猪繁殖与呼吸综合征病毒感染仔猪淋巴细胞亚群的动态

目的：研究SPF仔猪感染猪繁殖与呼吸综合征病毒后对猪瘟苗的免疫应答受到抑制的机理。方法：利用流式细胞术检测了SPF仔猪感染PRRS病毒BJ-4后外周血淋巴细胞亚群的动态。结果：外周血CD3^ 、CD4^ 、CD8^ 和SLA-DR^ 表达细胞在感染早期比例下降;感染猪扁桃体的CD3^ 和CD4^ CD8^ 细胞亚群比例下降;肠系膜淋巴结的CD3^ 细胞亚群在感染后细胞在感染早期比例下降;感染猪扁桃体的CD3^ 和CD4^ CD8^ 细胞亚群比例下降;肠系膜淋巴结的CD3^ 细胞在感染后下降,但是SLA-DR^ 细胞亚群有逐渐升高的趋势。结论：仔猪感染PRRS病毒后淋巴细胞各亚群的比例下降可能会抑制机体对其它病原体的免疫反应,扁桃体的细胞比例变化有利于其它呼吸道病原体的混合感染或继发感染。     

环孢霉素A对OVA免疫TCR转基因DO11.10小鼠CD4+CD25+T细胞的影响

目的：研究免疫抑制剂Csh对处于免疫应答状态的小鼠脾脏调节性CD4^＋CD25^＋T细胞影响。方法：采用流式细胞术检测卵白蛋白（OVA）免疫的DO11．10小鼠脾脏CD4^＋CD25^＋T细胞及其中Foxp 3^＋T细胞的变化。结果：OVA免疫后脾脏CD4^＋CD25^＋T细胞占CD4^＋T细胞百分数及Foxp 3^＋T细胞占CD4^＋CD25^＋T细胞百分数均增加，显示CsA可明显减少正常及免疫应答状态下小鼠脾脏CD4^＋CD25^＋T细胞及CD4^＋CD25^＋Foxp3^＋T细胞百分数。结论：CsA在抑制免疫应答的同时也可能抑制了免疫耐受的诱导。     

中国HIV感染者细胞毒性淋巴细胞内穿孔素的差异性表达

目的 了解中国HIV感染者细胞毒性相关的NK细胞及CD8^＋T细胞内穿孔素表达水平，探讨HIV感染过程中穿孔素表达与机体免疫功能的关系。方法 采集31例未经抗病毒治疗的HIV感染者和经过高效抗逆转录病毒疗法（HAAS）治疗的17例HIV／AIDS患者以及15例健康对照的抗凝全血，应用流式细胞仪胞内染色法检测CD56^＋／CD3^-、CD3^-／CD16^＋NK细胞及CD8^＋／CD3^＋内穿孔素表达的百分数，分析其与NK细胞绝对值、NK细胞百分数、CD4^＋T、CD8^＋T淋巴细胞绝对值及血浆病毒载量的相关性。结果 中国HIV感染者的NK细胞CD56^＋／CD3^-及CD3^-／CD16^＋亚群穿孔素表达百分数（平均13．17％，平均24．05％）高于CD8^＋T细胞穿孔素表达百分数（平均9．03％）；NK细胞内穿孔素表达低于健康对照（P〈0．05，P〈0．05），CD8^＋T细胞内穿孔素表达高于健康对照（P〈0．05）；NK细胞及CD8^＋T细胞内穿孔素表达水平与其绝对计数显著相关，与疾病进展不相关。HAART治疗组NK细胞内穿孔素表达升高，CD8T^＋细胞内穿孔素表达无显著变化。结论 中国HIV感染者NK细胞内穿孔素表达降低，抗病毒治疗后升高；CD8^＋T细胞内穿孔素表达升高，抗病毒治疗后无显著变化。     

