Anaplasma phagocytophilum is an obligate intracellular, tick-borne bacterial pathogen capable of causing disease and even mortality in various mammals, including humans. Non-coding RNAs play important regulatory roles in multicellular organisms, including innate and adaptive immune pathways, which control bacterial, parasitic, and viral infections. However, the global transcriptomic landscape encompassing both ncRNAs and mRNAs in HL-60 cells invaded by A. phagocytophilum remains unexplored. Cell apoptosis was evaluated by flow cytometry at multiple time points after HL-60 cell infection with A. phagocytophilum. Total RNA was extracted and analyzed by RNA sequencing (RNA-seq) to delineate expression alterations of long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and messenger RNAs (mRNAs) at 24 h post-infection (hpi). Bioinformatics methods were employed for gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses to elucidate the potential functions of these differentially expressed genes. Furthermore, an integrated bioinformatics approach was applied to systematically construct a competing endogenous RNA (ceRNA) network involving lncRNAs, miRNAs, and mRNAs. A. phagocytophilum infection accelerated HL-60 cell apoptosis at multiple time points, with the most significant effect observed at 24 hpi. Transcriptome profiling at 24 hpi identified substantial differential expression, including 487 lncRNAs, 550 mRNAs, and 22 miRNAs with statistically significant changes in expression. Then, expression patterns of eight lncRNAs, eight mRNAs, and seven miRNAs were experimentally validated through reverse transcription quantitative polymerase chain reaction (RT-qPCR), demonstrating strong correlation with RNA-seq results. Bioinformatics analyses revealed significant enrichment of differentially expressed mRNAs in three key pathways: the PI3K/Akt signaling pathway, the actin cytoskeleton regulation pathway and the p53 signaling pathway. Differentially expressed lncRNAs were largely related to the phospholipase D signaling pathway and pathways related to cortisol and aldosterone synthesis/secretion. The altered miRNAs showed predominant enrichment in Rap1 and NF-κB signaling pathways. Notably, computational reconstruction of the lncRNA–miRNA–mRNA ceRNA network identified hsa–miR–4518 and hsa–miR–3609 as central regulatory nodes. This comprehensive transcriptome study elucidates complex gene regulatory networks activated in HL-60 cells after A. phagocytophilum invasion, with particular emphasis on pathogen-modulated miRNA signatures that coordinate critical pathways governing host immune responses and microbial survival strategies. These findings elucidate previously uncharacterized molecular mechanisms underlying A. phagocytophilum pathogenesis and may provide actionable targets for novel therapeutics.

Porcine parvovirus 1 (PPV1) is an important swine pathogen associated with reproductive disorders. The VP2 capsid protein is the major structural protein of PPV1 and is capable of self-assembly into virus-like particles (VLPs), providing a useful model for studying capsid structure and function. However, the specific VP2 residues involved in hemagglutination and cell attachment remain poorly defined. In this study, sequence alignment and structural comparison of representative protoparvoviruses were used to identify two candidate surface residues, Arg374 and Arg393, in PPV1 VP2. Site-directed mutagenesis was used to generate R374K and R393G mutants, which were expressed using a baculovirus-insect cell system. SDS-PAGE, Western blotting, and transmission electron microscopy confirmed that both mutants efficiently formed VLPs with morphology comparable to wild-type VP2, indicating that these substitutions do not affect capsid assembly. Functional assays demonstrated that both mutations abolished hemagglutination activity. In addition, indirect immunofluorescence assays showed that no detectable cell-associated VP2 signals were observed in PK-15 cells (porcine kidney epithelial cell line) treated with R374K or R393G mutant VLPs, whereas clear VP2-specific fluorescence signals were observed in cells treated with wild-type VLPs. These results identify Arg374 and Arg393 as VP2 surface residues associated with hemagglutination and capsid–cell interaction properties in PPV1 VLPs. This study provides residue-level functional evidence contributing to the understanding of PPV1 capsid surface properties and structure–function relationships in protoparvoviruses.

