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Type Species |
(FLUAV) |
Member viruses of the genus Influenzavirus A all have 8 genome segments. Hemagglutinin and the neuraminidase receptor-destroying enzyme are different glycoproteins. The conserved end sequences of the viral RNAs of the influenzaviruses A are 5-AGUAGAAACAAGG . . . , and 3-UCG(U/C)UUUCGUCC . . . The exact order of electrophoretic migration of the RNA segments varies with strain and electrophoretic conditions. On the basis of the gene sequences, for Influenza A virus the segments 1-3 encoded PB1, PB2 and PA proteins are estimated to have an Mr ± 87 103 (observed: ± 96 103), 84 103 (observed: 87 103) and 83 103 (observed: 85 103), respectively. The segment 4 encoded (unglycosylated) HA is ± 63 103 (glycosylated HA1 is ± 48 103, HA2 is ± 29 103). The segment 5 encoded NP is ± 56 103 (observed: 50-60 103). The segment 6 encoded NA is ± 50 103 (observed: 48-63 103). The segment 7 encoded M1 and M2 proteins are ± 28 103 (observed: 25 103) and 11 103 (observed: 15 103), respectively. The segment 8 encoded NS1 and NS2 are 27 103 (observed: 25 103) and 14 103 (observed: 12 103) respectively.
Antigenic variation occurring within the HA and NA antigens of influenzaviruses A has been analyzed in detail. Fifteen subtypes of HA and nine subtypes of NA are recognized for influenzaviruses A, with minimal serological cross-reaction between subtypes. Additional variation occurs within subtypes. By convention, new isolates are designated by their serotype/host species/site of origin/strain designation/and year of origin and (HA [H] and NA [N] subtype), e.g., A/tern/South Africa/1/61 (H5N3). In humans, continual evolution of new strains occurs and older strains apparently disappear from circulation. Antibody to HA neutralizes infectivity. If NA antibody is present during multicycle replication it inhibits virus release and thus reduces virus yield. Antibody to the amino terminus of M2 reduces virus yield in tissue culture.
Epidemics of respiratory disease in humans during the 20th century have been caused by influenzaviruses A having the antigenic composition H1N1, H2N2 and H3N2. Limited outbreaks of respiratory disease in humans caused by antigenically novel viruses occurred in 1976 in Fort Dix, New Jersey when classical swine H1N1 viruses infected military recruits, in 1997 in Hong Kong when H5N1 viruses caused outbreaks in poultry and contemporaneous illnesses and deaths in humans, and in 1998 and 1999 when H9N2 viruses present in poultry caused illness in humans in China. Influenzaviruses A of subtype H7N7 and H3N8 (previously designated equine 1 and equine 2 viruses) cause outbreaks of respiratory disease in horses. Influenzaviruses A (H1N1), and (H3N2) have been isolated frequently from swine. The H1N1 viruses isolated from swine in recent years appear to be of three general categories: those closely related to classical “swine influenza” and which cause occasional human cases; those first recognized in avian specimens, but which have caused outbreaks and infections among swine in Europe and China; and those resembling viruses isolated from epidemics in humans since 1977. H3N2 viruses from swine appear to contain HA and NA genes closely related to those from human epidemic strains. Influenzaviruses A (H7N7 and H4N5) have caused outbreaks in seals, with virus spread to non-respiratory tissues in this host. In two separate cases, H7N7 viruses were isolated from conjunctival infections of a laboratory worker and a farm worker in 1980 and 1996, respectively. Pacific Ocean whales have reportedly been infected with type A (H1N1) virus. Other influenza subtypes have also been isolated from lungs of Atlantic Ocean whales in North America. FLUAV (H10N4) has caused outbreaks in mink. All subtypes of HA and NA, in many different combinations, have been identified in isolates from avian species, particularly wild aquatic birds, chickens, turkeys, and ducks. Pathology in avian species varies from inapparent infection (often involving replication in, and probable transmission via, the intestinal tract), to virulent infections (observed with subtypes H5 and H7) with spread to many tissues and high mortality rates. The structure of the HA protein, in particular the specificity of its receptor binding site and its cleavability by naturally occurring tissue protease(s), appears to be critical in determining the host range and organ tropisms of influenzaviruses. In addition, interactions between gene products determine the outcome of infection. Interspecies transmission apparently occurs in some instances without genetic reassortment (e.g., H1N1 virus from swine to humans and vice versa, H3N2 virus from humans to swine, and the recent transmissions of H5N1 and H9N2 viruses from poultry to humans). In other cases interspecies transmission may involve RNA segment reassortment in hosts infected with more than one strain of virus each with distinct host ranges, or epidemic properties (e.g., 1968 isolates of H3N2 viruses apparently were derived by reassortment between a human H2N2 virus and a virus containing an H3 HA; seal H7N7 virus probably was derived by reassortment of two or more avian influenzaviruses; and reassortment of human H1N1 and H3N2 viruses in 1978 and 1989 led to human infections by viruses with H1N1 or H1N2 surface proteins and 4 to 6 other genes of H3N2 origin). Laboratory animals that may be infected with influenzaviruses A include ferrets, mice, hamsters, and guinea pigs as well as some small primates such as squirrel monkeys.
List of Species Demarcation Criteria in the Genus
No separate species are currently recognized in the genus Influenzavirus A. This genus is comprised of a cluster of strains that replicate as a continuous lineage and can genetically reassort with each other. Therefore, although 15 different HA subtypes and 9 different NA subtypes are recognized among influenzaviruses A replicating in birds, separate species designations have not been accorded these subtypes
Official virus species names are in italics. Tentative virus species names, alternative names ( ), strains or serotypes are not italicized. Virus name, genome sequence accession numbers [ ], and assigned abbreviation ( ) are:
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Influenza A virus A/PR/8/3H (H1N1) |
[V00603, J02151, V01106, J02144, J02148, J02146, V01099, V01104] |
(FLUAV) |
No attempt has been made here to cite the accession numbers for the several hundred influenza virus nucleotide sequences deposited in the EMBL/GenBank database.
Tentative Species in the Genus
None reported.
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