Primate Hosts Research Articles

Gastrointestinal Parasites in Non-Human Primates in Zoological Gardens in Northern Italy.

Non-human primates (NHPs) host a variety of helminth and protist parasites that are able to cause infection in humans. Gastrointestinal parasites in NHPs living in two zoological gardens of Northern Italy were studied. An total of 96 faecal pools were collected from 26 groups of NHPs. The mini-Flotac method was applied to fecal samples to detect gastrointestinal helminthiases, while the detection of the protists Cryptosporidium spp., Blastocystis sp. and Giardia duodenalis was performed by targeting SSU rRNA through nested PCR and real-time PCR; they were further studied by sequencing the same gene for Blastocystis and βgiardine and triosephosphate isomerase (TPI) genes for Giardia. Twenty-two out of the 96 examined fecal pools (22.9%) were positive for one or more helminth species, including Hymenolepis diminuta, Trichurid, Capillariid and Strongylid eggs. All samples were negative for Cryptosporidium spp., while 16/26 (61.5%) animals were positive for G. duodenalis in the real-time PCR; the sequences obtained assigned them all to sub-assemblage BIV. Blastocystis sp. was detected in 22/26 of the NHPs (84.6%); molecular analyses attributed the isolates to ST 4, allele 92. Analyses of the feces of sympatric rats revealed the presence of the same allele, as well as of Hymenolepis diminuta eggs, raising concern about their role as parasite reservoirs in the facilities.

Evolution of the Cytomegalovirus RL11 gene family in Old World monkeys and Great Apes.

Cytomegalovirus (CMV) is a genus of herpesviruses, members of which share a long history of coevolution with their primate hosts including New World monkeys, Old World monkeys (OWMs), and Great Apes (GAs). These viruses are ubiquitous within their host populations and establish lifelong infection in most individuals. Although asymptomatic in healthy individuals, infection poses a significant risk to individuals with a weakened or underdeveloped immune system. The genome of human CMV is the largest among human-infecting viruses and comprises at least 15 separate gene families, which may have arisen by gene duplication. Within human CMV, the RL11 gene family is the largest. RL11 genes are nonessential in vitro but have immune evasion roles that are likely critical to persistence in vivo. These genes demonstrate an extreme level of inter-species and intra-strain sequence diversity, which makes it challenging to deduce the evolutionary relationships within this gene family. Understanding the evolutionary relationships of these genes, especially accurate ortholog identification, is essential for reconstructing ancestral genomes, deciphering gene repertoire and order, and enabling reliable functional analyses across the CMV species, thereby offering insights into evolutionary processes, genetic diversity, and the functional significance of genes. In this work, we combined in silico genome screening with sequence-based and structure-guided phylogenetic analysis to reconstruct the evolutionary history of the RL11 gene family. We confirmed that RL11 genes are unique to OWM and GA CMVs, showing that this gene family was formed by multiple early duplication events and later lineage-specific losses. We identified four main clades of RL11 genes and showed that their expansions were mainly lineage specific and happened independently in CMVs of GAs, African OWMs, and Asian OWMs. We also identified groups of orthologous genes across the CMV tree, showing that some human CMV-specific RL11 genes emerged before the divergence of human and chimpanzee CMVs but were subsequently lost in the latter. The extensive and dynamic species-specific evolution of this gene family suggests that their functions target elements of host immunity that have similarly coevolved during speciation.