Giardiasis, caused by Giardia duodenalis, is a prevalent and significant zoonotic disease.While nitroimidazole drugs are primarily used to treat giardiasis, the urgent need for the development and formulation of new drugs has arisen due to increasing drug resistance. Several plant derived medicine have been employed as antiparasitic drugs. This study has evaluated the anti-Giardia effect of Licochalcone A (Lic A) through both in vitro and in vivo experiments. We determined the 50% inhibitory concentration (IC50) of Lic A, analyzed the adhesive ability of G. duodenalis, and assessed intestinal morphology and various indicators in the gerbil model. The in vitro assays demonstrated that the IC50 value of Lic A against G. duodenalis was 27.42 μM. Additionally, Lic A significantly inhibited the adhesiveability of G. duodenalis trophozoites, impairing their cell structure and cytoskeleton. In vivo experiments showed that Lic A significantly mitigated weight loss due to G. duodenalis infection, and lowered the intestinal parasite load.Histopathological examinations in gerbils indicated that Lic A could reduce intestinal damage, increase the height of intestinal villi, decrease crypt depth, and maintain the integrity of intestinal structure. Furthermore, Lic A altered cytokine levels and enhanced the body's antioxidant capacity. In conclusion, Lic A exbibits significant anti-Giardia effects both in vitro and in vivo, suggesting its potential as a promising antiparasitic drug candidate against giardiasis.

BackgroundCryptosporidium spp., Enterocytozoon bieneusi, and Blastocystis sp. are common enteric parasites in humans and pigs. Ascertaining whether non-biting flies (NBFs) serve as potential vectors of these parasites on pig farms is a crucial aspect of disease control.MethodsNon-biting flies were collected and identified by morphology analysis together with sequence analysis of the mitochondrial cytochrome c oxidase I (CO1) gene as confirmation. In a cross-sectional study, the small-subunit ribosomal RNA (SSU rRNA) gene of Cryptosporidium spp., the internal transcribed spacer region (ITS) region of E. bieneusi and the SSU rRNA gene of Blastocystis sp. were investigated in fresh pig fecal samples and sympatric NBFs.ResultsThe results revealed the occurrence of five species of NBFs (Musca domestica, 91.2%; Lucilia sericata, 5.8%; Chrysomya megacephala, 1.7%; Aldrichina grahami, 0.6%; Helicophagella melanura, 0.6%) in the collected pig fecal samples. The prevalence of Cryptosporidium spp., E. bieneusi and Blastocystis sp. on the body surface of NBFs was 0.6% (2/342), 4.4% (15/342) and 20.8% (71/342), respectively. Similarly, the prevalence of these parasites in the lysates of NBFs (= in vivo carriage) was 0% (0/342), 2.7% (9/342) and 10.5% (36/342), respectively. The prevalence of Cryptosporidium spp., E. bieneusi and Blastocystis sp. in pigs from which fly samples were collected was 2.3% (41/1794), 12.6% (226/1794) and 30.8% (553/1794), respectively. The zoonotic Cryposporidium suis/C. scrofarum, E. bieneusi ITS genotypes EbpA/EbpC and Blastocystis sp. subtypes ST1/ST3/ST5 were identified in both NBFs and pig feces. NBFs were found to carry E. bieneusi and Blastocystis sp. on their body surface as well as in the lysates.ConclusionsThese findings demonstrate the role of NBFs as potential vectors in the dissemination of these zoonotic parasites in pig farms, and also highlight the possibility of their transmission to humans.

Cryptosporidium parvum infection can regulate apoptosis of host epithelial cells through both extrinsic and intrinsic apoptotic pathways, potentially involving various microRNAs (miRNAs). This study focuses on the role of miR-125b-5p in modulating apoptosis in HCT-8 cells in response to C. parvum infection. Expression levels of miR-125b-5p and C. parvum burden were estimated using real-time quantitative polymerase chain reaction (RT-qPCR) and cell apoptosis was detected by flow cytometry. The interaction between miR-125b-5p and Bak1 was studied by luciferase reporter assay, RT-qPCR, and western blotting. The expression of Cytochrome c (Cyt c), Caspase-3, and Caspase-9 were assessed by RT-qPCR, and western blotting. JC-1 assess mitochondrial membrane potential. MiR-125b-5p expression decreased at 3, 6, 12, and 24 h post-infection (hpi) but increased at 48 and 72 hpi. Upregulation of miR-125b-5p inhibited apoptosis and increased parasite burden in HCT-8 cells following C. parvum infection, whereas its downregulation promoted apoptosis and reduced the parasite burden. Luciferase reporter assays identified Bak1 as a target gene of miR-125b-5p. Suppression of Bak1 expression via small interfering RNA (siRNA) inhibited apoptosis and increased the C. parvum burden, while Bak1 overexpression promoted apoptosis and reduced the parasite burden. Co-transfection with miR-125b-5p mimics and pcDNA3.1-Bak1 demonstrated that miR-125b-5p regulates apoptosis and parasite burden by targeting Bak1. Further analysis showed that overexpression of miR-125b-5p significantly decreased the mRNA and protein levels of Cytochrome c (cyt-c), caspase-3, and caspase-9, as well as reduced mitochondrial membrane damage. Inhibition of miR-125b-5p produced opposite effects. Co-transfection with miR-125b-5p mimics and pcDNA3.1-Bak1 revealed that pcDNA3.1-Bak1 counteracted the inhibitory effects of miR-125b-5p on cyt-c, caspase-3, caspase-9, and mitochondrial membrane damage. The present data indicated that miR-125b-5p targets Bak1 to regulate apoptosis in HCT-8 cells in response to C. parvum infection via the mitochondrial pathway.

