Role of the PRRS virus in concurrent infections in swine

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Role of the PRRS virus in concurrent infections in swine

Concurrent infections with other pathogens, whether viruses and/or bacteria, are common in most PRRS virus infections in swine under field conditions.

The presence of these concurrent infections can not only increase the severity of the clinical manifestations of PRRS, but blur the clinical picture and complicate the diagnosis on the farm. It is a fact that PRRS virus infection in swine can increase the susceptibility of the animals to other infections or alternatively, other infections may exist simultaneously with the PRRS virus. A key example of this situation is the Porcine respiratory disease complex (PRDC), where the PRRS virus is one of the main primary agents. This phenomenon is especially noticeable in weaning and growing pigs.

There are several reasons which explain the role of the PRRS virus in the increase in the susceptibility of pigs to other infections. As a result, the PRRS virus may impair the host immune response to viral and bacterial infections:

  • The PRRS virus damages or affects the ultrastructure of the respiratory tract; this hampers bacterial clearance.
     
  • Alveolar macrophages, which are the main cells involved in the lungs’ defense, are the primary target cells for the PRRS virus in swine. More specifically, the virus replicates in the subset of alveolar macrophages with the maximal ability to phagocytose bacteria and produce components to destroy them. Also, the virus can interact with other antigen- presenting cells.

To sum up, the PRRS virus:

  • … can kill infected and non-infected macrophages by inducing direct/indirect necrosis or apoptosis.
  • … can decrease the bactericidal activity of macrophages.
  • … can inhibit cytokines with broad antiviral properties, such as type I IFNs, even in the presence of other viruses (coinfections).
  • … can induce an imbalance between pro- and anti-inflammatory cytokines.
  • … can impair the immune responses by inducing the release of certain cytokines.
  • … can interfere with the correct antigen presentation.
  • … can decrease the cytotoxicity of NK cells.
  • The magnitude of the above-mentioned phenomena may vary among strains.

Several groups have attempted to develop models to study PRRS virus co-infections with various bacteria and viruses. There is strong experimental evidence to support PRRS virus-induced predisposition to Streptococcus suis, Salmonella choleraesuis, Bordetella bronchiseptica, Mycoplasma hyopneumoniae, Porcine Circovirus type 2 (PCV2) and Swine Influenza Virus (SIV) infection and disease. The following table summarizes much of the information in the literature on experimental models using the PRRS virus and bacterial/viral co-infections.

 

 
 
 
 
 

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