Porcine reproductive and respiratory syndrome (PRRS) has become one of the most important pig diseases that cause huge economic losses worldwide. PRRS virus (PRRSV) is a single-stranded RNA virus with a high mutation rate. This disease is characterized by respiratory disease, weight loss, and poor growth performance, as well as by late-term abortions. 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 sulphate, CD151, vimentin, MYH9, etc. Infection of macrophages results in its death and may contribute to the frequent bacterial infections that complicate the respiratory disease. PRRSV has a highly restricted cell tropism both in vitro and in vivo. The virus's primary target is porcine alveolar macrophage (PAM), which plays a crucial role in the immune response. Consequently, PRRSV can destroy the immune system, thus resulting in severe bacterial super-infections. Although PRRS commercial modified live vaccines provide a certain degree of protection in pig farms with an outbreak of this disease, there are many side effects including the prolonged viremia of the vaccine strain, the interference with the immune effects of other vaccines, and the recombination of vaccine strain with field strains. Therefore, the PRRS vaccine may be a "double-edged sword". The pathogenesis of the virus remains unclear and requires further research.
The aim of this special issue is to gather a collection of Review or Original Research articles on PRRSV pathogenesis covering i) viral structural and non-structural protein function analysis; ii) host-pathogen interaction: the interaction of the virus with the cells of the immune system, particularly macrophages and different types of dendritic cells; iii) immune escape in the life cycle of the virus; iv) antivirals against the virus; v) future prospects for newer vaccines and vaccination strategies.
Contributions to the following themes are welcome but not limited to:
• PRRSV adsorption, entry and uncoating mediators correlated to relevant signalling pathways in target cells
• Function analysis of viral structural and non-structural proteins
• PRRSV variation and evolution under immune pressure
• PRRSV pathogenesis and immune-response mediator patterns to PRRSV infection
• Antiviral drug development against PRRSV infection
• New-type vaccine development against PRRSV infection
• PRRSV resistance by gene-editing
Porcine reproductive and respiratory syndrome (PRRS) has become one of the most important pig diseases that cause huge economic losses worldwide. PRRS virus (PRRSV) is a single-stranded RNA virus with a high mutation rate. This disease is characterized by respiratory disease, weight loss, and poor growth performance, as well as by late-term abortions. 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 sulphate, CD151, vimentin, MYH9, etc. Infection of macrophages results in its death and may contribute to the frequent bacterial infections that complicate the respiratory disease. PRRSV has a highly restricted cell tropism both in vitro and in vivo. The virus's primary target is porcine alveolar macrophage (PAM), which plays a crucial role in the immune response. Consequently, PRRSV can destroy the immune system, thus resulting in severe bacterial super-infections. Although PRRS commercial modified live vaccines provide a certain degree of protection in pig farms with an outbreak of this disease, there are many side effects including the prolonged viremia of the vaccine strain, the interference with the immune effects of other vaccines, and the recombination of vaccine strain with field strains. Therefore, the PRRS vaccine may be a "double-edged sword". The pathogenesis of the virus remains unclear and requires further research.
The aim of this special issue is to gather a collection of Review or Original Research articles on PRRSV pathogenesis covering i) viral structural and non-structural protein function analysis; ii) host-pathogen interaction: the interaction of the virus with the cells of the immune system, particularly macrophages and different types of dendritic cells; iii) immune escape in the life cycle of the virus; iv) antivirals against the virus; v) future prospects for newer vaccines and vaccination strategies.
Contributions to the following themes are welcome but not limited to:
• PRRSV adsorption, entry and uncoating mediators correlated to relevant signalling pathways in target cells
• Function analysis of viral structural and non-structural proteins
• PRRSV variation and evolution under immune pressure
• PRRSV pathogenesis and immune-response mediator patterns to PRRSV infection
• Antiviral drug development against PRRSV infection
• New-type vaccine development against PRRSV infection
• PRRSV resistance by gene-editing