Page 163 - Avian Virology: Current Research and Future Trends

156 | Liu et al.

Table 5.4 Reverse genetics system for recovery of infectious coronaviruses
System Description Developed for
BAC Clone full-length genomic cDNA into a BAC vector and Alphacoronavirus
transfect into cells. Initiate infection by transcribing infectious TGEV (Almázan et al., 2000)
gRNA from CMV promoter Betacoronavirus
HCoV-OC43 (St-Jean et al., 2006); SARS-CoV (Almázan et al.,
2006); MERS-CoV (Almázan et al., 2015)
In vitro ligation Clone smaller parts of the genomic cDNA as a set of smaller Alphacoronavirus
stable clones; assemble full length cDNA by directed in vitro PEDV (Beall et al., 2016); TGEV (Yount et al., 2000);
ligation HCoV-NL63 (Donaldson et al., 2008)
Betacoronavirus
MHV (Yount et al., 2002); SARS-CoV (Yount et al., 2003);
MERS-CoV (Scobey et al., 2013); Bat-CoV (Becker et al.,
2008)
Gammacoronavirus
IBV (Youn et al., 2005a; Fang et al., 2007)
Targeted Synthetic donor RNA bearing mutations of interest introduced Alphacoronavirus
recombination into cells infected by the recipient parent virus possessing mFIPV (Haijema et al., 2003)
characteristics which can be selected against Betacoronavirus
MHV (Koetzner et al., 1992); fMHV (Kuo et al., 2000)
Vaccinia virus Clone full-length genomic cDNA into Vaccinia virus genome; Alphacoronavirus
transcribe infectious gRNA and transfect into cells HCoV-229E (Thiel et al., 2001); FCoV (Tekes et al., 2008)
Betacoronavirus
MHV (Coley et al., 2005)
Gammacoronavirus
IBV (Casais et al., 2001)
BAC, Bacterial artificial chromosome; Bat-SCoV, severe acute respiratory syndrome-like coronavirus; fMHV, feline Mouse hepatitis virus;
HCoV-229E, Human coronavirus 229E; HCoV-NL63, Human coronavirus Netherlands 63; HCoV-OC43, Human coronavirus organ culture 43;
MERS-CoV, Middle East respiratory syndrome coronavirus; mFIPV, mutant Feline infectious peritonitis virus; MHV, Mouse hepatitis virus; PEDV,
Porcine epidemic diarrhoea virus; SARS-CoV, Severe acute respiratory syndrome coronavirus; TGEV, Transmissible gastroenteritis coronavirus.

homologous recombination can be used to modify or replace effects and mortality as they grow older (Albassam et al., 1986;
portions of the CoV cDNA, followed by transient dominant Crinion and Hofstad, 1972). Mortality rates induced by IBV
selection (TDS) system (Britton et al., 2005). With the exception vary among different inbred lines (Otsuki et al., 1990; Ignjatovic
of the modification introduced, the resultant rIBVs are isogenic as et al., 2003). Genetic difference in IBV susceptibility was noted,
they are derived from the same cDNA sequence. with the light breeds more susceptible than the heavy breeds
Collectively, reverse genetics have been used to study the (Cumming and Chubb, 1988; Jones, 2008). Nephropathogenic
molecular biology of CoV interactions and functions of the rep- IBV (NIBV) has also been shown to induce a higher mortality in
licase, structural and accessory proteins, providing a powerful broilers than layers (Ignjatovic, 1988; Lambrechts et al., 1993),
means to unravel the complexities of the CoV genome. and male chicks were shown to be twice as susceptible as females
to nephritis (Cumming, 1969). Nutrition and environment also
appear to affect host susceptibility to IBV infection. Chickens on
Pathogenesis and clinical features high protein diets, such as meat meals and poultry by-product
Domestic chickens have usually been regarded as the exclusive meat-based diets are more prone to IBV-induced nephrosis
host of IBV, but respiratory disease and decreased egg production and mortality (Cumming, 1969; Cumming and Chubb, 1988).
have also been reported in other avian species including pheas- Low temperature appears to have a significant impact on NIBV-
ants, pigeons, peacock, partridge and mallard, indicating that the induced mortality (Cumming, 1969) and IBV-induced tracheal
host range of IBV extends beyond chickens (Wickramasinghe et lesions (Ratanasethakul and Cumming, 1983a). The associated
al., 2015). mortality rate also increased to up to 50%. This has important
implications for assessing vaccine protection, since cold exposure
Virulence factors influencing pathogenesis can be used to increase the severity of challenge imposed (Klieve
and Cumming, 1990).
Host and environment factors
Age, breed, nutrition and environment may affect the pathogenesis Viral virulence factors
of IBV. All ages are susceptible to IBV, but clinical manifestations IBV virulence is a crucial frontier of IB pathogenesis, as deter-
are pronounced in young chicks, and can often lead to perma- mined by successful entry, replication, and final release of the
nent damages to the organs involved (Crinion and Hofstad, mature virion. S protein plays an essential role in the attach-
1972; Smith et al., 1985). Chicks will become more resistant to ment and entry of host cells and therefore, contributes to virus
IBV-induced clinical signs such as oviduct lesions, nephropathic infection. Amino acid substitutions in the S1 subunit of IBV