Climate change is aggravating dengue and yellow fever transmission risk

Dengue and yellow fever have complex cycles, involving urban and sylvatic mosquitoes, and non‐human primate hosts. To date, efforts to assess the effect of climate change on these diseases have neglected the combination of such crucial factors. Recent studies only considered urban vectors. This is the first study to include them together with sylvatic vectors and the distribution of primates to analyse the effect of climate change on these diseases. We used previously published models, based on machine learning algorithms and fuzzy logic, to identify areas where climatic favourability for the relevant transmission agents could change: 1) favourable areas for the circulation of the viruses due to the environment and to non‐human primate distributions; 2) the favourability for urban and sylvatic vectors. We obtained projections of future transmission risk for two future periods and for each disease, and implemented uncertainty analyses to test for predictions reliability. Areas currently favourable for both diseases could keep being climatically favourable, while global favourability could increase a 7% for yellow fever and a 10% increase for dengue. Areas likely to be more affected in the future for dengue include West Africa, South Asia, the Gulf of Mexico, Central America and the Amazon basin. A possible spread of dengue could take place into Europe, the Mediterranean basin, the UK and Portugal; and, in Asia, into northern China. For yellow fever, climate could become more favourable in Central and Southeast Africa; India; and in north and southeast South America, including Brazil, Paraguay, Bolivia, Peru, Colombia and Venezuela. In Brazil, favourability for yellow fever will probably increase in the south, the west and the east. Areas where the transmission risk spread is consistent to the dispersal of vectors are highlighted in respect of areas where the expected spread is directly attributable to environmental changes. Both scenarios could involve different prevention strategies.

Landscape drives zoonotic malaria prevalence in non-human primates.

Zoonotic disease dynamics in wildlife hosts are rarely quantified at macroecological scales due to the lack of systematic surveys. Non-human primates (NHPs) host Plasmodium knowlesi, a zoonotic malaria of public health concern and the main barrier to malaria elimination in Southeast Asia. Understanding of regional P. knowlesi infection dynamics in wildlife is limited. Here, we systematically assemble reports of NHP P. knowlesi and investigate geographic determinants of prevalence in reservoir species. Meta-analysis of 6322 NHPs from 148 sites reveals that prevalence is heterogeneous across Southeast Asia, with low overall prevalence and high estimates for Malaysian Borneo. We find that regions exhibiting higher prevalence in NHPs overlap with human infection hotspots. In wildlife and humans, parasite transmission is linked to land conversion and fragmentation. By assembling remote sensing data and fitting statistical models to prevalence at multiple spatial scales, we identify novel relationships between P. knowlesi in NHPs and forest fragmentation. This suggests that higher prevalence may be contingent on habitat complexity, which would begin to explain observed geographic variation in parasite burden. These findings address critical gaps in understanding regional P. knowlesi epidemiology and indicate that prevalence in simian reservoirs may be a key spatial driver of human spillover risk.

Landscape drives zoonotic malaria prevalence in non-human primates

Zoonotic disease dynamics in wildlife hosts are rarely quantified at macroecological scales due to the lack of systematic surveys. Non-human primates (NHPs) host Plasmodium knowlesi, a zoonotic malaria of public health concern and the main barrier to malaria elimination in Southeast Asia. Understanding of regional P. knowlesi infection dynamics in wildlife is limited. Here, we systematically assemble reports of NHP P. knowlesi and investigate geographic determinants of prevalence in reservoir species. Meta-analysis of 6322 NHPs from 148 sites reveals that prevalence is heterogeneous across Southeast Asia, with low overall prevalence and high estimates for Malaysian Borneo. We find that regions exhibiting higher prevalence in NHPs overlap with human infection hotspots. In wildlife and humans, parasite transmission is linked to land conversion and fragmentation. By assembling remote sensing data and fitting statistical models to prevalence at multiple spatial scales, we identify novel relationships between P. knowlesi in NHPs and forest fragmentation. This suggests that higher prevalence may be contingent on habitat complexity, which would begin to explain observed geographic variation in parasite burden. These findings address critical gaps in understanding regional P. knowlesi epidemiology and indicate that prevalence in simian reservoirs may be a key spatial driver of human spillover risk.

Strain-specific requirements of susceptibility to rhesus enteric calicivirus infection.

