Page 9 - Avian Virology: Current Research and Future Trends

2 | Perez et al.

referenced and kindly encourage the reader to explore beyond Influenzavirus D (type D), Isavirus, Thogotovirus and Quaranja-
those mentioned in this chapter. virus (McCauley, 2014). Orthomyxoviruses have in common a
lipid bi-layer envelope derived from the host’s cell membrane
and a segmented, negative-sense, RNA genome that requires
Historical perspective a virus-encoded RNA-dependent RNA polymerase for replica-
Avian influenza was first described in 1878 in Northern Italy as tion (Fig. 1.1). In contrast to the majority of RNA viruses, IAV
a high mortality disease affecting chickens, initially termed ‘fowl transcribes and replicates in the nucleus of the cell (Martin and
plague’ (Perroncito, 1878). Outbreaks of HPAI were subsequently Helenius, 1991a; Holsinger et al., 1994). The genome of IAVs
reported in 1894 and 1901 starting in Italy, quickly spreading to contains eight RNA segments (McGeoch et al., 1976; Palese,
Austria, Germany, Belgium and France. By 1901, as a result of the 1977), totalling approximately 14 kilobases, that encode between
Brunswick Fowl Exposition, the HPAI virus reached every corner 12 to 16 viral proteins depending on the strain (Table 1.2 and
of Germany (Perez et al., 2005; Perez and de Wit, 2016). In the Fig. 1.1) (Lamb, 1989; Bouvier and Palese, 2008). Approxi-
1920s, HPAI activity was also reported in North Africa, Asia, mately half of the total genome encodes for the three viral
Middle East and the Americas and remained endemic in most polymerase proteins (Palese et al., 1977). Within the family
of Europe until it disappeared around the mid 1930s. The first Orthomyxoviridae, only IAVs are divided into subtypes. In 1980,
outbreak of HPAI in the USA occurred in 1924–1925 and started the World Health Organization established the nomenclature of
in the live bird markets of New York and then spread to other IAVs to contain the type of host (if different from human, lower
bird markets in New Jersey and Pennsylvania. By 1925, the virus case), the geographical region of origin, number of isolate or
had spread to markets and farms in Connecticut, West Virginia, laboratory code, and the year of isolation separated by forward
Indiana, Illinois, Michigan and Missouri. The HPAI reappeared slashes and followed by the HA and NA subtype combination
in New Jersey in 1929 affecting few flocks. After it’s disappearance in parentheses, described by letter and number, H1 to H16,
in the 1930s, no outbreaks were recorded until 1959 (Lupiani and and N1 to N9. Thus, a simple example could be the fifth IAV
Reddy, 2009). strain of the H7N3 subtype isolated from a chicken in Pakistan
The terminology ‘highly pathogenic avian influenza’ (HPAI) in 2017, which would be labelled A/chicken/Pakistan/5/2017
was officially adopted in 1981 at the 1st International Sympo- (H7N3). Of note, new IAVs were recently discovered in fruit
sium on Avian Influenza to designate the highly virulent forms bat species in Guatemala and Peru (Tong et al., 2012, 2013)
of influenza affecting poultry, replacing the term ‘fowl plague’ with haemagglutinin-like (HL) and neuraminidase-like (NL)
that was used for almost a century (Bankowski, 1981). Although surface proteins, which constitute new subtypes, HL17NL10
the causative agent was determined to be filtrable in 1901, it and HL18NL11, respectively.
was only in 1955 that the virus was classified as an influenza A In common with other members in the family, IAVs are
virus (Schäfer, 1955), two decades after both human and swine pleomorphic particles of about 80–120 nm in diameter. IAVs
influenza A viruses were identified (Shope, 1931; Smith et al., particles may adopt a spherical or filamentous shape, with the
1933). Based on records of the last two centuries, outbreaks of latter associated with higher infectivity and RNA content than
highly pathogenic avian influenza (HPAI) have occurred inter- the former (Kilbourne and Murphy, 1960; Roberts et al., 1998).
mittently in all continents. Since 1959, more than 70 outbreaks The combined effects of cellular factors and viral proteins mod-
of avian influenza have been recorded, more than 50 of those in ulate virus morphology (Höglund and Ciampor, 1975; Roberts
the past two decades, resulting in the loss of approximately 120 and Compans, 1998; Roberts et al., 1998; Zhang et al., 2000; Liu
million birds since 2013 (OIE, 2017). In recent years the most et al., 2002; Bourmakina and García-Sastre, 2003; Burleigh et
affected areas have been Europe and Southeast Asia (OIE, 2017). al., 2005; McCown and Pekosz, 2005; Peiris et al., 2009; Noda,
The apparent increase in the number of reported outbreaks of 2011; Bialas et al., 2012, 2014; Roberts et al., 2013; Campbell et
HPAI in the last two decades may be the result of a combination al., 2014; Chlanda et al., 2015; Frensing et al., 2016). Filamen-
of factors including more scrutinized AI monitoring and, perhaps tous particles are predominant in clinical samples (Sieczkarski
most importantly, the worldwide increase in the production of and Whittaker, 2005). Spherical particles are more common
commercial and non-commercial poultry under conditions that in viruses grown in in vitro culture systems (Kilbourne and
do not necessarily prevent contact with feral birds and/or carriers Murphy, 1960; Mitnaul et al., 1996; Liu et al., 2002; Burleigh et
of AI. Table 1.1 summarizes the most impactful as well as most al., 2005; Sieczkarski and Whittaker, 2005; Bruce et al., 2012;
recent outbreaks of avian influenza. Badham and Rossman, 2016). Heat, extreme changes of pH,
non-isotonic conditions, and dryness can readily inactivate IAVs
(Perez et al., 2005). On the surface, IAV virions carry project-
Infectious agent ing glycoprotein spikes corresponding to the viral HA and NA
glycoproteins (Lamb, 1989) (Fig. 1.1). The HA and NA are pre-
Classification, morphology, genome structure sent as homotrimers and homotetramers, respectively. IAV also
and organization carry several copies of the transmembrane M2 protein inserted
IAVs belong to the genus Influenzavirus A in the family in the envelope. Under the lipid bi-layer and protecting the viral
Orthomyxoviridae. This family of viruses includes six more genome, there are multiple copies of the matrix 1 (M1) protein.
genera: Influenzavirus B (type B), Influenzavirus C (type C), Each of the viral RNA (vRNA) segments contains 12 and 13