PRRS IMMUNOLOGY
PRRSV enters pigs through skin breaks or at mucosal surfaces and infects macrophages and dendritic cells. It replicates over a period of hours and exits the cell. Within a day it has infected macrophages throughout the body, especially in the lung and lymph nodes. During this time the pig is largely unaware that it has been infected. The innate immune response is slow and weak, The anti-PRRSV effector adaptive immune response, i.e. antibodies and cytotoxic T cells,are slow to develop. Thus a long viremia of a month or so occurs, followed by a prolonged persistent infection in lymph nodes. The load of virus reaches peak levels in about a week and diminishes steadily. Most of the virus is eliminated before neutralizing antibodies are detected, and in apparent absence of an effective T cell response. The mechanism of viral elimination may involve a reduction in the abundance of permissive macrophages. The prolonged period of viremia and extended persistent infection of lymph nodes increases opportunities for transmission and establishment of endemic infection of herds with continuous flow management. Even though PRRSV becomes established, pigs that are infected once are largely resistant to reinfection. There is little or no viremia and little or no change in antibody titers.At the individual pig level, attenuated PRRSV vaccines grow in pigs, induce antibody responses, and substantially or completely prevent infection by field viruses. The great genetic variation in PRRSV allows for situations in which previous exposure to field or vaccine PRRSV does not completely protect against reinfection. Incomplete immunity to rechallenge is common for many pathogens and hosts, such as influenza virus in swine, humans and chickens. For PRRSV in swine, incomplete immunity may be sufficient to block disease spread or it may not be sufficient. The outcome is influenced by herd size, by the specific viruses that are present in the herd, and by management practices. At present it is not possible to predict the level of protection that will be afforded by one PRRSV against another based on genetic similarity or other factors, and experimental comparisons generally show that previous exposure to one virus produces a high level of protection against re-challenge by a spectrum of unrelated viruses. Improved diagnostics for quantitative assessment of viral load and differentiation of antibody response to vaccines versus field viruses will be helpful in determining the effectiveness of control and elimination programs, and the virological and immunological status of herds. Improved diagnostics, combined with a better understanding of PRRSV interactions with its host, will help to control PRRS.
MICHAEL MURTAUGH
University of Minnesota, St.Paul, MN, USA
国际会议
亚洲猪病学会第三届学术会议(Proceedings the 3rd Congress of the Asian Pig Veterinary Society)
武汉
英文
73-79
2007-04-22（万方平台首次上网日期，不代表论文的发表时间）