Recently, we identified the coxsackie and adenovirus receptor (CAR) as the entry receptor for rhesus enteric calicivirus (ReCV) isolate FT285 and demonstrated that co-expression of the CAR and the type B histo-blood group antigen (HBGA) is required to convert the resistant CHO cell line susceptible to infection. To address whether the CAR is also the functional entry receptor for other ReCV isolates and the requirement for specific HBGAs or other glycans, here we used a panel of recombinant CHO cell lines expressing the CAR and the type A, B, or H HBGAs alone or in combination. Infection studies with three diverse ReCV strains, the prototype GI.1 Tulane virus (TV), GI.2 ReCV-FT285, and GI.3 ReCV-FT7, identified that cell surface expression of the CAR is an absolute requirement for all three strains to promote susceptibility to infection, while the requirement for HBGAs varies among the strains. In addition to the CAR, ReCV-FT285 and TV require type A or B HBGAs for infection. In the absence of HBGAs, TV, but not Re-CV FT285, can also utilize sialic acids, while ReCV-FT7 infection is HBGA-independent and relies on CAR and sialic acid expression. In summary, we demonstrated strain-specific diversity of susceptibility requirements for ReCV infections and that CAR, type A and B HBGA, and sialic acid expression control susceptibility to infection with the three ReCV isolates studied. Our study also indicates that the correlation between in vitro HBGA binding and HBGAs required for infection is relatively high, but not absolute. This has direct implications for human noroviruses.IMPORTANCEHuman noroviruses (HuNoVs) are important enteric pathogens. The lack of a robust HuNoV cell culture system is a bottleneck for HuNoV cell culture-based studies. Often, cell culture-adapted caliciviruses that rapidly replicate in conventional cell lines and recapitulate biological features of HuNoVs are utilized as surrogates. Particularly, rhesus enteric caliciviruses (ReCVs) display remarkable similarities, including the primate host, clinical manifestation of gastroenteritis, genetic/antigenic diversity, and reliance on histo-blood group antigens (HBGAs) for attachment. While the HuNoV entry receptor(s) is unknown, the coxsackie and adenovirus receptor (CAR) has recently been identified as the ReCV entry receptor. Here, we identified the CAR, the type A and B HBGAs, and sialic acids as critical cell surface molecules controlling susceptibility to ReCV infections. The CAR is required for all ReCV isolates studied. However, the requirement for the different carbohydrate molecules varies among different ReCV strains. Our findings have direct implications for HuNoVs.

Adaptation of SIVmac to baboon primary cells results in complete absence of in vivo baboon infectivity.

While simian immunodeficiency virus (SIV) infection is non-pathogenic in naturally infected African nonhuman primate hosts, experimental or accidental infection in rhesus macaques often leads to AIDS. Baboons, widely distributed throughout Africa, do not naturally harbor SIV, and experimental infection of baboons with SIVmac results in transient low-level viral replication. Elucidation of mechanisms of natural immunity in baboons could uncover new targets of antiviral intervention. We tested the hypothesis that an SIVmac adapted to replicate in baboon primary cells will gain the capacity to establish chronic infections in vivo. Here, we generated SIVmac variants in baboon cells through serial passage in PBMC from different donors (SIVbn-PBMC s1), in PBMC from the same donors (SIVbn-PBMC s2), or in isolated CD4 cells from the same donors used for series 2 (SIVbn-CD4). While SIVbn-PBMC s1 and SIVbn-CD4 demonstrated increased replication capacity, SIVbn-PBMC s2 did not. Pharmacological blockade of CCR5 revealed SIVbn-PBMC s1 could more efficiently use available CCR5 than SIVmac, a trait we hypothesize arose to circumvent receptor occupation by chemokines. Sequencing analysis showed that all three viruses accumulated different types of mutations, and that more non-synonymous mutations became fixed in SIVbn-PBMC s1 than SIVbn-PBMC s2 and SIVbn-CD4, supporting the notion of stronger fitness pressure in PBMC from different genetic backgrounds. Testing the individual contribution of several newly fixed SIV mutations suggested that is the additive effect of these mutations in SIVbn-PBMC s1 that contributed to its enhanced fitness, as recombinant single mutant viruses showed no difference in replication capacity over the parental SIVmac239 strain. The replicative capacity of SIVbn-PBMC passage 4 (P4) s1 was tested in vivo by infecting baboons intravenously with SIVbn-PBMC P4 s1 or SIVmac251. While animals infected with SIVmac251 showed the known pattern of transient low-level viremia, animals infected with SIVbn-PBMC P4 s1 had undetectable viremia or viral DNA in lymphoid tissue. These studies suggest that adaptation of SIV to grow in baboon primary cells results in mutations that confer increased replicative capacity in the artificial environment of cell culture but make the virus unable to avoid the restrictive factors generated by a complex multicellular organism.

