细小病毒 (PV) 影响各种动物物种，导致不同的疾病。迄今为止，在猪群中已发现八种不同的猪细小病毒（PPV1 至 PPV8），所有这些病毒均分布在细小病毒科的亚科和属中。 PPV1 是最古老的，被认为是 SMEDI 的主要药物，而其余的 PPV（PPV2 到 PPV8）被称为新型 PPV（nPPV）。 nPPV 的发病机制仍不明确，这些病毒是否是推定的致病因子尚不清楚。从结构上看，PPV 非常相似；差异主要发生在基因组（ssDNA）水平，其中编码基因的数量和位置存在差异。此外，人们认为PV的基因组具有与ssRNA病毒相似的突变率，即大约10−5–10−4个核苷酸/替换/年。这些突变主要表现在构成病毒衣壳的VP蛋白中，影响毒力、向性和病毒抗原性。对于 nPPV，突变率已经确定，与已经描述的类似；然而，在这组病毒中，PPV7 的突变率最高。除了突变外，还报道了重组，主要是PPV2、PPV3和PPV7；这些已在家猪和野猪品系之间发现，并且在 VP 序列中占有更显着的比例。关于对细胞类型的亲和力，已检测到 nPPV 在不同类型的器官和组织中存在不同的流行率；这导致人们认为它们具有广泛的趋向性，尽管在肺和淋巴组织（如脾、扁桃体和淋巴结）中发现的比例更多。 就其流行病学而言，nPPV 存在于各大洲（PPV8 除外，仅在亚洲），并且在养猪场内，检测到病毒基因组的最高流行率出现在育肥组和育肥组中。 nPPV 与临床表现之间的关系的确定十分复杂。然而，已经有一些证据表明存在关联。其中之一是 PPV2 与猪呼吸道疾病综合征 (PRDC)，其中因果关系测试（PCR、ISH 和组织病理学）导致提出 PPV2 病毒可能是参与该综合征的病原体。对于其他 nPPV，仍然没有与任何病理学明确的关联。这些已在不同系统（呼吸系统、生殖系统、胃肠系统、泌尿系统和神经系统）中检测到，但仍然没有足够的证据将它们归类为致病因子。在这方面，nPPV（PPV8 除外）已被发现会导致猪繁殖失败（PRF），其中最常见的是 PPV4、PPV6 和 PPV7。就 PRDC 而言，还检测到了 nPPV，其中 PPV2 在受影响猪的肺部中病毒载量最高。关于混合感染，在健康猪和病猪中同时检测到 nPPV，以及原发性 PRDC 和 PRF 病毒，例如 PCV2、PCV3 和 PRRSV。这些合并感染的影响并不明显；目前尚不清楚它们是否有利于主要药物的复制、临床表现的严重程度或没有效果。 nPPV 研究中最显着的限制是它们的分离是不可能的。因此，目前还没有对其发病机制的体外和体内研究。 对于上述所有问题，有必要对 nPPV 进行基础和应用研究，以确定它们是否是假定的疾病病原体，确定它们对混合感染的影响，并衡量它们对生猪生产的影响。
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The Novel Porcine Parvoviruses: Current State of Knowledge and Their Possible Implications in Clinical Syndromes in Pigs
Parvoviruses (PVs) affect various animal species causing different diseases. To date, eight different porcine parvoviruses (PPV1 through PPV8) are recognized in the swine population, all of which are distributed among subfamilies and genera of the Parvoviridae family. PPV1 is the oldest and is recognized as the primary agent of SMEDI, while the rest of the PPVs (PPV2 through PPV8) are called novel PPVs (nPPVs). The pathogenesis of nPPVs is still undefined, and whether these viruses are putative disease agents is unknown. Structurally, the PPVs are very similar; the differences occur mainly at the level of their genomes (ssDNA), where there is variation in the number and location of the coding genes. Additionally, it is considered that the genome of PVs has mutation rates similar to those of ssRNA viruses, that is, in the order of 10−5–10−4 nucleotide/substitution/year. These mutations manifest mainly in the VP protein, constituting the viral capsid, affecting virulence, tropism, and viral antigenicity. For nPPVs, mutation rates have already been established that are similar to those already described; however, within this group of viruses, the highest mutation rate has been reported for PPV7. In addition to the mutations, recombinations are also reported, mainly in PPV2, PPV3, and PPV7; these have been found between strains of domestic pigs and wild boars and in a more significant proportion in VP sequences. Regarding affinity for cell types, nPPVs have been detected with variable prevalence in different types of organs and tissues; this has led to the suggestion that they have a broad tropism, although proportionally more have been found in lung and lymphoid tissue such as spleen, tonsils, and lymph nodes. Regarding their epidemiology, nPPVs are present on all continents (except PPV8, only in Asia), and within pig farms, the highest prevalences detecting viral genomes have been seen in the fattener and finishing groups. The relationship between nPPVs and clinical manifestations has been complicated to establish. However, there is already some evidence that establishes associations. One of them is PPV2 with porcine respiratory disease complex (PRDC), where causality tests (PCR, ISH, and histopathology) lead to proposing the PPV2 virus as a possible agent involved in this syndrome. With the other nPPVs, there is still no clear association with any pathology. These have been detected in different systems (respiratory, reproductive, gastrointestinal, urinary, and nervous), and there is still insufficient evidence to classify them as disease-causing agents. In this regard, nPPVs (except PPV8) have been found to cause porcine reproductive failure (PRF), with the most prevalent being PPV4, PPV6, and PPV7. In the case of PRDC, nPPVs have also been detected, with PPV2 having the highest viral loads in the lungs of affected pigs. Regarding coinfections, nPPVs have been detected in concurrence in healthy and sick pigs, with primary PRDC and PRF viruses such as PCV2, PCV3, and PRRSV. The effect of these coinfections is not apparent; it is unknown whether they favor the replication of the primary agents, the severity of the clinical manifestations, or have no effect. The most significant limitation in the study of nPPVs is that their isolation has been impossible; therefore, there are no studies on their pathogenesis both in vitro and in vivo. For all of the above, it is necessary to propose basic and applied research on nPPVs to establish if they are putative disease agents, establish their effect on coinfections, and measure their impact on swine production.
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