Cryptosporidium parvum is an important zoonotic pathogen that is studied worldwide. MicroRNAs (miRNAs) act as post-transcriptional regulators and may play a key role in modulating host epithelial responses following Cryptosporidium infection. Our previous study has shown that C. parvum downregulates the expression of miR-181d through the p50-dependent TLRs/NF-κB pathway. However, the mechanism by which miR-181d regulates host cells in response to C. parvum infection remains unclear. The present study found that miR-181d downregulation inhibited cell apoptosis and increased parasite burden in HCT-8 cells after C. parvum infection. Bioinformatics analysis and luciferase reporter assays have shown that BCL2 was a target gene for miR-181d. Moreover, BCL2 overexpression and miR-181d downregulation had similar results. To further investigate the mechanism by which miR-181d regulated HCT-8 cell apoptosis during C. parvum infection, the expression of molecules involved in the intrinsic apoptosis pathway was detected. Bax, caspase-9, and caspase-3 expression was decreased at 4, 8, 12, and 24 hpi and upregulated at 36 and 48 hpi. Interfering with the expression of miR-181d or BCL2 significantly affected the expression of molecules in the intrinsic apoptosis pathway. These data indicated that miR-181d targeted BCL2 to regulate HCT-8 cell apoptosis and parasite burden in response to C. parvum infection via the intrinsic apoptosis pathway. These results allowed us to further understand the regulatory mechanisms of host miRNAs during Cryptosporidium infection, and provided a theoretical foundation for the design and development of anti-cryptosporidiosis drugs.

The objective of the present study was to develop a real-time PCR (qPCR) technique for the diagnosis of Eimeria spp. in Ovis aries and Capra hircus. The qPCR technique was developed using SYBR Green, resulting in a PCR with high sensitivity, specificity, and reproducibility.

Cryptosporidium parvum is a zoonotic parasite of the intestine and poses a threat to human and animal health. However, it is difficult to obtain a large number of oocysts for genome sequencing using in vitro culture. To address this challenge, we employed the strategy of whole-genome amplification of 10 oocysts followed by long-read sequencing and obtained a high-quality genome assembly of C. parvum IIdA19G1 subtype isolated from a pre-weaning calf with diarrhea. The assembled genome was 9.13 Mb long and encompassed eight chromosomes with six capped by telomeric sequences at one or both ends. In total, 3,915 protein-coding genes were predicted, exhibiting a high completeness with 98.2% single-copy BUSCO genes. To our current knowledge, this represents the first chromosome-level genome assembly of C. parvum achieved through the combined use of whole-genome amplification of 10 oocysts and long-read sequencing. This achievement not only advances our understanding of the genomic landscape of this zoonotic intestinal parasite, but also provides valuable resources for comparative genomics and evolutionary analyses within the Cryptosporidium clade.

