Hepatitis E virus (HEV) is increasingly recognized as a cause of neurological disease beyond its hepatic manifestations. Neurological complications are the most frequently reported extrahepatic presentations and include both peripheral nervous system disorders, such as Guillain–Barré syndrome (GBS) and neuralgic amyotrophy (NA), and central nervous system (CNS) involvement, including encephalitis and myelitis, often in the absence of overt hepatitis. This review summarizes the clinical spectrum of HEV-associated neurological disease and integrates evidence from human studies and experimental models. Current evidence supports multifactorial pathogenesis, with direct viral neuroinvasion of the CNS and immune-mediated mechanisms predominating in peripheral neuropathies. Experimental in vivo and in vitro systems demonstrate that HEV can cross the blood–brain barrier (BBB) and replicate within neural tissues, providing biological plausibility for CNS involvement. By synthesizing clinical and experimental findings, this review highlights the dual pathogenic pathways underlying HEV-associated neurological injury and outlines key unresolved questions relevant to diagnosis, pathogenesis, and clinical management.

BackgroundArtemisia argyi is a traditional medicinal herb with established anti-inflammatory and immunomodulatory properties. Its aqueous extract (AEAA), enriched in water-soluble bioactive constituents, exhibits favorable safety and bioavailability; however, its potential protective effects against acute lung injury (ALI) and its associations with systemic immunometabolic regulation remain incompletely understood.MethodsAn LPS-induced ALI mouse model was established following 28 days of AEAA pretreatment. Lung histopathology, pulmonary edema, and inflammatory cytokines were evaluated. Integrated multi-omics analyses—including gut microbiota profiling, untargeted metabolomics of colonic contents and serum, and lung transcriptomics—were performed to characterize treatment-associated microbial, metabolic, and transcriptional alterations.ResultsAEAA pretreatment dose-dependently alleviated lung injury, reduced pulmonary edema, and suppressed pro-inflammatory cytokines while restoring anti-inflammatory IL-10 levels. AEAA treatment was associated with partial reversal of LPS-induced gut dysbiosis, characterized by reduced abundance of inflammation-associated taxa and enrichment of beneficial genera, particularly Akkermansia and Lactobacillus. Metabolomic analyses revealed treatment-associated normalization of intestinal and systemic metabolic disturbances, including increased homeostasis-related metabolites and reduced inflammation-associated metabolites. Lung transcriptomic profiling suggested attenuation of LPS-associated transcriptional signatures related to NF-κB, MAPK, Toll-like receptor, and PI3K–AKT signaling pathways. Cross-omics integration further revealed coordinated associations among microbial shifts, metabolic remodeling, and pulmonary inflammatory gene expression.ConclusionThese findings suggest that aqueous Artemisia argyi extract is associated with mitigation of LPS-induced acute lung injury, accompanied by coordinated alterations in gut microbiota composition, host metabolic profiles, and pulmonary inflammatory gene expression. Although causal relationships were not established, this integrated multi-omics analysis provides a systems-level, hypothesis-generating framework supporting the potential of AEAA as a multi-target botanical candidate for ALI.

ABSTRACT Hepatitis E virus (HEV) is a globally prevalent zoonotic pathogen that is primarily spread through the fecal-oral route, such as by consuming undercooked or contaminated pork. HEV infection leads to an estimated 3.3 million symptomatic cases of viral hepatitis and 70,000 deaths in human populations each year. Therefore, a rapid and accurate method for detecting HEV in serum or stool samples is essential. In this study, we aimed to develop and evaluate two methods for the rapid and convenient detection of HEV RNA: reverse transcription recombinase-aided amplification with lateral flow dipstick (RT-RAA-LFD) and quantitative real-time reverse transcription recombinase-aided amplification (qRT-RAA). We optimized the reaction conditions and assessed their sensitivity and specificity. The RT-RAA-LFD assay completed its reaction at 39°C within 15 minutes, achieving a 95% limit of detection (LOD) of 247 copies/μL. The qRT-RAA assay, completed at 42°C within 20 minutes, had a 95% LOD of 25 copies/μL. Both assays demonstrated no cross-reactivity with other porcine pathogens and exhibited strong specificity. In testing 245 porcine bile and fecal samples, the RT-RAA-LFD assay showed a kappa value of 0.943 ( P < 0.001) with a 97.14% (238/245) coincidence rate compared with quantitative reverse transcription PCR. Similarly, the qRT-RAA assay achieved a kappa value of 0.976 ( P < 0.001) with a 98.78% (242/245) coincidence rate. In conclusion, these two RT-RAA assays show promising potential as effective diagnostic tools for broad and efficient screening of swine HEV in veterinary clinics. IMPORTANCE Hepatitis E virus (HEV) is a globally widespread zoonotic pathogen that poses a significant public health risk. Swine serve as the primary natural host for zoonotic HEV. This study introduces a rapid and precise method for detecting swine HEV RNA, showcasing its potential as an effective diagnostic tool for comprehensive and efficient screening of swine HEV in veterinary clinics.

