Rectal temperatures equal or above 41?C (41?C) were defined as fever. well- known to stay in lungs and lymphoid organs of infected pigs for a long time. It was reported that an infected sow was able to transmit PRRSV up to 157?days post initial infection . Others had detected PRRSV in lymph organs up to 132?days when the piglets were infected in the uterus . PRRSV was also detected more than 180?days post-infection . The mechanism of PRRSV persistence is not completely understood but is likely related to the emergence of viral variants which can escape host immune response . PRRS has Pyrithioxin dihydrochloride now emerged as the most prevalent disease of swine in the world. In the United States, annual loss due to PRRS is estimated at 560 million dollars . In early 2006, a highly pathogenic disease emerged in some swine farms in Jiangxi province of China, and then spread rapidly to the rest of China . This disease remains a major threat to swine industry all over the world . Infected pigs of all ages presented with clinical signs including continuous high fever of above 41?C, depression, dyspnea, anorexia, red discoloration of the ears and skin, conjunctivitis, mild diarrhea, shivering and limping. The morbidity rate was 50C100?% with mortality rate of 20C100?% . Studies demonstrated that highly pathogenic porcine reproduction and respiratory syndrome virus (HP-PRRSV) was the major pathogen that caused the outbreak. HP-PRRSV TJ strain was originally isolated from a piglet that died of a high fever in Tianjin, China, in 2006, and it had the same characteristics as those of other HP-PRRSV strains observed in China. HP-PRRSV strain TJ was culturally passaged on MARC-145 cells for attenuation so that it could be used Pyrithioxin dihydrochloride for the development of a modified live virus (MLV) vaccine . Genetic analysis indicates that the HP-PRRSV isolated from China has a discontinuous deletion of 30 amino acids (AA) in non-structural protein 2 (Nsp2), compared with the North American type of PRRSV strain. However, the mechanisms contributing to the molecular pathogenesis of the HP-PRRSV have not been elucidated. Some preliminary studies reported that PRRSV modulates the host immune responses and alters host gene expression [14C17]. In order to further investigate the immunological characteristics of HP-PRRSV, ten five-week-old pigs were experimentally infected with HP-PRRSV TJ strain and pathological changes, humoral and cell-mediated immune responses were evaluated in the present study. Results Clinical signs observations post infection All piglets infected with HP-PRRSV TJ strain virus developed typical clinical signs of HP-PRRS, such as severe depression and anorexia, lameness and shivering, dyspnea, skin cyanosis and death. Pyrithioxin dihydrochloride Four of five PRRSV-infected piglets died of acute respiratory disease. Conversely, no clinical signs were observed in the control ones. Infected animals had persistently high fever Pyrithioxin dihydrochloride (41?C) Pyrithioxin dihydrochloride at 4?day post infection (dpi), which lasted 9?days (Fig.?1a). In contrast, control piglets remained healthy with normal body temperature throughout the experiment. Animals in group 1 showed significantly higher average clinical scores than the control group ( ?0.01) (Fig.?1b). As shown in Fig.?1c, animals infected with HP-PRRSV TJ strain in group 1 lost significantly more body weight than those in control group. IL22 antibody Open in a separate window Fig. 1 Clinical evaluation for each piglet post infection. After infection, mean rectal temperatures (a), mean clinical score (b) and body weight (c) of each animal were measured daily in HP-PRRSV inoculation group (PRRSV, em n /em ?=?5) and control group (Control, em n /em ?=?5). Rectal temperatures equal or above 41?C (41?C) were defined as fever. Data are presented as mean values??SD..