BALB/C小鼠对不同佐剂SARS灭活疫苗的早期免疫反应

目的：研究含不同佐剂的SARS灭活疫苗免疫小鼠后，小鼠的早期细胞免疫和体液免疫反应。方法：灭活的SAPS冠状病毒F69株分别与弗氏佐剂、氢氧化铝、CpG佐剂配伍，制备灭活疫苗。接种6周龄SPF’级BALB／C小鼠。定时采血，分析小鼠外周血中CD4^ 、CD8^ T细胞亚群动态变化，同时测定鼠血清中特异性IgG抗体及抗体的病毒中和活性。结果：由3种佐剂制备的SARS灭活疫苗免疫小鼠后，CD4^ 、CD8^ T细胞百分比升高或无明显改变，CD4／CD8比值无显著性改变。其中，弗氏佐剂疫苗免疫小鼠的CD4^ T细胞百分比升高较明显，且在一段时间内，维持在一个较高的水平；铝佐剂疫苗免疫小鼠后，未观察到明显T细胞亚群改变；而CoG佐剂疫苗免疫小鼠的CD8^ T细胞百分比改变较其它佐剂疫苗改变更明显。与此相异的是，3种疫苗均可诱导小鼠产生较高滴度特异性IgG抗体，并且所产生的抗体具有中和活性。在初免后第34天，3种佐剂组的IgG抗体滴度分别为1：12800、1：3200和1：1600，中和效价分别为1：2560、1：960和1：320。结论：SARS灭活疫苗接种小鼠后，可诱导较强的体液免疫反应，同时轻度上调CD4^ 、CD8^ T细胞活性，程度因佐剂而异。     

重症胰腺炎大鼠肠道免疫功能改变及精氨酸的调节作用

目的：探讨重症急性胰腺炎（Severe Acute Pancreatitis，SAP）大鼠肠道黏膜免疫功能变化及L-精氨酸（L-Arg）对SAP大鼠肠道黏膜免疫功能的影响。方法：成年、雄性Wistar大鼠随机分为胰腺炎组、假手术组和L．精氨酸治疗组。分别于造模后24、48和72小时取标本检测：鲎试剂法检测大鼠门静脉血内毒索水平、免疫组化方法检测并计数小肠黏膜固有层内CD3、CD4、CD8阳性T淋巴细胞百分数、放射免疫法检测盲肠内容物中分泌型IgA（sIgA）含量。结果：SAP组大鼠各时段门静脉血内毒素水平显著升高，回肠末段黏膜固有层CD3^＋、CD4^＋T淋巴细胞百分数明显减少，CD^＋／CD8^＋T淋巴细胞比值降低，盲肠内容物sIgA含量明显降低；与SAP组比较，L-精氨酸组大鼠各时段门静脉血内毒素水平明显降低，回肠末段黏膜固有层CD3^＋、CD4^＋T淋巴细胞百分数明显增加，CD4^＋／CD8^＋T淋巴细胞数比值升高，盲肠内容物SIgA含量增加。结论：SAP大鼠早期即发生肠黏膜免疫功能明显下降，可能是导致肠道内毒素移位的主要原因，L-精氨酸可以改善SAP大鼠肠道黏膜免疫功能，降低SAP大鼠肠道内毒索移位发生。     

CD4+CD25+调节性T细胞与系统性红斑狼疮病情活动性关系的研究

目的：检测系统性红斑狼疮患者外周血CD4^＋CD25^＋、CD4^＋CD8^＋调节性T细胞亚群，探讨其与疾病活动性、肾脏损伤、血清抗ds-DNA抗体及免疫球蛋白和补体C3含量的关系。方法：采用流式细胞术检测北京协和医院住院和门诊SLE患者（n=37）外周血CD4^＋CD25^＋T、CD4^＋CD8^＋T细胞群比例，以15例RA和15例SS组成自身免疫性疾病对照，30例健康体检者作为正常对照，观察调节性T细胞亚群与SLE患者疾病活动性指标SLEDAI、IgG、C3及血清抗ds-DNA抗体的关系。结果：①疾病活动期SLE患者外周血CD4^＋CD25^＋调节性T细胞群比例显著低于正常对照组（P〈0.01），疾病稳定期和风湿性疾病对照组与正常对照组结果差异无统计学意义。疾病活动期和稳定期SLE患者CD4＋CD8＋T细胞群比例都略高于正常对照组，但未发现结果差异有统计学意义（P〉0.05）。②疾病活动期SLE患者外周血CD4^＋CD25^＋T细胞比例及CD4^＋CD25^＋/CD4^＋值显著低于稳定期患者（P〈0.01）。SLE患者外周血CD4^＋CD25^＋/CD4^＋值与SLEDAI、补体C3呈低度相关（r分别为-0.491、0.368，P〈0.05），CD4^＋CD25^＋T细胞数量与SLEDAI呈负相关（r=-0.578，P〈0.05）。③SLE并发肾病组外周血CD4^＋CD25^＋T细胞群比例及CD4^＋CD25^＋/CD4^＋值显著低于非肾病组（P〈0.01；P〈0.05）。同一SLE患者治疗前后CD3^＋CD4^-CD8^-细胞和NK细胞降低，CD4^＋CD25^＋细胞、CD4^＋CD25^＋/CD4^＋值及CD8^＋T细胞增加，但未发现这些结果差异有统计学意义。本次研究未发现NK细胞、CD4^＋CD8＋T细胞、CD4^＋CD25^＋T细胞群比例在ds-DNA＋组与ds-DNA-组之间结果差异有统计学意义。结论：SLE患者外周血CD4^＋CD25^＋T细胞群比例与SLEDAI成负相关，与肾脏的损害也有密切关系，但与血清抗ds-DNA抗体产生的关系不明显。活动期SLE患者外周血CD4^＋CD25^＋T细胞减少，稳定期CD4^＋CD25^＋T细胞比例回升，因此推测CD4^＋CD25^＋T细胞的变化可能是导致疾病发生和病情发展及相关器官（如肾脏）损伤的关键环节之一。     