Heat stress (HS) is a major concern in poultry production worldwide due to its adverse effects on feed intake, weight gain, carcass weight, and metabolic conditions. Several strategies have been explored to ameliorate the negative effects of HS in broiler chickens, among which antimicrobial peptides (AMPs) represent a promising approach. Previously, we isolated chicken hemoglobin antimicrobial peptides (CHAP) and further demonstrated that CHAP has strong bactericidal activity. However, whether CHAP can improve growth performance and maintain intestinal mucosal immunity under chronic HS conditions remains unclear. In the present study, a total of 141 one-day-old broilers were divided into two groups. A total of 36 broilers were used to establish a chronic HS model to evaluate the effects of CHAP on intestinal mucosal immunity, and the remaining 105 birds were used to monitor the inductive effects of CHAP on two vaccines, including Newcastle disease virus (NDV) and avian influenza virus (AIV) vaccines, in broilers. As expected, HS-stimulated broiler chickens supplemented with CHAP showed a significant increase in villus height in the duodenum (p < 0.01), jejunum (p < 0.05), and ileum (p < 0.01) compared to those who did not receive CHAP under chronic HS conditions. The levels of alkaline phosphatase (AKP) and the number of secretory IgA (sIgA)-producing cells were markedly decreased in the chronic HS group (p < 0.01), whereas both significantly recovered after CHAP administration (p < 0.01). CHAP administration improved the birds' body weight and average daily gain (ADG), as well as the feed utilization rate, under HS conditions. Moreover, CHAP effectively mitigated HS-induced bursa injury by inhibiting excessive bursal apoptosis through the downregulation of caspase-3 and Bax, as well as the upregulation of Bcl-2 (p < 0.01). Interestingly, CHAP supplementation enhanced the antibody titer of both NDV and AIV in the broilers. Finally, CHAP administration enhanced the proliferation of splenic lymphocytes. In summary, our data demonstrate that CHAP not only maintains intestinal stability to improve growth performance but also inhibits excessive apoptosis in immune organs and upregulates vaccination effects.

Previous studies here have demonstrated that the rabbit sacculus rotundus-derived antimicrobial peptides (RSRP) could alter the intestinal mucosal immune responses in specific-pathogen-free (SPF) chickens, however, the protective effects of RSRP on chickens against infection remain questionable. In the present study, eighty SPF chickens were randomly divided into five groups and challenged with very virulent infectious bursal disease virus (vvIBDV) to determine the protective effects and its underlying mechanism of RSRP. Histopathology examination found that vvIBDV-infection caused severe damage in the bursa of Fabricius, especially the bursal lymphoid follicles underwent severe necrosis, depletion, hemorrhage, and edema. Unexpectedly, RSRP intervention significantly reduced the necrosis and depletion of lymphoid follicles in the vvIBDV-infected chickens. Moreover, RSRP treatment significantly decreased the expression of Bax (P<0.01) as well as remarkably promoted the expression of Bcl-2 (P<0.01), concomitantly alleviated the excessive apoptosis in the immune organs such as the bursa of Fabricius during vvIBDV infection. Notably, consistent with our previous reports that increased mast cell activation and degranulation in the bursa after vvIBDV infection, RSRP administration considerably reduced the mast cell density and the expression of tryptase, a marker for activated mast cells. Collectively, the present study indicates that rabbit sacculus rotundus-derived antimicrobial peptides could effectively protect the major immune organs including the bursa of Fabricius from the damage caused by vvIBDV infection, which provides the possibility and a promising perspective for the future application of antimicrobial peptides for poultry production.

