About this Research Topic
Porcine reproductive and respiratory syndrome (PRRS) is one of the most important pig diseases that cause important economic losses worldwide. PRRS virus (PRRSV), is a single-stranded RNA virus with a high mutation rate. PRRSV infection may result in reproductive failure in sows and respiratory disease in pigs of all ages that often lead to secondary bacterial infections. At present two species (PRRSV1 and PRRSV2) are recognized, each one showing a high genetic diversity. Highly virulent variants emerged in China and the United States (PRRSV 2) as well as in Eastern Europe (PRRSV 1), showing more severe clinical symptoms as well as a broader cell tropism.
PRRSV invades the host mainly by targeting the macrophages via the core receptor CD163 together with the joint forces from several other co-receptors such as Siglecs, heparan sulfate, CD151, vimentin, MYH9, etc. The infection of macrophages results in its death and may contribute to the frequent bacterial infections that complicate the respiratory disease. Most often, viremia persists for weeks and after its clearance, and the virus may remain in lymphoid tissues for weeks or even months. Early studies showed that some of the immunological features of this infection are uncommon. While the antibody response develops early and is strong, substantial amounts of neutralizing antibodies are not consistently demonstrated in the first month of infection. Cell-mediated response is also irregular at first. Additionally, while the virus is known to inhibit interferon beta responses, it seems not to be able to inhibit plasmacytoid cells. At present several valuable vaccines are marketed. However, those vaccines are limited tools since vaccinated animals can get infected and may potentially transmit the infection.
The aim of this Research Topic is to gather a collection of basic Review articles and Original Research articles on PRRSV to improve our understanding of (i) the interaction of the virus with the cells of the immune system, particularly macrophages and different types of dendritic cells, ii) the mechanisms exploited by the virus to escape the immune response, iii) the role of the humoral and cell-mediated immune responses in protection, iv) future prospects for newer vaccines and vaccination strategies. Better insights will lead to research-driven development of new generation treatments and vaccines.
We welcome authors to submit on the following topics:
• PRRSV variation and evolution under immune pressure (selection of immune escape variants)
• PRRSV entry and uncoating mediators correlated to relevant signaling pathways in target cells
• Function analysis of viral proteins and their roles in the immune response
• Glycan-protein interactions in viral pathogenesis and immune recognition
• Interaction of PRRSV with dendritic cells and macrophages and impact on their functionality
• Inhibition/regulation of the immune response by PRRSV
• Role of neutralizing antibodies in protection, especially broadly neutralizing antibodies
• T-cell response: cytotoxicity
• Immunological memory in PRRS
• Homologous and heterologous immunity/Relevant epitopes for broad or universal protection
• New vaccine developments and new adjuvants for PRRSV vaccines
PRRSV invades the host mainly by targeting the macrophages via the core receptor CD163 together with the joint forces from several other co-receptors such as Siglecs, heparan sulfate, CD151, vimentin, MYH9, etc. The infection of macrophages results in its death and may contribute to the frequent bacterial infections that complicate the respiratory disease. Most often, viremia persists for weeks and after its clearance, and the virus may remain in lymphoid tissues for weeks or even months. Early studies showed that some of the immunological features of this infection are uncommon. While the antibody response develops early and is strong, substantial amounts of neutralizing antibodies are not consistently demonstrated in the first month of infection. Cell-mediated response is also irregular at first. Additionally, while the virus is known to inhibit interferon beta responses, it seems not to be able to inhibit plasmacytoid cells. At present several valuable vaccines are marketed. However, those vaccines are limited tools since vaccinated animals can get infected and may potentially transmit the infection.
The aim of this Research Topic is to gather a collection of basic Review articles and Original Research articles on PRRSV to improve our understanding of (i) the interaction of the virus with the cells of the immune system, particularly macrophages and different types of dendritic cells, ii) the mechanisms exploited by the virus to escape the immune response, iii) the role of the humoral and cell-mediated immune responses in protection, iv) future prospects for newer vaccines and vaccination strategies. Better insights will lead to research-driven development of new generation treatments and vaccines.
We welcome authors to submit on the following topics:
• PRRSV variation and evolution under immune pressure (selection of immune escape variants)
• PRRSV entry and uncoating mediators correlated to relevant signaling pathways in target cells
• Function analysis of viral proteins and their roles in the immune response
• Glycan-protein interactions in viral pathogenesis and immune recognition
• Interaction of PRRSV with dendritic cells and macrophages and impact on their functionality
• Inhibition/regulation of the immune response by PRRSV
• Role of neutralizing antibodies in protection, especially broadly neutralizing antibodies
• T-cell response: cytotoxicity
• Immunological memory in PRRS
• Homologous and heterologous immunity/Relevant epitopes for broad or universal protection
• New vaccine developments and new adjuvants for PRRSV vaccines
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