Physiological and genomic characterization of Lactiplantibacillus plantarum isolated from Indri indri in Madagascar.

Indri indri is a lemur of Madagascar which is Critically Endangered. The analysis of the microbial ecology of the intestine offers tools to improve conservation efforts. This study aimed to achieve a functional genomic analysis of three Lp. plantarum isolates from indris. Samples were obtained from 18 indri; 3 isolates of Lp. plantarum were obtained from 2 individuals. The three isolates were closely related to each other, with fewer than 10 single nucleotide polymorphisms, suggesting that the two individuals shared diet-associated microbes. The genomes of the three isolates were compared to 96 reference strains of Lp. plantarum. The three isolates of Lp. plantarum were not phenotypically resistant to antibiotics but shared all 17 genes related to antimicrobial resistance that are part of the core genome of Lp. plantarum. Genomes of the three indri isolates of Lp. plantarum also encoded for the 6 core genome genes coding for enzymes related to metabolism of hydroxybenzoic and hydroxycinnamic acids. The phenotype for metabolism of hydroxycinnamic acids by indri isolates of Lp. plantarum matched the genotype. Multiple antimicrobial resistance genes and gene coding for metabolism of phenolic compounds were identified in the genomes of the indri isolates, suggesting that Lp. plantarum maintains antimicrobial resistance in defense of antimicrobial plant secondary pathogens and that their metabolism by intestinal bacteria aids digestion of plant material by primate hosts.

African ZIKV lineage fails to sustain infectivity in an in vitro mimetic urban cycle.

Zika virus (ZIKV) is an arbovirus maintained in nature in two distinct cycles of transmission: urban and sylvatic. Each cycle includes specific vertebrate and invertebrate hosts, and through alternate infections, a conserved consensus sequence is maintained that might vary depending on the cycle. The current study aimed to investigate the ability of ZIKVAF and ZIKVBR to maintain an infectious cycle by alternating passages in cells mimicking the urban (UC) and semi-sylvatic (SC) cycles. The complete genome of the original inoculum and the last passages for each cycle were sequenced by Sanger. Ten passages were performed, as planned, for ZIKVBR UC, ZIKVAF SC, and ZIKVBR SC. ZIKVBR SC showed significant variation in viral titers along the passages, suggesting that the virus is not well adapted to the non-human primate host. ZIKVAF passage in UC was abrogated in the third passage, showing the inability of the African lineage to sustain cycles in human cells, suggesting a low capacity to establish an urban cycle. Several mutations were found in both strains along the passages, but not occurring at equivalent positions. Further studies are needed to elucidate whether any of these specific mutations affect viral fitness. ZIKV strains behave differently in artificial transmission cycles in vitro: Brazilian ZIKV was able to establish urban and semi-sylvatic cycles in vitro. African ZIKV proved unable to cycle among human and mosquito cells and is compatible only with the semi-sylvatic cycle. The main mutations arose in the NS2A region after artificial transmission cycles for both ZIKV strains but not at equivalent positions.

Host-related and environmental factors influence long-term ectoparasite infestation dynamics of mouse lemurs in northwestern Madagascar.