Hepatitis E virus (HEV) is a foodborne zoonotic pathogen that is supposed to be one of the most common causes of acute viral hepatitis. However, HEV infection has been recently associated with a wide spectrum of extrahepatic manifestations, particularly neurological disorders. Previous studies have shown that HEV is able to cross the blood-brain barrier (BBB) and induce inflammatory response of the central nervous system. However, the pathogenesis of HEV-induced neuroinflammation and tissue injury of the central nervous system have yet to be fully elucidated. In this study, activation of NLRP3 inflammasome following HEV infection were investigated. In a gerbil model infected by HEV, brain histopathological changes including gliosis, neuronophagia and neuron injury were observed and expression of NLRP3, caspase-1, IL-1 beta and IL-18 were elevated. Brain microvascular endothelial cells (BMECs) are key components of the BBB that protects the brain from various challenges. Following HEV infection, virus-like particles range from 30 to 40 nm in diameter were observed in human BMECs (hBMECs). Enhanced expression levels of NLRP3 and subsequent ASC, caspase-1, IL-1 beta and IL-18 were detected in infected cells. Treatment with MCC950 alleviated HEV infection induced activation of NLRP3 inflammasome, mitochondrial damage and VE-cadherin degradation. The findings provide new insights into HEV-associated neuroinflammation. Moreover, targeting NLRP3 inflammasome signalling is a promising therapeutic in HEV-induced neurological disorder.

戊型肝炎病毒(HEV)是单股正链RNA病毒,主要经粪口途径在人和动物间传播.HEV感染已经成为全球性的公共卫生问题,多流行于卫生条件较差的地区.尽管HEV感染多为自限性,但仍有较高几率导致孕妇以及妊娠动物发生流产甚至死亡,并且越来越多的证据表明其可导致诸如神经系统症状等在内的肝外损伤.HEV作为一种人畜共患病原,具有广泛的宿主适应性,对猪、兔等经济动物的健康造成了较大威胁,同时也危害人类动物性食品安全,因此,有关HEV流行和感染机制的研究成为公共卫生和医学领域的热点问题.近年,随着HEV体外培养和动物模型探索成果的相继问世,HEV的生活史及其致病机制也有了新的研究进展.本文综合近年来HEV相关的研究进展,对其流行病学、分类、致病机制、研究模型以及面临的问题等进行简要阐述.

Chronic hepatitis E virus (HEV) infection is frequently reported in immunocompromised patients, but has also been increasingly reported in non-immunocompromised individuals. We characterized the course of chronic HEV infection in immunocompetent rabbits. In two independent experiments, 40 specific-pathogen-free rabbits were infected with a rabbit HEV genotype 3 strain in serial diluted titers (108 to 104 copies/mL). Serum and fecal samples were collected weekly and were tested for HEV RNA, antigen, anti-HEV and liver enzymes. Rabbits that spontaneously cleared the infection before 10 weeks post-inoculation (wpi) were kept to the end of the study as recovery control. Liver tissues were collected from HEV-infected rabbits at 5, 10 and 26 wpi for histopathological analysis. Nineteen rabbits (47.5%) developed chronic HEV infection with persistent viraemia and fecal HEV shedding for >6 months. Seroconversion to anti-HEV was observed in 84.2% (16/19) of the chronically infected rabbits. Serum levels of aminotransferase were persistently elevated in most of the rabbits. Characterizations of chronic HEV infection in immunocompetent settings could be recapitulated in rabbits, which can serve as a valuable tool for future studies on pathogenesis.

戊型肝炎病毒(Hepatitis E virus,HEV)是一种重要的人兽共患病病原,在全球范围内广泛流行.猪是HEV的重要自然宿主,自然感染率较高,通常为亚临床感染或与其他病原混合感染.HEV主要通过粪口途径在人和动物之间传播,国内外均可见人群HEV聚集性感染的报道.由此可见,HEV的流行不仅对畜牧业生产造成威胁,还严重危害人类的食品安全.因此,了解猪群HEV的流行情况和防控措施具有重要的公共卫生学意义.本文调研近年来HEV相关的研究进展,对HEV在猪群中的流行情况、传播方式、诊断和防控等方面展开论述.

如何诊断大熊猫(Ailuropoda melanoleuca)是否患有心肌炎,以及在心肌炎发生发展过程中心脏功能和结构的改变对大熊猫的健康有何意义,现阶段研究报道还很少见.因此,为了解大熊猫心脏病理学变化特点,通过组织病理学方法,对北京动物园过去22年中11例死亡大熊猫的心脏组织进行了系统观察.结果显示:11例大熊猫的心脏均出现了明显的心肌变性和坏死.在轻度情况下,心肌纤维仅呈现颗粒变性、轻度脂肪变性;重症病例,心肌纤维则呈水泡变性和蜡样坏死,甚至断裂、溶解,并可见钙盐沉着.病理诊断表明,11例大熊猫均患有实质性心肌炎.从病理学角度对大熊猫实质性心肌炎进行系统论述,为今后大熊猫相关疾病防治提供病理学依据.