发作期哮喘患者外周血T细胞亚群、B细胞和NK细胞的变化及临床意义

目的：探讨发作期哮喘患者外周血T细胞亚群、B细胞和NK细胞变化及临床意义。方法：采用直接免疫荧光法,用流式细胞术检测30例发作期哮喘患者和30例正常人对照的T细胞亚群、B细胞和NK细胞的变化。结果：与正常对照组比较,发作期哮喘患者CD4^＋T细胞、CD19^＋B细胞和CD4^＋／CD8^＋比值显著增高（P〈0．01）,CD8^＋T细胞显著下降（P〈0．01）和CD56^＋CD16^＋NK细胞下降（P〈0．05）。CD3^＋T细胞无明显变化。结论：发作期哮喘患者的免疫功能紊乱在哮喘发病中起着重要作用。     

胃癌患者红细胞C3b受体与淋巴细胞免疫功能的相关性研究

目的：研究胃癌患者红细胞C3b受体（RBC-C3bR）与淋巴细胞免疫功之间的关系。方法：利用酵母菌花环试验、MTT法及克隆抗体致敏花环法对51例胃癌患者及30例正常人的RBC-C3bR、自然杀伤细胞（NK）活性及T淋巴细胞（TC）亚群进行测定。结果：胃癌患者RBC-C3bR阳性率、NK细胞杀伤活性、CD3^＋、CD4^＋、CD4^＋／CD8^＋比值均比正常对照组显著低下（P〈0．05、P〈0．01）。经统计学相关性分析显示，RBC-C3bR阳性率与CD4^＋／CD8^＋比值、NK细胞杀伤活性间呈正相关（P〈0．05，P〈0．01）。结论：胃癌患者红细胞免疫功能与淋巴细胞免疫功能一样受到抑制，二者免疫功能密切联系、相互影响。     

当归多糖对细胞免疫功能的增进作用

目的：观察当归多糖（AP）对细胞免疫功能的影响。方法：用机械分散法制备小鼠单个脾细胞悬液，用MTT比色法检测脾细胞和T细胞的增殖。以免疫磁珠法从小鼠脾细胞中分离纯化T细胞后，用流式细胞术观察AP对CD4^＋T细胞比率的影响。结果：当归总多糖AP-0及其3个组分AP-1、AP-2和AP-3在30—100mg／L剂量的范围内，能显著促进脾细胞的增殖（P〈0．01）；其中组分AP-3能显著促进混合淋巴细胞和T细胞的增殖反应，显著增加培养的脾细胞中CD4^＋T细胞亚群的比率。结论：AP对细胞免疫功能具有增强作用，T细胞是当归多糖的靶细胞之一。     

