Emergency vaccination is a useful tool for controlling animal and human infectious diseases after exposure to pathogens, such as the foot-and-mouth disease virus (FMDV) , the classical swine fever virus (CSFV) , and rabies virus . Emergency vaccination diminishes economic losses by reducing morbidity and mortality, as well as virus transmission. Post-exposure vaccination for typical PRRS has significantly reduced the number of persistently infected pigs at 127 DPI and reduced viral shedding to within 97 DPI . In the present study, emergency vaccination successfully alleviated the clinical signs of HPPRRSV infection and reduced the mortality rate. Emergency vaccination was more efficient in controlling HPPRRSV, an acute form of the disease with epidemiologic characteristics that differed from typical PRRS.
The mechanism for emergency vaccination may be related to a quick adaptive immune response to restrict viral replication and proliferation, which could explain the immune protection conferred by the C strain of CSFV  and FMDV emergency vaccine . Emergency vaccination might induce innate immunity. During rabies vaccination, the attenuated rabies virus spreads from the peripheral sites of inoculation to the CNS tissues, and triggers the substantial immune cell infiltration into the CNS. These cells had a major function in the early containment of rabies viral infections (i.e., cleaning rabies or preventing them from entering the CNS), particularly through the production of type I interferon . If the attenuated rabies vaccines entered the CNS after the wild-type rabies virus, the vaccination would be ineffective [14, 15]. Previous studies have provided very little explanation on the mechanism of PRRSV emergency vaccination. PRRSV variants possess different capacities for inducing or controlling innate immunity, which appears similar with rabies vaccination. Thus, we speculated that the attenuated PRRSV might trigger an innate immune response that subsequently controls HPPRRSV infection.
The significantly higher level of serum IFN-γ in the vaccine-treated group at 10 DPI lasted until the end of the experiment (21 DPI). This process probably influenced the protection obtained by piglets from the vaccinated group. In a previous report , a swine serum IFN-γ response was detected immediately after PRRSV infection and lasted for approximately 3 weeks. IFN-γ is important for controlling PRRSV infection . IFN-γ could inhibit PRRSV replication more effectively than the type I interferon in vitro[18, 19]. Furthermore, no neutralizing activities were detected in all of the serum samples (data not shown). This observation underlines the protective function of IFN-γ during the early stages of PRRSV infection.
The viral load in tissues of infected pigs under the acute infection phase was one of indexes used to indicate PRRSV pathogenicity. The more virulent the strain is, the higher is the viral load in pigs . In our study, the serum viral RNA load was significantly lower in the vaccinated group (p < 0.05) at 7 and 10 DPI. The severity of a clinical disease is highly associated with the viral load . Thus, the lower serum viral RNA load might account for the minimal clinical signs and tissue lesions observed in the vaccinated group.
In this study, we developed an HPPRRSV contact-infection model by intramuscular infection. The infected pigs exhibited higher levels of viraemia at 3 DPI, thereby suggesting that the pigs transmitted the virus within 2 DPI, which may account for the rapid spread of the virus in herds . PRRSV transmission is primarily via the respiratory route . Our data indicated that the virus from the inoculation sites rapidly reached the lungs.