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Chaphamaparvovirus (CHPV) is a recently characterized genus of the Parvoviridae family whose members can infect different hosts, including bats, which constitute the second most diverse order of mammals and are described worldwide as important transmitters of zoonotic diseases. In this study, we identified a new CHPV in bat samples from the municipality of Santarém (Pará state, North Brazil). A total of 18 Molossus molossus bats were analyzed using viral metagenomics. In five animals, we identified CHPVs. These CHPV sequences presented the genome with a size ranging from 3797 to 4284 bp. Phylogenetic analysis-based nucleotide and amino acid sequences of the VP1 and NS1 regions showed that all CHPV sequences are monophyletic. They are also closely related to CHPV sequences previously identified in bats in southern and southeast Brazil. According to the International Committee on Taxonomy of Viruses (ICTV) classification criteria for this species (the CHPV NS1 gene region must have 85% identity to be classified in the same species), our sequences are likely a new specie within the genus Chaphamaparvovirus, since they have less than 80% identity with other CHPV described earlier in bats. We also make some phylogenetic considerations about the interaction between CHPV and their host. We suggest a high level of specificity of CPHV and its hosts. Thus, the findings contribute to improving information about the viral diversity of parvoviruses and show the importance of better investigating bats, considering that they harbor a variety of viruses that may favor zoonotic events.

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.

In line with the Latin expression “ sed parva forti” meaning “small but mighty,” the family Parvoviridae contains many of the smallest known viruses, some of which result in fatal or debilitating infections. In recent years, advances in metagenomic viral discovery techniques have dramatically increased the identification of novel parvoviruses in both diseased and healthy individuals. While some of these discoveries have solved etiologic mysteries of well-described diseases in animals, many of the newly discovered parvoviruses appear to cause mild or no disease, or disease associations remain to be established. With the increased use of animal parvoviruses as vectors for gene therapy and oncolytic treatments in humans, it becomes all the more important to understand the diversity, pathogenic potential, and evolution of this diverse family of viruses. In this review, we discuss parvoviruses infecting vertebrate animals, with a special focus on pathogens of veterinary significance and viruses discovered within the last four years.

Parvoviridae, a diverse family of small single-stranded DNA viruses was established in 1975. It was divided into two subfamilies, Parvovirinae and Densovirinae, in 1993 to accommodate parvoviruses that infect vertebrate and invertebrate animals, respectively. This relatively straightforward segregation, using host association as the prime criterion for subfamily-level classification, has recently been challenged by the discovery of divergent, vertebrate-infecting parvoviruses, dubbed “chapparvoviruses”, which have proven to be more closely related to viruses in certain Densovirinae genera than to members of the Parvovirinae. Viruses belonging to these genera, namely Brevi-, Hepan- and Penstyldensovirus, are responsible for the unmatched heterogeneity of the subfamily Densovirinae when compared to the Parvovirinae in matters of genome organization, protein sequence homology, and phylogeny. Another genus of Densovirinae, Ambidensovirus, has challenged traditional parvovirus classification, as it includes all newly discovered densoviruses with an ambisense genome organization, which introduces genus-level paraphyly. Lastly, current taxon definition and virus inclusion criteria have significantly limited the classification of certain long-discovered parvoviruses and impedes the classification of some potential family members discovered using high-throughput sequencing methods. Here, we present a new and updated system for parvovirus classification, which includes the introduction of a third subfamily, Hamaparvovirinae, resolves the paraphyly within genus Ambidensovirus, and introduces new genera and species into the subfamily Parvovirinae. These proposals were accepted by the ICTV in 2020 March.

Seven novel porcine parvoviruses (nPPVs) (PPV2 through PPV8) have been described, although their pathogenicity and possible effects on porcine reproductive failure (PRF) are undefined. In this study, these nPPVs were assessed in gilts from Colombia; their coinfections with PPV1, PCV2, PCV3, PCV4, and PRRSV and an association between the nPPVs and the reproductive performance parameters (RPPs) in sows were determined. For this, 234 serum samples were collected from healthy gilts from 40 herds in five Colombian regions, and the viruses were detected via real-time PCR. The results confirmed the circulation of PPV2 through PPV7 in Colombia, with PPV3 (40%), PPV5 (20%), and PPV6 (17%) being the most frequent. Additionally, no PCV4 or PPV8 was detected. PPV2 to PPV7 were detected in concurrence with each other and with the primary PRF viruses, and these coinfections varied from double to sextuple coinfections. Additionally, the association between nPPVs and PRF primary viruses was statistically significant for the presence of PPV6 in PCV3-positive (p < 0.01) and PPV5 in PPRSV-positive (p < 0.05) gilts; conversely, there was a significant presence of PPV3 in both PCV2-negative (p < 0.01) and PRRSV-negative (p < 0.05) gilts. Regarding the RPPs, the crude association between virus detection (positive or negative) and a high or low RPP was only statistically significant for PCV3 and the farrowing rate (FR), indicating that the crude odds of a low FR were 94% lower in herds with PCV3-positive gilts. This finding means that the detection of PCV3 in gilts (PCV3-positive by PCR) is associated with a higher FR in the farm or that these farms (with positive gilts) have lower odds (OR 0.06, p-value 0.0043) of a low FR. Additionally, a low FR tended to be associated with the detection of PPV4 and PPV5 (p-value < 0.20). This study is important for establishing the possible participation of nPPVs in PRF.

