2.2 Porcine Reproductive and Respiratory Syndrome
Virus
Porcine Reproductive and Respiratory Syndrome Virus (PRRSV), is an
enveloped, single-stranded, positive sense RNA virus in the family ofArteriviridae (Kavanova et al., 2018) and an etiologic agent that
causes porcine reproductive and respiratory syndrome (PRRS), which has
been estimated to be the cause of a lost $600 million in the US swine
industry at least every year (Neumann et al., 2005). The typical
symptoms of PRRSV are characterized by blue-ear and failure in pregnant
pigs (Lunney et al., 2016), also these infections can induce cell lysis,
apoptosis, changes in T-cell subpopulations etc (Labarque, Van Gucht,
Nauwynck, Van Reeth, & Pensaert, 2003; Shimizu et al., 1996;
Thanawongnuwech, Thacker, & Halbur, 1997).
It has been reported that, the concurrent infection with Mhp and PRRSV
is common (Chae, 2016; Fablet, Marois-Crehan, Grasland, Simon, & Rose,
2016b; Pallares et al., 2002). Scott and colleagues have proved their
hypothesis that PRRSV and Mhp can be transported via airborne route
(Dee, Otake, Oliveira, & Deen, 2009; Otake, Dee, Corzo, Oliveira, &
Deen, 2010), these characteristics of pathogens increased the difficulty
to control these diseases. PRRSV replicates mainly in porcine alveolar
macrophages (PAMs), dendritic cells (DC) in lungs and the upper
respiratory tract (Lunney et al., 2016), resulting in viremia as early
as 12 h post infection at the early infection stage(Wills, Doster,
Galeota, Sur, & Osorio, 2003). For the persistence period, viral
replication is primarily localized in lymphoid organs, including tonsil
and lymph nodes but not spleen (Allende et al., 2000; Rowland, Lawson,
Rossow, & Benfield, 2003; Wills et al., 1997) and gradual decays until
the virus becomes extinct in the host (Christopher-Hennings, Nelson,
Althouse, & Lunney, 2008; Wills et al., 2003).
The PAMs from pigs infected with PRRSV have significantly downregulated
the ability to kill bacteria (Solano, Bautista, Molitor, Segales, &
Pijoan, 1998). Although, some researchers have demonstrated that
co-infection with Mhp and PRRSV show no potentiating effect (Van
Alstine, Stevenson, & Kanitz, 1996). Thacker and colleagues suggested
that the Mhp potentiated and prolonged PRRSV-induced pneumonia
clinically, macroscopically and microscopically regardless of the
inoculation sequence of infection to both pathogens, whereas PRRSV did
not aggravate Mhp infection in piglets when inoculated before Mhp under
experimental conditions (Thacker, Halbur, Ross, Thanawongnuwech, &
Thacker, 1999; Tzika et al., 2015; Van Alstine et al., 1996).
Furthermore, Fablet suggested that, the infection by Mhp was associated
with PRRSV seropositive status (Fablet, Marois-Crehan, Grasland, Simon,
& Rose, 2016a). Moreover, in the concurrent infection with Mhp and
PRRSV, many vital functional genes were detected as being differentially
expressed (DE) in PAMs (Li et al., 2015), especially, IL-1β was
considerably higher, which is a key component for downstream signal
pathways. In addition, the co-infection of Mhp and PRRSV significantly
increased the severity and duration of pneumonia in experimentally
infected pigs, which was associated with induction of several
proinflammatory cytokines (Thacker, Thacker, Kuhn, Hawkins, & Waters,
2000), such as IL-1α, IL-1β, IL-6, IL-8, IL-10, IL-12 and Tumor Necrosis
Factor-alpha (TNF-α) (Thanawongnuwech, Thacker, Halbur, & Thacker,
2004; Thanawongnuwech & Thacker, 2003; Thanawongnuwech, Young, Thacker,
& Thacker, 2001). Other group also found increased levels of both IL-12
and IL-10 in the respiratory tract of pigs experimentally infected with
either Mhp and/or PRRSV, IFN-γ and Insulin-like Growth Factor-I (IGF-I)
production were lower and delayed in pigs co-infected with PRRSV and
Mhp(Roberts & Almond, 2003; Thanawongnuwech & Thacker, 2003). These
results suggest that the exacerbation Mhp respiratory disease may be due
to viral infection which induces regulatory T cells (Tregs) (LeRoith et
al., 2011). In contrast, Fano et al suggested that Mhp did not affect
these epidemiological features of PRRSV-associated disease under the
conditions of study (Fano, Pijoan, & Dee, 2007).
Other studies also implicated that a single-dose vaccination against Mhp
alone decreased the levels of PRRSV viremia and PRRSV-associated
pulmonary lesions, whereas single-dose
vaccination
against PRRSV alone did not decrease nasal shedding of Mhp and
Mhp-associated pulmonary lesions in the co-infected pigs (S. J. Park,
Seo, Park, & Chae, 2014). Combining vaccines with Mhp and PRRSV did not
induce negative interaction which would reduce the efficacy of each
individual vaccine (Bourry, Fablet, Simon, & Marois-Crehan, 2015).
These results indicated that, the combined vaccination is more efficient
than single ones, consequently, further research should focus on the
developing of combined vaccine, which can improve the convenient and
efficient pig production simultaneously.