The microRNAs (miRNAs) of their hosts play an important role in regulating both the innate and adaptive immune responses to Cryptosporidium parvum infection. The mechanisms of autophagy and apoptosis are important components of the defense system against C. parvum infection. In this study, we investigate the role of miRNA-199a-3p in regulating MTOR-mediated autophagy and apoptosis in HCT-8 cells induced by C. parvum. The expression of miR-199a-3p increased at 3, 6 and 12 hours postinfection (hpi) but decreased at 24 and 48 hpi. The upregulation of miR-199a-3p promoted autophagy and apoptosis and limited the parasite burden in HCT-8 cells after C. parvum infection. The downregulation of miR-199a-3p inhibited the autophagy and apoptosis induced by C. parvum and enhanced the parasite burden in HCT-8 cells. A luciferase reporter showed that MTOR was a target gene of miR-199a-3p. Suppressed expression of MTOR by small interfering RNA (siRNA) promoted autophagy and apoptosis and limited C. parvum burden in HCT-8 cells. Co-transfection with miR-199a-3p inhibitor or si-mTOR revealed that miR-199a-3p regulates autophagy and apoptosis in HCT-8 cells through MTOR, to resist C. parvum infection. In conclusion, intestinal epithelial cells defend against C. parvum infection by regulating their autophagy and apoptosis through the miR-199a-3p-MTOR axis. Autophagy and apoptosis play a role in the defense against C. parvum. This study shows that miR-199a-3p targets MTOR transcripts, thus downregulating MTOR function, and subsequently reduces the C. parvum burden by promoting autophagy and apoptosis.

Taenia solium taeniasis/cysticercosis is an important global food-borne infectious disease transmitted between humans and pigs. According to both national surveys and field investigations, the prevalence of the disease in China has significantly decreased in recent decades. The primary disease control measures are health education and promotion, meat inspection, and chemotherapy. Other factors that influence or fundamentally affect human and pig T. solium taeniasis/cysticercosis have been identified, such as pig farming patterns shift and a revolution in sanitary toilets, which block T. solium transmission routes. Pig farming practices have shifted from backyard to large-scale intensive farming, thus decreasing pig contact with, and consumption of, human excreta. The increased in the use of sanitary toilets has facilitated hygiene by preventing of human excreta from contacting humans, or polluting the environment, feed, or water. The occurrence of human T. solium infections has markedly decreased as a result of these social changes. The objective of this review is to describe the ecological determinants of the cysticercosis decline in China.

吉尔吉斯斯坦位于中亚东北部,天山山脉西麓,属于内陆国家.在地理位置上北边与哈萨克斯坦相接,西边为乌兹别克斯坦,西南为塔吉克斯坦,东边紧邻中国.吉尔吉斯斯坦划分为7州(省)2市:楚河州、塔拉斯州、奥什州、贾拉拉巴德州、纳伦州、伊塞克湖州、巴特肯州和比什凯克市、奥什市.吉尔吉斯斯坦是一个以农业和畜牧业为主的国家,拥有九万多平方公里的牧场和天然割草场,全年光照充足,气候适宜,这使吉尔吉斯斯坦的畜牧业拥有得天独厚的资源优势.吉尔吉斯斯坦主要以养殖牛、羊、马为主,活动物出口、牛羊肉、皮、奶等具有极强的出口优势,近几年,每年出口量都有小幅上涨.吉尔吉斯斯坦的农产品加工业是经济重点领域之一,每年的农产品及其加工品的贸易额都超过10亿美元.本文通过对吉尔吉斯斯坦养殖业和疫病防控科技现状进行分析,为中、吉两国农业合作提供理论依据.

Cryptosporidiosis is a zoonotic disease in humans and animals that is caused by infection with the oocysts of Cryptosporidium. MicroRNAs (miRNAs) are important players in regulating the innate immune response against parasitic infection. Public miRNAs data for studying pathogenic mechanisms of cryptosporidiosis, particularly in natural hosts, are scarce. Here, we compared miRNA profiles of the glandular stomach of C. muris-infected and uninfected BALB/c mice using microarray sequencing. A total of 10 miRNAs (including 3 upregulated and 7 downregulated miRNAs) with significant differential expression (|FC| ≥ 2 and P value < 0.05) were identified in the glandular stomach of BALB/c mice 8 h after infection with C. muris. MiRWalk and miRDB online bioinformatics tools were used to predict the target genes of differentially expressed miRNAs. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed to annotate the target genes. GO analysis indicate that gene transcription-related and ion transport-related GO terms were significantly enriched. In addition, the KEGG analyses showed that the target genes were strongly related to diverse types of tumor disease progression and anti-pathogen immunity pathways. In the current study, we firstly report changes in miRNA expression profiles in the glandular stomach of BALB/c mice at the early phase of C. muris invasion. This dysregulation in miRNA expression may contribute to our understanding of cryptosporidiosis pathology. This study provides a new perspective on the miRNA regulatory mechanisms of cryptosporidiosis, which may help in the development of effective control strategies against this pathogen.