蕈样肉芽肿患者外周血单一核细胞CD45RA及CD45RO表达的研究

目的探讨蕈样肉芽肿（Mycosis fungoides,MF）患者外周血单个核细胞CD45RA及CD45RO的表达及其与MF发病的关系。方法应用双荧光抗体标记、流式细胞仪检测15例MF患者外周血单个核细胞CD45RA及CD45RO的表达。结果（1）MF患者外周血CD3^＋、CD3^＋CD8^＋细胞与正常对照比较差异不显著（P〉0.05）。（2）MF患者外周血CD4^＋细胞低于正常对照,差异非常显著（P〈0.001）。（3）MF患者外周血T细胞CD3^＋CD4^＋/CD3^＋CD8^＋比值低于正常对照,差异显著（P〈0.001）。（4）MF患者外周血CD45RA^＋细胞低于正常对照,差异非常显著（P〈0.001）,CD45RO^＋细胞高于正常对照,差异非常显著（P〈0.001）。（5）MF患者外周血CD45RO^＋/CD45RA^＋比值高于正常对照,差异非常显著（P〈0.001）。（6）MF患者外周血CD4^＋CD45RA^＋细胞低于正常对照,差异非常显著（P〈0.001）。（7）MF患者外周血CD4^＋CD45RO^＋细胞及CD8^＋CD45RO^＋细胞均高于正常对照,差异非常显著（均P〈0.001）。（8）MF患者外周血CD4^＋CD45RO^＋/CD4^＋CD45RA^＋比值及CD8^＋CD45RO^＋/CD8^＋CD45RA^＋比值均高于正常对照,差异非常显著（P〈0.01及P〈0.001）。结论MF患者外周血中,不仅存在CD4^＋亚群失调和CD4^＋/CD8^＋比值降低,而且在CD4^＋和CD8^＋亚群中也存在CD45RA^＋、CD45RO^＋亚群失调和CD45RO^＋/CD45RA^＋比值升高,从而导致的机体免疫功能紊乱,可能与MF的发病或病情加剧有关。     

Gradual development of the interferon-gamma response of swine to porcine reproductive and respiratory syndrome virus infection or vaccination

Infection of swine with virulent porcine reproductive and respiratory syndrome (PRRS) virus induced a rapid, robust antibody response that comprised predominantly nonneutralizing antibodies and waned after approximately 3 months. In contrast, the initial onset of virus-specific interferon (IFN)-gamma-secreting cells (SC) in the pig lymphocyte population remained at a fairly low level during this period and then increased gradually in frequency, plateauing at 6 months postinfection. A similar polarization of the host humoral and cellular immune responses was also observed in pigs immunized with a PRRS-modified live virus (MLV) vaccine. Even coadministration of an adjuvant that enhanced the immune response to a pseudorabies (PR) MLV vaccine failed to alter the induction of PRRS virus-specific IFN-gamma SC (comprising predominantly CD4/CD8 alpha double positive memory T cells with a minority being typical CD4(-)/CD8 alpha beta(+) T cells) and the generation of neutralizing antibodies. Moreover, unlike inactivated PR virus, nonviable PRRS virus did not elicit virus-neutralizing antibody production. Presumably, an intrinsic property of this pathogen delays the development of the host IFN-gamma response and preferentially stimulates the synthesis of antibodies incapable of neutralization.     

Porcine reproductive and respiratory syndrome (PRRS) virus-specific interferon-gamma(+) T-cell responses after PRRS virus infection or vaccination with an inactivated PRRS vaccine

Although field studies have found porcine reproductive and respiratory syndrome (PRRSV) inactivated vaccines to be beneficial in reducing losses linked to PRRSV infection, immune mechanisms induced by these vaccines need better understanding. In the study reported here, we examined the interferon-gamma(+) (IFNgamma(+)) PRRS-specific T cell responses induced after infection and vaccination with an inactivated PRRS vaccine. Autologous monocyte-derived dendritic cells loaded with the PRRSV P120 strain were used to re-stimulate ex vivo T cells that had been primed in vivo by either the virus or the vaccine, or both. Virus-specific IFNgamma(+) T cells were quantified by using a porcine IFNgamma- ELISpot assay. A specific but low live virus-induced response was observed between days 35 and 70 for most of the pigs tested, while a significant inactivated vaccine-induced PRRSV-specific IFNgamma(+) T-cell response was measured soon after vaccination. Moreover, we observed that vaccination of pre-challenged pigs clearly favoured the PRRSV-specific cell-mediated immunity primed by the live virus. To characterize further the nature of the PRRSV-specific T cells, the different T-cell subsets involved in PRRSV immunity were analyzed by flow cytometry. We showed that the inactivated vaccine was able to prime both CD4(+)CD8(int+) and CD8(high) virus-specific T cells and that CD4(+)CD8(int+) were preferentially recalled by the live virus.     