Parasite infestations depend on multiple host-related and environmental factors. In the case of ectoparasites, which are exposed to the environment beyond the host, an impact of climate, expressed by seasonal or yearly variations, can be expected. However, long-term dynamics of ectoparasite infestations are rarely studied in nonhuman primates. We investigated the yearly variations in ectoparasite infestations of two small primates, the gray (Microcebus murinus) and the golden-brown (Microcebus ravelobensis) mouse lemur. For a more comprehensive evaluation, we also analyzed the potential effects of yearly and monthly climatic variation (temperature, rainfall) in addition to habitat, host sex, age, species, and body mass, on ectoparasite infestation. Individuals of both host species were sampled in two study sites within the Ankarafantsika National Park in northwestern Madagascar during several months (March-November) and across 4 years (2010, 2011, 2015, 2016). Our results show significant monthly and yearly variations in the infestation rates of three native ectoparasite taxa (Haemaphysalis spp. ticks, Schoutedenichia microcebi chigger mites, Lemurpediculus spp. sucking lice) and in ectoparasite species richness in both mouse lemur species. In addition, significant impacts of several host-related (species, sex, body mass) and environmental factors (habitat, temperature, rainfall) were found, but with differences in relevance for the different parasite taxa and partly deviating in their direction. Although some differences could be attributed to either permanent or temporary presence of the parasites on the host or to ecological differences between the host species, the lack of specific knowledge regarding the life cycle and microhabitat requirements of each parasite taxon precludes a complete understanding of the factors that determine their infestation dynamics. This study demonstrates the presence of yearly and monthly dynamics in lemur-parasite interactions in tropical, seasonal, dry deciduous forests in Madagascar, which call out for broad ecological long-term studies focusing both on primate hosts and their parasites.

Genetic characterization of Strongyloides fuelleborni infecting free-roaming African vervets (Chlorocebus aethiops sabaeus) on the Caribbean island of St. Kitts.

Human strongyloidiasis is an important neglected tropical disease primarily caused by the nematode Strongyloides stercoralis, and to a lesser extent Strongyloides fuelleborni which mainly infects non-human primates. Zoonotic sources of infection have important implications for control and prevention of morbidity and mortality caused by strongyloidiasis. Recent molecular evidence suggests that for S. fuelleborni, primate host specificity is variable among genotypes across the Old World, and consequently that these types likely vary in their capacity for human spillover infections. Populations of free-roaming vervet monkeys (Chlorocebus aethiops sabaeus), introduced to the Caribbean Island of Staint Kitts from Africa, live in close contact with humans, and concern has arisen regarding their potential to serve as reservoirs of zoonotic infections. In this study, we sought to determine the genotypes of S. fuelleborni infecting St. Kitts vervets to explore whether they are potential reservoirs for human-infecting S. fuelleborni types. Fecal specimens were collected from St. Kitts vervets and S. fuelleborni infections were confirmed microscopically and by PCR. Strongyloides fuelleborni genotypes were determined from positive fecal specimens using an Illumina amplicon sequencing-based genotyping approach targeting the mitochondrial cox1 locus and 18S rDNA hypervariable regions I and IV of Strongyloides species. Phylogenetic analysis of resultant genotypes supported that S. fuelleborni from St. Kitts vervets is of an exclusively African variety, falling within the same monophyletic group as an isolate which has been detected previously in a naturally infected human from Guinea-Bissau. This observation highlights that St. Kitts vervets may serve as potential reservoirs for zoonotic S. fuelleborni infection, which warrants further exploration.

Non-structural genes of novel lemur adenoviruses reveal codivergence of virus and host.

Adenoviruses (AdVs) are important human and animal pathogens and are frequently used as vectors for gene therapy and vaccine delivery. Surprisingly, there are only scant data regarding primate AdV origin and evolution, especially in the most basal primate hosts. We detect and sequence AdVs from faeces of two Madagascan lemur species. Complete genome sequence analyses define a new AdV species with a particularly large gene encoding a protein of unknown function in the early gene region 3. Unexpectedly, the new AdV species is not most similar to human or other simian AdVs but to bat adenovirus C. Genome characterisation shows signals of virus-host codivergence in non-structural genes, which show lower diversity than structural genes. Outside a lemur species mixing zone, recombination less frequently separates structural genes, as in human adenovirus C. The evolutionary history of lemur AdVs likely involves both a host switch and codivergence with the lemur hosts.

Surveillance, isolation and genomic characterization of Pteropine orthoreovirus of probable bat origin among patients with acute respiratory infection in Malaysia.