凋亡是宿主与寄生虫长期进化过程中形成的调节机制之一,对寄生虫感染引起宿主先天免疫反应具有重要的调控作用.隐孢子虫、十二指肠贾第虫和芽囊原虫等寄生性原虫感染可诱导宿主胃肠道上皮细胞发生凋亡.NF-κB信号通路和非编码RNA等参与调控隐孢子虫感染诱导的宿主上皮细胞凋亡,已报道的凋亡途径包括Fas/FasL和TRAI/TRAIL途径;十二指肠贾第虫感染通过内、外两种凋亡途径调控宿主上皮细胞的凋亡,TNFR1信号通路参与细胞凋亡的调控;芽囊原虫和十二指肠贾第虫感染在诱导宿主上皮细胞凋亡水平上存在虫株间的差异.因此,探索隐孢子虫、十二指肠贾第虫和芽囊原虫诱导宿主上皮细胞凋亡机制,对研究寄生性原虫入侵机制及开发设计抗寄生性原虫药物和疫苗具有重要意义.

Background Cryptosporidium is second only to rotavirus as a cause of moderate-to-severe diarrhea in young children. There are currently no fully effective drug treatments or vaccines for cryptosporidiosis. MicroRNAs (miRNAs) are involved in regulating the innate immune response to Cryptosporidium parvum infection. In this study, we investigated the role and mechanism of miR-3976 in regulating HCT-8 cell apoptosis induced by C. parvum infection. Methods Expression levels of miR-3976 and C. parvum burden were estimated using real-time quantitative polymerase chain reaction (RT-qPCR) and cell apoptosis was detected by flow cytometry. The interaction between miR-3976 and B-cell lymphoma 2-related protein A1 ( BCL2A1 ) was studied by luciferase reporter assay, RT-qPCR, and western blotting. Results Expression levels of miR-3976 were decreased at 8 and 12 h post-infection (hpi) but increased at 24 and 48 hpi. Upregulation of miR-3976 promoted cell apoptosis and inhibited the parasite burden in HCT-8 cells after C. parvum infection. Luciferase reporter assay indicated that BCL2A1 was a target gene of miR-3976. Co-transfection with miR-3976 and a BCL2A1 overexpression vector revealed that miR-3976 targeted BCL2A1 and suppressed cell apoptosis and promoted the parasite burden in HCT-8 cells. Conclusions The present data indicated that miR-3976 regulated cell apoptosis and parasite burden in HCT-8 cells by targeting BCL2A1 following C. parvum infection. Future study should determine the role of miR-3976 in hosts’ anti- C. parvum immunity in vivo. Graphical Abstract

为了解我国部分地区近10年羊肠道寄生虫感染情况,探讨羊肠道寄生虫流行特征,采用显微镜检查法对2012年1月至2021年12月来自全国17个省份46个地区的6 745份羊粪便样品进行肠道寄生虫感染情况调查.结果显示,在这些样品中共检测出原虫(艾美耳球虫、隐孢子虫、贾第虫及阿米巴等)、线虫(毛尾线虫也称为鞭虫、毛细线虫、羊仰口线虫、细颈线虫和毛圆线虫等)、绦虫、吸虫(前后盘吸虫、歧腔吸虫及绵羊斯克里亚宾吸虫等)共4纲寄生虫.肠道寄生虫总感染率为82.15％,其中球虫感染率最高(73.73％),其次是阿米巴(37.49％);2012年感染率最高(97.58％),2018年最低(50.77％);放牧羊感染率(87.85％)高于舍饲羊(80.59％).说明我国羊肠道寄生虫感染情况普遍存在,10年来寄生虫感染率无显著下降,应加强肉羊寄生虫病的防控.

