Infectious salmon anemia virus ISAV A

probable virus in the family Orthomyxoviridae. Placed on the number one list of the most dangerous fish viruses by the European Union, the disease is characterized by severe anemia, ascites and hemorrhagic liver necrosis, with a mortality rate of 15-100%. An enveloped virus, diameter 130-140 nm, with a single stranded RNA genome with negative polarity and eight segments. Total size of the genome is 14.5 kb. The virus replicates optimally at 15°C and does not replicate above 25°C. Hemagglutinates piscine but not mammalian or avian erythrocytes, and has a receptor-destroying enzyme that is an acetylesterase.

infectious units Rarely, single virus particles or, in most cases, groups of virions which plaque or titrate as units. The number of virus particles is often very much larger (up to 106 times) than the number of infectious units.

infectivity A measure of the ability of a virus to replicate within its host's cells. Usually determined by endpoint dilution, or plaque titration, and expressed as infectious units.

Influenzavirus A A genus of the family Orthomyxoviridae containing one species, Influenza A virus. The members of this genus all have eight genome segments. Hemagglutination and the neuramin-idase 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 elec-trophoretic 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 a mol. wt. ± 87 x 103, 84 x 103 and 83 x 103, respectively. The segment 4 encoded (unglycosylated) HA is ± 63 x 103 (glyco-sylated HA1 is ± 48 x 103, HA2 is ±29 x 103). The segment 5 encoded NP is ±56 x 103. The segment 6 encoded NA is ± 50 x 103. The segment 7 encoded M1 and M2 proteins are ± 28 x 103 and 11 x 103, respectively. The segment 8 encoded NS1 and NS2 (NEP) are 27 x 103 and 14 x 103, respectively. Antigenic variation occurring within the HA and NA antigens of Influenzavirus 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 twentieth 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, USA 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. Influenza-viruses 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 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. Influenza-viruses 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 influenza viruses. 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 transmission 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 four to six 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.

Influenza A virus (FLUAV) A species in the genus Influenzavirus A. Type species A/PR/8/34 (H1N1). All species of the genus share a common ribonucleoprotein antigen, the NP protein. It is demonstrated by CF test or immunodiffusion and is found as part of the nucleocapsid or as soluble antigen. The genome (mol. wt. 4.5 x 106, 13.6kb) is comprised of eight segments of linear negative-stranded RNA which range in length from approximately 900 to 2500 nucleotides. Conserved sequences are present at the 5' and 3' termini (13 and 12 nucleotides, respectively). The segments encode 10 proteins: 1, PB2; 2, PB1; 3, PA; 4, HA; 5, NP; 6, NA; 7, M1 and M2; and 8, NS1 and NS2 (nuclear export protein, NEP). The internal virion RNA transcriptase complex includes the PB1, PB2, PA and NP proteins. This is surrounded by the matrix or M protein that underlies the outer lipid bilayer envelope in which are inserted the HA (hemagglutinin), NA (neuraminidase) and M2 proteins. The HA and NA are both species- and type-specific antigens, as demonstrated for HA by hemagglutination inhibition (HI) or neutralization, and for NA by enzymeinhibition tests. In avian influenza viruses, 15 HA subtypes and nine NA subtypes can be demonstrated, some of which occur in various combinations in influenza viruses from humans, horses or pigs. To date, only three HA subtypes (H1-H3) and two NA subtypes (N1 and N2) have been found in human Influenza A viruses. Gene reassortment is frequent between Influenza A viruses in mixed infections, and may result in dramatic changes in antigenicity termed 'antigenic shift', which may precipitate pandemic disease. In addition, all strains undergo antigenic drift. Transmission is by airborne virus or direct contact causing epidemic and sporadic respiratory disease. Natural hosts are humans, pigs, horses, birds and occasionally nonhuman primates, dogs and cattle. Ferrets are experimentally susceptible to mammalian strains. Less susceptible are mice, hamsters and guinea pigs. Most influenza strains replicate in eggs and primary cultures of monkey, human and chick cells. Laboratory strains may be adapted to grow in cell lines.

Banks J et al (1998) Arch Virol 143, 781

Cox NJ and Subbarao K (1999) Lancet 354,1277

influenza virus A avian Strains of Influenzavirus A whose natural hosts are birds: fowl, quail, ducks, turkey, pheasant, etc. They have also been isolated from aquatic mammals such as seals and dolphins. Isolates fall into one of 15 anti-genic groups based on hemagglutination inhibition, and nine based on neu-raminidase. Natural infection is widespread in birds, particularly water fowl in which infection is waterborne, and usually silent and intestinal. They may excrete the virus over prolonged periods. Many strains of virus are present and may provide a source of new mammalian strains. In 1997 an unusual avian virus, H5N1, which was highly pathogenic for birds, caused 18 human cases of influenza with six deaths in Hong Kong.