Heat and social rank impact behavior and physiology of PRRS-virus-infected pigs

Changes in thermal environment can invoke a stress response in pigs, which in turn can potentially impact their immune system and disease susceptibility. We investigated effects of heat stress and social rank on behavior, immune responsiveness, and performance of pigs challenged with porcine reproductive and respiratory syndrome (PRRS) virus. Sixty-four 7-week-old PRRS-na?ve pigs were assigned to each of four experimental treatments consisting of a 2 x 2 factorial design: PRRS (PRRS- or PRRS+) and environmental temperature (24 degrees C or 32 degrees C). Blood samples were taken prior to and at days 7 and 14 post-inoculation, and alveolar macrophages were collected via bronchoalveolar lavage at day 14. Total white blood cell counts, natural killer cytotoxicity, macrophage numbers, macrophage subpopulations, and performance measures were all significantly affected by social rank, heat stress, and/or infection status of the pig. Heat stress and PRRS status also significantly influenced the amount of time pigs spent lying with or without contacting another animal. Cortisol and various immune measures were also affected by PRRS status. These results show not only that intranasal inoculation with PRRS virus affects physiological, behavioral, and performance measures in growing pigs, but that social rank influences pigs' immune responsiveness to PRRS as well. Moreover, heat stress does not have additive negative impact on physiological or performance traits in pigs challenged with PRRS virus.     

Different European-type vaccines against porcine reproductive and respiratory syndrome virus have different immunological properties and confer different protection to pigs

Immunization of piglets with two different European-type modified live vaccines against porcine reproductive and respiratory syndrome (PRRS) virus produced different outcomes. After vaccination, pigs became viremic (42 days), neutralizing antibodies did not develop, and frequencies of virus-specific gamma-interferon-secreting cells (IFN-gamma-SC) were low. Levels of interleukin-10 (IL-10) produced by peripheral blood mononuclear cells (PBMC) seemed to inversely correlate with interferon-gamma responses. After a challenge with a virulent Spanish strain, one vaccine (V3) protected piglets against viremia while the other (V1) did not. The vaccine V3 induced the highest IFN-gamma-SC frequencies. IL-2, IL-4 or transforming growth factor-beta responses were not detected at any time for neither of the vaccines. In contrast, haptoglobin rose in sera of viremic pigs after the challenge. These results indicated a strong involvement of IFN-gamma, and maybe IL-10, in the development of immunity against PRRS virus.     

Phylogenetically important regions of the influenza A H1 hemagglutinin protein

The cellular immune response to a European isolate of porcine reproductive and respiratory syndrome (PRRS) virus in animals recovered from the experimental infection has been studied in vitro. Peripheral blood mononuclear cells (PBMC) from these pigs proliferated specifically when they were stimulated with PRRS virus. This response was not detectable until 4 weeks after inoculation and remained for more than 3 months. Addition of blocking monoclonal antibodies to the cultures showed that this proliferation was mainly dependent on CD4(+) cells with the participation of SLA-class II molecules. T-cell cultures established by stimulating responding cells with PRRS virus and maintained in culture for up to 3 weeks showed an increase of CD8(+) CD4(+) and CD4(-) CD8(+) subsets within activated cells, gated according to their light scatter parameters, whereas CD4(+) CD8(-) cells declined along the time in culture. Within the activated cells, those expressing the TcR gammadelta receptor also increased, being most of them also positive for the CD8 marker. By RT-PCR, T-cells responding to the virus showed a Th1 type cytokine production pattern. During the culture period the cytotoxic activity against K-562 cells increased from 15 to 35% of specific lysis. This cellular immune response may play a relevant role in the clearance of PRRS virus and the recovery of the infection.     

Porcine reproductive and respiratory syndrome virus vaccines: Immunogenicity,efficacy and safety aspects

Porcine reproductive and respiratory syndrome virus (PRRSV) infection is the leading cause of economic casualty in swine industry worldwide. The virus can cause reproductive failure, respiratory disease, and growth retardation in the pigs. This review deals with current status of commercial PRRS vaccines presently used to control PRRS. The review focuses on the immunogenicity, protective efficacy and safety aspects of the vaccines. Commercial PRRS modified-live virus (MLV) vaccine elicits delayed humoral and cell-mediated immune responses following vaccination. The vaccine confers late but effective protection against genetically homologous PRRSV, and partial protection against genetically heterologous virus. The MLV vaccine is of concern for its safety as the vaccine virus can revert to virulence and cause diseases. PRRS killed virus (KV) vaccine, on the other hand, is safe but confers limited protection against either homologous or heterologous virus. The KV vaccine yet helps reduce disease severity when administered to the PRRSV-infected pigs. Although efforts have been made to improve the immunogenicity, efficacy and safety of PRRS vaccines, a better vaccine is still needed in order to protect against PRRSV.     