Rhipicephalus microplus is a major threat to the cattle industry worldwide. The intensive use of acaricides and repellents has resulted in drug resistance. Hence, effective and eco-friendly pest control alternatives are urgently needed, especially from natural plant resources. In this study, the acaricidal and repellent activities of nine herbs against the larvae and eggs of R. microplus were evaluated. The results showed that ethanol extracts of star anise (Illicium verum), chaulmoogra (Hydnocarpus anthelmintica), motherwart (Leonurus artemisia), mandarin orange peel (citri reticulatae pericarpium, i.e., peel of Citrus reticulata fruit), and stemona (Stemona sessilifolia) had good contact acaricidal activities of 100, 98, 94, 88 and 86%, respectively, whereas star anise and clove (Syzygium aromaticum) had good fumigant acaricidal activities of 98 and 96%, respectively. The hatching inhibition rate of star anise against R. microplus eggs was 100%. All nine herbs had good real-time repellent rates, but only castor bean and star anise had repellent effects after 48 h (81.3 and 79.6%, respectively). This is the first report of the acaricidal and repellent activities of these medicinal herbs against R. microplus. Ethanol extracts of these herbs might be considered as potential alternatives to chemical acaricides for control of R. microplus.

The genus Anaplasma comprises eight bacterial species that are obligate intracellular pathogens that affect human and animal health. The zoonotic species A. phagocytophilum is the causative agent of tick-borne fever in ruminants, and of granulocytic anaplasmosis in horses, dogs, and humans. Recently, novel strains related to A. phagocytophilum (A. phagocytophilum-like 1/Japanese variant and A. phagocytophilum-like 2/Chinese variant) have been identified. The aim of this study was to reveal the prevalence and phylogeny of A. phagocytophilum and related stains in small ruminants and ticks in China based on sequences of the 16S rRNA combined restriction fragment length polymorphism (RFLP) and groEL genes. PCR-RFLP and phylogenetic analyses based on the 16S rRNA gene showed the presence of A. phagocytophilum-like 1 and 2 variants in sampled animals from China, with prevalence rates of 22.6% (303/1338) and 0.7% (10/1338), respectively. Only A. phagocytophilum-like 1 DNA was found in Haemaphysalis longicornis. The phylogeny based on the groEL gene showed inclusion of A. phagocytophilum-like 1 and some A. phagocytophilum-like 2 strains in two unique clades distinct from, but related to, Japanese and Chinese strains of related A. phagocytophilum, respectively. One noteworthy result was that the SSAP2f/SSAP2r primers detected Ehrlichia spp. strains. Moreover, the A. phagocytophilum-like 1 and 2 strains should be considered in the differential diagnosis of caprine and ovine anaplasmosis. Further investigations should be conducted to provide additional epidemiological information about A. phagocytophilum and A. phagocytophilum-like variants in animals and ticks.

隐孢子虫是一种人兽共患寄生性原虫,其致病机理及宿主防御机制尚不完全清楚.凋亡是宿主细胞抵抗隐孢子虫感染的重要防御机制之一,宿主细胞通过细胞凋亡防御隐孢子虫感染,而隐孢子虫则抑制宿主细胞凋亡以促进虫体发育.目前已知的参与隐孢子虫调控细胞凋亡的因子主要有Caspase家族、microRNAs、B7-H1基因、凋亡抑制蛋白(IAPs)、表皮生长因子(EGF)、TAT蛋白等;隐孢子虫调控上皮细胞凋亡通路包括外源性通路(Fas/FasL,TRAI/TRAIL)和内源性通路(线粒体通路).文章综述了隐孢子虫感染调控上皮细胞凋亡的研究进展,以期为设计和开发抗隐孢子虫病的疫苗和药物提供新的理论依据和策略.

隐孢子虫病(Cryptosporidiosis)是由隐孢子虫(Cryptosporidium)寄生于人和动物胃肠道上皮细胞内并引起以腹泻为特征的一种重要的机会性原虫病,该病严重威胁人类健康,给畜牧养殖业造成巨大的经济损失.有研究显示,隐孢子虫需借助顶端复合体分泌的蛋白分子入侵宿主细胞,因此,阐明隐孢子虫入侵相关蛋白分子的作用机制具有重要意义.论文主要对磷脂酶A2、Cp2、Cpa135、CpSUB和CpMuc等5种隐孢子虫入侵相关蛋白分子的结构和功能进行综述,以期为研究隐孢子虫入侵机制和抗隐孢子虫药物与疫苗的研究提供参考.