis[edit]

Targets of anti-influenza agents that are licensed or under investigation

Vaccines and drugs are available for the prophylaxis and treatment of influenza virus infections. Vaccines are composed of either inactivated or live attenuated virions of the H1N1 and H3N2 human influenza A viruses, as well as those of influenza B viruses. Because the antigenicities of the wild viruses evolve, vaccines are reformulated annually by updating the seed strains.

When the antigenicities of the seed strains and wild viruses do not match, vaccines fail to protect the vaccinees. In addition, even when they do match, escape mutants are often generated.

Drugs available for the treatment of influenza include Amantadine and Rimantadine, which inhibit the uncoating of virions by interfering with M2, and Oseltamivir (marketed under the brand name Tamiflu), Zanamivir, and Peramivir, which inhibit the release of virions from infected cells by interfering with NA. However, escape mutants are often generated for the former drug and less frequently for the latter drug.[53]

See also[edit]

  • Dog flu
  • Influenza-like illness

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Further reading[edit]

  • Hoyle, L. (1969). The Influenza Viruses. Virology Monographs. 4. Springer-Verlag. ISBN 978-3-211-80892-4. ISSN 0083-6591. OCLC 4053391.

External links[edit]

  • Health-EU Portal EU work to prepare a global response to influenza.
  • Influenza Research Database Database of influenza genomic sequences and related information.
  • European Commission—Public Health EU coordination on Pandemic (H1N1) 2009
  • 3D Influenza-virus-related structures from the EM Data Bank(EMDB)
  • Viralzone: Orthomyxoviridae
  • ICTV