The Presence of Alpha Interferon at the Time of Infection Alters the Innate and Adaptive Immune Responses to Porcine Reproductive and Respiratory Syndrome Virus

Porcine reproductive and respiratory syndrome (PRRS) is one of the most devastating and costly diseases to the swine industry worldwide. Overall, the adaptive immune response to PRRS virus (PRRSV) is weak, which results in delayed elimination of virus from the host and inferior vaccine protection. PRRSV has been shown to induce a meager alpha interferon (IFN-α) response, and we hypothesized that elevated IFN-α levels early in infection would shorten the induction time and increase elements of the adaptive immune response. To test this, we measured both antibody and cell-mediated immunity in pigs after the administration of a nonreplicating human adenovirus type 5 vector expressing porcine IFN-α (Ad5–pIFN-α) at the time of PRRSV infection and compared the results to those for pigs infected with PRRSV alone. Viremia was delayed, and there was a decrease in viral load in the sera of pigs administered the Ad5–pIFN-α. Although seroconversion was slightly delayed in pigs receiving Ad5–pIFN-α, probably due to the early reduction in viral replication, little difference in the overall or neutralizing antibody response was seen. However, there was an increase in the number of virus-specific IFN-γ-secreting cells detected in the pigs receiving Ad5–pIFN-α, as well as an altered cytokine profile in the lung at 14 days postinfection, indicating that the presence of IFN-α at the time of infection can alter innate and adaptive immune responses to PRRSV.     

Natural infection with torque teno sus virus 1 (TTSuV1) suppresses the immune response to porcine reproductive and respiratory syndrome virus (PRRSV) vaccination

To evaluate the effect of natural infection with TTSuV1 on the antibody response to vaccination with PRRS vaccine and clinical signs when co-infected with virulent PRRSV, 15 4-week-old TTSuV1-positive piglets and 20 TTSuV1-negative piglets were selected by PCR from two pig farms in Jiangsu province. TTSuV1-negative pigs were divided into four groups, and TTSuV1-positive pigs were divided into three groups. Experimental pigs were vaccinated with a PRRSV modified live virus (MLV) at 6 weeks of age and subsequently challenged with a virulent strain of PRRSV at 10 weeks of age. A TTSuV1-negative control group and an unvaccinated PRRS MLV control group were tested at the same time. The levels of antibody/cytokine and protective efficiency against PRRS MLV vaccine were evaluated. TTSuV1-infected/PRRSV-vaccinated pigs had lower levels of PRRSV antibody, as well as IFN-γ, IL-10 and T lymphocyte proliferation, than the TTSuV1-uninfected/PRRSV-vaccinated group (P < 0.05, except IL-10) after vaccination at only one time point. TTSuV1-infected/PRRS MLV-vaccinated/PRRSV-challenged pigs had more severe clinical signs (P > 0.05), more macroscopic lung lesions (P < 0.05) and lower levels of PRRSV antibody (P < 0.05 at 7 to 14 days post-PRRSV-challenge) than TTSuV1-uninfected/PRRSV-vaccinated/PRRSV-challenged pigs. These data indicate that TTSuV1 natural infection has an adverse effect on the development of host immune responses, suppresses immunization by the PRRS MLV vaccine, and exacerbates PRRS to a certain extent in pigs.     

Vaccination with a Porcine Reproductive and Respiratory Syndrome (PRRS) Modified Live Virus Vaccine Followed by Challenge with PRRS Virus and Porcine Circovirus Type 2 (PCV2) Protects against PRRS but Enhances PCV2 Replication and Pathogenesis Compared to Results for Nonvaccinated Cochallenged Controls

Coinfections involving porcine reproductive and respiratory syndrome virus (PRRSV) and porcine circovirus type 2 (PCV2) contribute to a group of disease syndromes known as porcine circovirus-associated disease (PCVAD). Presumably, PRRSV infection enhances PCV2 replication as a result of modulation of host immunity. The purpose of this study was to evaluate PCV2 replication and pathogenesis in pigs vaccinated with a PRRS modified live virus (MLV) vaccine and subsequently challenged with a combination of PRRSV and PCV2. During the early postchallenge period, the number of pigs with PRRSV-associated clinical signs was decreased, and average daily gain (ADG) was increased, in the vaccinated group, demonstrating the protective effect of PRRS vaccination. However, during the later postchallenge period, more pigs in the vaccinated group showed increased PCV2 viremia, decreased ADG, increased PCVAD clinical signs, and increased mortality. In this disease model, the early benefits of PRRSV vaccination were outweighed by the later amplification of PCVAD.