The toxicity of melamine (MA) and its analogue cyanuric acid (CA) in multiple organs has been widely investigated. The purpose of this study was to characterize the pathological lesions of the liver caused by melamine alone or in combination with CA. Mice were oral administered 0, 25, 50, or 100 mg/kg/day MA and CA mixture (MC), or 25, 50, and 100 mg/kg/day MA alone for 7 days. We found MC caused increase of liver weight index and elevations of the serum concentrations of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and creatinine (Cr). Histopathologically, both MA and MC caused scattered necrosis and inflammation cell infiltration in liver. Notably, at 100 mg/kg/day MC, melamine-related crystals were observed in hepatic sinusoid. The liver at high-dose MA and MC groups were further examined by TEM. There were marked degeneration of the mitochondria, and crystal deposition in the Disse space or cytoplasm of hepatic cells and Kupffer cells. TUNEL staining revealed that MA and MC caused apoptosis of hepatocytes and Kupffer cells. Western blotting showed the expression of Bcl-2 decreased, and Bax and caspase-3 increase in liver. The analysis of oxidative stress showed that the expression and activities of two key antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GPX) decreased, and the concentration of malondialdehyde (MDA) elevated in MA- and MC-treated mice. These results from this study demonstrated that both MA and MC caused pathological damage to the liver in mice, especially when ingested in high concentration.

Rabbit hepatitis E virus（HEV） has been reported for years and is thought to have the potential for zoonotic transmission from rabbits to humans. As reported, HEV genotype 3（gt3） is the most prevalent form of HEV in rabbits. To determine the prevalence of HEV in commercial rabbit livers, 176 liver samples were collected from an abattoir in Hebei Province, China.Three（1.7%） samples tested positive for RNA of HEV-ORF2（open reading frames-2）. Sequence analysis showed that the three isolates shared high identities with each other（94.08–98.85%）. Further analysis showed that all the rabbit strains clustered together in the branch of HEV gt3. Further study by immunohistochemistry（IHC） assays showed that 131（74.4%）liver samples were positive for HEV ORF2 protein. Pathological changes including cell degeneration, inflammatory cell infiltration and bile duct epithelial cell hyperplasia were observed under microscopy. These findings indicated the presence of HEV in commercial livers of rabbits. Additional studies should be conducted to investigate the infectivity of rabbit HEV（rHEV） and the potential risks of zoonotic transmission of rHEV from rabbits to human beings.

目的 建立输血感染戊型肝炎病毒(hepatitis E virus,HEV)兔模型,了解HEV全血输注传播的可能性,并观察感染后的指标动态.方法 以兔HEV接种4只SPF兔,经腹腔静脉窦采集抗凝血,然后立即以约10 mL/kg经耳缘静脉注射输血方式分别给予正常SPF受体兔5只,每周监测受体兔粪便和血清抗原、抗体和核酸,连续13周.结果 静脉输血后,5只受体兔均出现粪便排毒,其中3只受体兔引起慢性戊肝,排毒时间超过13周,同时出现病毒血症和HEV抗原阳性,HEV抗体阴性或弱阳性;2只受体兔引起急性戊肝,排毒时间均小于6周,同时HEV抗体检测Sample/Cut-off(S/CO)值均大于13、HEV抗原阴性、无病毒血症.结论 通过输全血方式可以感染兔,并引起急性或慢性HEV感染.