Viruses have long been considered potential triggers of autoimmune diseases. Here we defined the intestinal virome from birth to the development of autoimmunity in children at risk for type 1 diabetes (T1D). A total of 220 virus-enriched preparations from serially collected fecal samples from 11 children (cases) who developed serum autoantibodies associated with T1D (of whom five developed clinical T1D) were compared with samples from controls. Intestinal viromes of case subjects were less diverse than those of controls. Among eukaryotic viruses, we identified significant enrichment of Circoviridae-related sequences in samples from controls in comparison with cases. Enterovirus, kobuvirus, parechovirus, parvovirus, and rotavirus sequences were frequently detected but were not associated with autoimmunity. For bacteriophages, we found higher Shannon diversity and richness in controls compared with cases and observed that changes in the intestinal virome over time differed between cases and controls. Using Random Forests analysis, we identified disease-associated viral bacteriophage contigs after subtraction of age-associated contigs. These disease-associated contigs were statistically linked to specific components of the bacterial microbiome. Thus, changes in the intestinal virome preceded autoimmunity in this cohort. Specific components of the virome were both directly and inversely associated with the development of human autoimmune disease.

The canine parvovirus, with its many variants, is responsible for a pivotal and common viral infection affecting millions of dogs and other carnivore species worldwide, particularly the wild ones, which are considered as the main reservoir hosts. To that end, this study investigated the presence of canine parvovirus (CPV) in red foxes (Vulpes vulpes) living in wild habitats of several regions of Turkey. We randomly collected 630 archival fox stool specimens from rural areas of 22 provinces and used real-time PCR to detect CPV. Two of the 630 (0.3%) stool samples were positive for CPV-DNA, named Tr-Fox/128(Aydin) and Tr-Fox/159(Manisa). We attempted to isolate the virus in a MDCK cell line, and cytopathic effects were observed four days post-inoculation. Three regions corresponding to the CPV capsid protein VP2 gene from extracted DNA of positive samples were amplified by conventional PCR, and the products were visualised, purified, and Sanger sequenced. Three overlapping DNA raw sequence fragments, were read, assembled, and aligned to obtain approximately 1.5 kb-long regions that cover most of the VP2 gene, then deposited in GenBank. After comparing the isolates with parvovirus sequences data of domestic and wild carnivores by BLAST processing, our isolates' similarity rate with each other was 99.40%, with base differences in 9 nucleotide positions. They were classified as 2b variant closely related to isolates from dogs in Turkey, Egypt, Iraq, Italy, Thailand, and China. This study presents evidence of interspecies transmission of CPV, of which there are no reports on prevalence in wildlife carnivores of our country. Identification of CPV in red foxes threatens local and hunting dogs, which may contract the infection or disseminate it to other wild animal species or vice-versa.

In the past decade, recombinant vectors based on a non-pathogenic parvovirus, the adeno-associated virus (AAV), have taken center stage as a gene delivery vehicle for the potential gene therapy for a number of human diseases. To date, the safety of AAV vectors in 176 phase I, II, and III clinical trials and their efficacy in at least eight human diseases are now firmly documented. Despite these remarkable achievements, it has also become abundantly clear that the full potential of first generation AAV vectors composed of naturally occurring capsids is not likely to be realized, since the wild-type AAV did not evolve for the purpose of therapeutic gene delivery. In this article, we provide a brief historical account of the progress that has been made in the development of capsid-modified next-generation AAV vectors to ensure both the safety and efficacy of these vectors in targeting a wide variety of human diseases.

Eight porcine parvovirus (PPV) species, designated as PPV1 through PPV8, have been identified in swine. Despite their similarities, knowledge about their distribution and genetic differences remains limited, resulting in a gap in the genetic classification of these viruses. In this study, we conducted a comprehensive analysis using PPV1 to PPV7 genome sequences from Colombia and others available in the GenBank database to propose a classification scheme for all PPVs. Sera from 234 gilts aged 180 to 200 days were collected from 40 herds in Colombia. Individual detection of each PPV (PPV1 through PPV7) was performed using end-point PCR. Complete nucleotide (nt) sequencing was performed on the PPV1 viral protein (VP), and near-complete genome (NCG) sequencing was carried out for novel porcine parvoviruses (nPPVs) (PPV2 through PPV7). Phylogenetic analyses were conducted by comparing PPV1-VP sequences to 94 available sequences and nPPVs with 565 NCG, 846 nPPV-VP, and 667 nPPV–nonstructural protein (NS) sequences. Bayesian phylogenetic analysis was used to estimate substitution rates and the time to the most recent common ancestor for each PPV. The highest prevalence was detected for PPV3 (40.1%), followed by PPV5 (20.5%), PPV6 (17%), PPV1 (14.5%), PPV2 (9.8%), PPV4 (4.2%), and PPV7 (1.3%). Notably, all tested sera were negative for PPV8 genomes. An analysis of the PPV1-VP sequences revealed two main clades (PPV1-I and PPV1-II), with the sequences recovered in this study grouped in the PPV1-II clade. Comparative analysis showed significant genetic distances for PPV2 to PPV7 at the NCG (>6.5%), NS (>6.3%), and VP (>7.5%) regions, particularly when compared to equivalent regions of PPV genomes recovered worldwide. This study highlights the endemic circulation of nPPVs in Colombian pig herds, specifically among gilts. Additionally, it contributes to the phylogenetic classification and evolutionary studies of these viruses. The proposed method aims to categorize and divide subtypes based on current knowledge and the genomes available in databanks.