Fate and Transport of Zoonotic Bacterial, Viral, and - The Pork Store ...

3. Common Viruses of Swine
inf l u e n z a
Influenza viruses are enveloped, segmented,
single-stranded (ss), negative-sense ribonucleic
acid (RNA) viruses belonging to the family
Orthomyxoviridae (Lamb and Krug 2001). The
Orthomyxoviridae family consists of four genera:
influenza A virus, influenza B virus, influenza C
virus, and thogotovirus (Lamb and Krug 2001).
Swine influenza virus belongs to the influenza A
virus genus. Type A influenza viruses cause disease
in lower mammals, birds, and humans (Wright and
Webster 2001). Although type B influenza viruses
primarily have been associated with disease in humans,
there is evidence for rare type B influenza infections
outside humans reported in the United Kingdom
(U.K.) and China in pigs that were shown to possess
antibodies against influenza B virus (Brown, Harris,
and Alexander 1995; Mu et al. 1988), and a single report
of an infection in a marine mammal (Wright and
Webster 2001). Type C influenza viruses are isolated
only occasionally, and although they can infect humans,
dogs, and swine, there is little evidence that they
circulate widely in swine (Brown, Harris, and Alexander
1995; CDC 2005; Matsuzaki et al. 2002; Youzbashi et
al. 1996). Because swine influenza is caused primarily
by influenza A viruses, this genus will be discussed in
detail in this chapter.
The influenza A virus genome consists of eight
RNA genes (Lamb and Krug 2001) that encode for 11
different viral proteins (Chen et al. 2001; Gibbs et al.
2003). Two of the genes—hemagglutinin (HA) and
neuraminidase (NA)—encode for surface glycoproteins
that project from the viral envelope, and because they
possess distinct antigenic properties, they are used
to subtype influenza viruses into 16 HA types (1–16)
(Fouchier et al. 2005) and 9 NA types (1–9) (Lamb and
Krug 2001). Two internal genes—nucleoprotein and
matrix—are conserved highly within the three types (A,
B, and C) of influenza viruses and often are targeted in
detection assays.
3.
COMMON VIruSeS OF SwINe
Influenza A viruses are named by their HA and
NA type, (e.g., H1N1), and often are given “strain”
names that include their genus or type, host species
if other than human, location of isolation, arbitrary
laboratory number, and year of isolation (e.g., A/Swine/
Iowa/15/1930).
Epidemiology
Swine influenza virus (SIV) has evolved from a
seasonal disease caused by a stable genotype to a yearround
endemic respiratory disease caused by multiple
genotypes undergoing continual change (Erickson
and Gramer 2003). These changes are caused by two
mechanisms: antigenic shift (or reassortment) and
antigenic drift (Lamb and Krug 2001). Antigenic shift is
a dramatic change that occurs when virus gene segments
are exchanged between two viruses infecting the same
host cell (Hilleman 2002). Antigenic drift is a more
subtle change that occurs through accumulations of
point mutations made during replication of the virus
genome (Schweiger, Zadow, and Heckler 2002). For
80 yr, pigs in North America had only one endemic
strain of SIV, classical H1N1, until 1998 when a human
reassortant H3N2 SIV was detected in U.S. swine (Brown
2000). In 1998, reassortant H3N2 SIVs emerged in the
swine population that either were double reassortant
with human and avian strains of influenza (A/Sw/NC/98)
or triple reassortment with human, avian, and swine
influenza strains (A/Sw/TX/98). In early 1999, the HA of
the preexisting classical H1N1 SIV reassorted with H3N2
SIV virus to create a second reassortant virus, H1N2
(Karasin, Olsen, and Anderson 2000). Control then was
complicated further as evidenced by multiple outbreaks
of swine influenza resulting from H1N2 infection despite
possible preexisting vaccinal immunity against classical
H1N1 SIV (Erickson and Gramer 2003; Karasin, Olsen,
and Anderson 2000). Further reassortment occurred
in late 2002 when both the HA and NA of H3N2 SIV
were replaced by the classical H1 and N1 genes, thereby
creating a reassortant novel H1N1 SIV with avian internal
(PA and PB2) genes (Webby et al. 2004).
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