Recently, hepatitis E virus (HEV) has caused large outbreaks and presented a significant public health problem. Thus, the mechanism of HEV has attracted increasing research attention. Previous studies revealed that HEV infection induced hepatocyte injuries and structural and functional changes in mitochondria. These pathological changes affected the life cycle of hepatocytes. However, the precise underlying mechanism and the effector protein responsible for this process remain unclear. In the present study, mitochondrial function and the expression of mitophagy-associated mRNA transcripts and proteins were detected in an HEV- infected Mongolian gerbil model. Observation of ultrastructural changes in the liver of the inoculated group revealed the disappearance of mitochondrial cristae of mitochondrion, blurring of the bilayer structure and cavitation in the cytoplasm. The results showed that the mitochondrial transmembrane potential of decreased, mitochondrial transition pore (MPTP) opening increased, reactive oxygen species (ROS) production increased, and glutathione peroxidase (GSH-Px) activity decreased in the HEV-inoculated group. Moreover, the LC3, Beclin1, BNIP3L, Parkin, PINK1 and P62 mRNA levels were significantly increased (p < 0.05 and p < 0.01) in the inoculated group. Western blot and immunohistochemistry assay analyses detected the upregulation of the mitophagyassociated proteins LC3, Beclin1, BNIP3L, Parkin, PINK1 and P62 (p < 0.05 and p < 0.01) in HEV-infected gerbils. All these data demonstrated that HEV infection in vivo induced mitochondrial dysfunction and the activation of the mitophagy pathway, which might be one of the key factors in hepatocyte injury.

戊型肝炎(HE)是由戊型肝炎病毒(HEV)引起的一种急性的自限性病毒性疾病,主要以粪口途径传播,在全球范围内呈暴发流行或散发传播,目前已被世界卫生组织认定为一个重要的公共卫生疾病.随着对戊型肝炎深入研究,越来越多的HEV动物宿主被证实,这促进了更多动物模型的建立.常见的实验动物模型有非人灵长类动物、猪、兔、啮齿类动物等.HEV动物模型在研究HEV传播、致病机制等方面具有非常重要的意义.本文就近年来HEV动物模型的研究进展进行综述.

将从胶东地区疑似Ⅰ群禽腺病毒(FAdV)感染的发病鸡的肝组织病料中分离鉴定出的FAdV-8b(FXWH-8b)株和FAdV-4 (FXWH-4)株,通过腿部肌肉注射方式,以TCID50 108.0 0.2 mL/羽的剂量,接种15日龄的SPF鸡,临床观察其发病情况及临床表现,研究其毒力和致病性.临床观察和剖检结果显示:FXWH-8b株和FXWH-4株均能在24 h引起试验鸡只发病,表现明显的临床症状和典型的剖检病理变化.H.E.染色结果显示:2株分离株均在脑、胸腺、气管、心脏、肝脏、脾脏、肺脏、肾脏、腺胃、胰腺、十二指肠、空肠、盲肠和法氏囊有较明显的病理变化,但均未发现核内包涵体.PCR检测结果显示:FXWH-8b株攻毒后72 h,FXWH-4株攻毒后48 h,在肝脏、肺脏、肾脏、腺胃、空肠和盲肠呈现100％的阳性率.免疫组化结果显示:FXWH-8b株和FXWH-4株均在肝脏存在强阳性信号;FXWH-4株在肾脏、十二指肠和空肠存在阳性信号.表明FXWH-8b株和FXWH-4株均对15日龄SPF鸡有较强的致病性,可侵害多个组织和器官.

为探明斑点叉尾(Ictalunes punctatus)溃烂症的病因,从4尾患鱼肝脾中分离纯化出4株优势菌株,并进行病原鉴定、毒力基因检测、动物回归感染和药敏试验.4株优势菌经鉴定并命名为杀鲑气单胞菌无色亚种(Aeromonas salmonicida subsp achromogenes)X-G1,杀鲑气单胞菌杀鲑亚种(A.s subsp salmonicida)X-P2、X-P3和嗜水气单胞菌(A.hydrophila)X-P4.15℃时,杀鲑气单胞菌X-G1、X-P2和X-P3的世代时间(约14 min)均小于嗜水气单胞菌X-P4(约20 min);25℃时,杀鲑气单胞菌X-G1、X-P2和X-P3株的世代时间(约20 min)均大于嗜水气单胞菌X-P4株(约16 min).X-G1株可检到弹性蛋白酶、溶血素和甘油磷脂胆固醇酰基转移酶等3种毒力基因;X-P2株仅可检到弹性蛋白酶1种毒力基因;X-P3株可检测到弹性蛋白酶、溶血素、细胞毒性肠毒素、丝氨酸蛋白酶、酯酶、气溶素和甘油磷脂胆固醇酰基转移酶等7种毒力基因;X-P4株可检测到鞭毛、弹性蛋白酶、气溶素、细胞毒性肠毒素、热不稳定性肠毒素、丝氨酸蛋白酶和溶血素等7种毒力基因.分离株X-G1、X-P2、X-P3和X-P4在15～17℃水温下腹腔注射攻毒的半数致死浓度(LD50)依次为0.49×104、0.78×104、0.53×104、3.84×104 CFU/g;而在23～26℃水温下测得的LD50依次为1.48×104、1.80×104、0.82×104、0.68×104 CFU/g.分离株混合感染比单一株感染均表现出更强的致死能力.分离菌株对多西环素、恩诺沙星、氟苯尼考均敏感,但因患病鱼不能摄食药饵而导致治疗失败.