More than a million chickens were slaughtered in Hong Kong and since 1998 the virus has not reappeared. Infection of chickens and turkeys with virulent strains, usually called fowl plague and of subtype H5 or H7, is a serious and commercially important disease which varies from a mild respiratory to a rapidly fatal pneumonic disease with CNS involvement. Stress may increase susceptibility. Transmission is probably airborne. A vaccine can protect birds but may not be economically practical. Mice, ferrets and other mammals have been infected experimentally usually by i.c. inoculation. Can be propagated in eggs and in primary fowl or monkey kidney cells. Most strains produce plaques in chick embryo fibroblasts.

Synonym: avian plague virus; fowl plague virus.

Webster RG and Kawaoka Y (1988) Crit Rev Poult Biol 1, 211

Webster RG (1999) In Encyclopedia of Virology, Second edition, edited by A Granoff and RG Webster. London: Academic Press, p. 824

influenza virus A equine Strains of Influenzavirus A whose natural host is the horse. Two distinct antigenic subtypes of HA have been found: H3 and H7. Antibodies are also found in human sera. Causes respiratory illness in horses and may be fatal in young animals. Causes inapparent infection in ferrets and can be adapted to produce pneumonia in mice. Replicates in eggs, primary cultures of bovine, human, monkey and chick cells. Agglutinates horse, pig, calf, rhesus, fowl, human and guinea pig erythrocytes. Synonym: equine influenza virus. Webster RG and Guo Y (1991) Nature 351, 527

influenza virus A hominis Strains of Influenzavirus A whose natural host is humans. The virus was first isolated in 1933. Causes sporadic and epidemic respiratory disease. The HA and NA antigens of the virus change slowly (anti-genic drift), but periodically a radical change occurs (antigenic shift) due to gene reassortment with replacement of the HA and/or NA gene by a new subtype. The human population has only slight immunity to the new strain, resulting in a pandemic. To date, three HA subtypes (H1-3) and two NA subtypes

(N1 and N2) have been found in human influenza viruses. Viruses isolated from 1933 to 1957 were H1N1 (swine-like); in 1957 they were replaced by H2N2 viruses (Asian); in 1968 these were replaced by H3N2 (Hong Kong); and H3N2 strains continue to circulate globally in the human population. However in 1977, H1N1 (swine-like) viruses reappeared and have also continued to circulate globally. Inactivated influenza virus vaccines consequently include H1N1, H3N2 and influenza virus B components (triva-lent), with annual changes in one or more of these components to accommodate minor changes due to antigenic drift. Influenza virus is usually isolated in the amniotic cavity of embryonated eggs or in primary monkey kidney cell cultures. Virus multiplication is observed by hemadsorption or hemagglutination of human or guinea pig erythrocytes. Ferrets can be infected experimentally and after adaptation, pneumonia can be produced in mice and hamsters. In monkeys, horses, dogs, sheep, guinea pigs and rats infection is usually inapparent. O-phase (original) or recently isolated strains replicate better in the amniotic than in the allantoic cavity, and agglutinate human and guinea pig erythrocytes better than fowl cells. After adaptation to the allantoic cavity they are termed D-phase (derived) and then they agglutinate fowl cells equally well. This phenomenon is termed O/D variation.

Cox NJ and Kawaoka Y (1998) In Virology, vol. 1 of Topley & Wilson's Microbiology and Microbial Infections, Ninth edition, edited by BWJ Mahy and L Collier. London: Arnold, p. 385 Wilson IA and Cox NJ (1990) Annu Rev Immun 8, 737

influenza virus A porcine Strains of Influenzavirus A whose natural host is the pig. Antibodies reacting with swine virus hemagglutinin are present in many human sera, especially from older people, and it has been suggested that the pandemic of 1918-19 in humans was caused by a virus which spread from humans to pigs. Sporadic fatal influenza cases in pig farmers and other persons in close contact with pigs continue to be reported. Causes pneumonia in pigs especially when associated with Haemo-philus suis. Ferrets and mice are also susceptible to infection. Transmission is by airborne droplets. Human and avian influenza viruses may also infect pigs, and epidemics of H3N5 subtype viruses in swine are common in several parts of the world.

Synonym: swine influenza virus.

Hinshaw VS et al (1985) Bull Wld Hlth Org 62, 870

Wells DL et al (1991) J Am Med Assoc 265, 478

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