Dear Editor, The COVID-19 pandemic caused by the SARS-CoV-2 virus has caused a significant public health crisis worldwide.Recent studies show that excessive inflammatory response is critical for SARS-CoV-2 pathogenesis and COVID-19 severity,1 which can lead to acute lung injury(ALI)and acute respiratory distress syndrome(ARDS).2 One major factor for acute inflammation in SARS-CoV-2 infection is the inflammatory macrophages,which has been considered important for the production of large amounts of proinflammatory cytokines.3 Autopsy identified an intense infiltra-tion of macrophages in the lung tissues of fatal COVID-19 patients.4 Furthermore,single-cell RNA sequencing(scRNA-seq)showed a higher proportion of macrophages presenting in bronchoalveolar lavage fluid(BALF)of severe COVID-19 patients.5 Consistent with studies of SARS-CoV-2,infiltration and accumula-tion of macrophages in the lung were also found in other coronavirus diseases.6 Depletion of macrophages protected mice from lethal SARS-CoV infection,highlighting the important roles of macrophages in coronavirus-induced symptoms.7 Therefore,targeting macrophages to regulate hyperinflammation in SARS-CoV-2 infection could be an effective strategy to treat COVID-19 patients.

In previous studies, it was found that blocking the low hydraulic resistance channel (LHRC) along meridian in minipigs could lead to the hyperalgesia, a series of abnormal behavioral changes, traditional Chinese medicine (TCM) syndromes and abnormal autopsy in internal organs. The objective of this paper is to investigate the pathology of these changes. Mini-pigs were randomly divided into a stomach meridian blocking group (SBG, n=8), a kidney meridian blocking group (KBG, n=8) and a control group (CG, n=6). The hydraulic gel was injected separately into LHRCs along the stomach meridian and the kidney meridian. The pigs were then fed 7 to 9 weeks, and several indexes were observed. The results showed that the blood serum creatinine increased extremely in all 3 groups and the level in the KBG was lower than that in the SBG by 13.76% (P<0.05) and in the CG by 14.51% (P<0.01). HE staining results showed that more than half of the pigs had the heart abnormalities in the CG, the liver abnormalities in the SBG and the kidney and testicles abnormalities in the KBG. Intestinal sections in the SBG showed that the intestinal crypt depth of the duodenum and the colon, and the total mucosal thickness of the large intestine were significantly higher than those of the CG. The jejunal V/C and the ileal crypt depth were significantly lower than those of the KBG, and the ileal V/C was significantly higher than that of the KBG. Compared with the CG, intestinal sections of the KBG showed that the duodenal crypt depth and the thickness of the colon was significantly higher than that of the CG. The GAS in the KBG was significantly higher than those of the CG and the SBG. The results verify that the blockage of LHRC along the stomach meridian and the kidney meridian can lead to different pathological phenomena, which provided a scientific basis for the syndromes induced by meridian stasis.

为了研究鸡血抗菌肽(CBAP)对保育猪促生长与免疫调节的影响,本试验选取20头65日龄杜洛克种猪,随机分为2组,口服饲喂30 d CBAP.试验结果表明,与对照组相比,饲喂CBAP的保育猪表现出更好的生长性能,日增重比对照组增长88 g/d,提高了 13.7％,CBAP组猪群料肉比与对照组相比降低0.18,下降了 10.4％,日增重与料肉比效果差异显著(P＜0.05).从先天免疫效果来看,CBAP组猪群血清补体C3、C4,γ-干扰素差异显著(P＜0.05),脾淋巴细胞转化率差异极显著(P＜0.01).体液免疫方面,CBAP对猪伪狂犬病(PR)疫苗免疫后的gB抗体,猪口蹄疫(FMD)O型、A型二价灭活疫苗O、A抗体效价提升差异显著(P＜0.05),对猪瘟(CSF)疫苗免疫抗体效价改善差异不显著(P＞0.05).上述结果表明,CBAP对保育猪有明显促生长与免疫调节作用.