Pteropine orthoreovirus (PRV), an emerging bat-borne virus, has been linked to cases of acute respiratory infections (ARI) in humans. The prevalence, epidemiology and genomic diversity of PRV among ARI of unknown origin were studied. Among 632 urban outpatients tested negative for all known respiratory viruses, 2.2% were PRV-positive. Patients mainly presented with moderate to severe forms of cough, sore throat and muscle ache, but rarely with fever. Phylogenetic analysis revealed that over 90% of patients infected with the Melaka virus (MelV)-like PRV, while one patient infected with the Pulau virus previously found only in fruit bats. Human oral keratinocytes and nasopharyngeal epithelial cells were susceptible to clinical isolates of PRV, including the newly isolated MelV-like 12MYKLU1034. Whole genome sequence of 12MYKLU1034 using Nanopore technique revealed a novel reassortant strain. Evolutionary analysis of the global PRV strains suggests the continuous evolution of PRV through genetic reassortment among PRV strains circulating in human, bats and non-human primate hosts, creating a spectrum of reassortant lineages with complex evolutionary characteristics. In summary, the role of PRV as a common etiologic agent of ARI is evident. Continuous monitoring of PRV prevalence, pathogenicity and diversity among human and animal hosts is important to trace the emergence of novel reassortants.

Walk on the wild side: SIV infection in African non-human primate hosts-from the field to the laboratory.

HIV emerged following cross-species transmissions of simian immunodeficiency viruses (SIVs) that naturally infect non-human primates (NHPs) from Africa. While HIV replication and CD4+ T-cell depletion lead to increased gut permeability, microbial translocation, chronic immune activation, and systemic inflammation, the natural hosts of SIVs generally avoid these deleterious consequences when infected with their species-specific SIVs and do not progress to AIDS despite persistent lifelong high viremia due to long-term coevolution with their SIV pathogens. The benign course of natural SIV infection in the natural hosts is in stark contrast to the experimental SIV infection of Asian macaques, which progresses to simian AIDS. The mechanisms of non-pathogenic SIV infections are studied mainly in African green monkeys, sooty mangabeys, and mandrills, while progressing SIV infection is experimentally modeled in macaques: rhesus macaques, pigtailed macaques, and cynomolgus macaques. Here, we focus on the distinctive features of SIV infection in natural hosts, particularly (1): the superior healing properties of the intestinal mucosa, which enable them to maintain the integrity of the gut barrier and prevent microbial translocation, thus avoiding excessive/pathologic immune activation and inflammation usually perpetrated by the leaking of the microbial products into the circulation; (2) the gut microbiome, the disruption of which is an important factor in some inflammatory diseases, yet not completely understood in the course of lentiviral infection; (3) cell population shifts resulting in target cell restriction (downregulation of CD4 or CCR5 surface molecules that bind to SIV), control of viral replication in the lymph nodes (expansion of natural killer cells), and anti-inflammatory effects in the gut (NKG2a/c+ CD8+ T cells); and (4) the genes and biological pathways that can shape genetic adaptations to viral pathogens and are associated with the non-pathogenic outcome of the natural SIV infection. Deciphering the protective mechanisms against SIV disease progression to immunodeficiency, which have been established through long-term coevolution between the natural hosts and their species-specific SIVs, may prompt the development of novel therapeutic interventions, such as drugs that can control gut inflammation, enhance gut healing capacities, or modulate the gut microbiome. These developments can go beyond HIV infection and open up large avenues for correcting gut damage, which is common in many diseases.

A nonstandard finite difference scheme for a time-fractional model of Zika virus transmission.

In this work, we investigate the transmission dynamics of the Zika virus, considering both a compartmental model involving humans and mosquitoes and an extended model that introduces a non-human primate (monkey) as a second reservoir host. The novelty of our approach lies in the later generalization of the model using a fractional time derivative. The significance of this study is underscored by its contribution to understanding the complex dynamics of Zika virus transmission. Unlike previous studies, we incorporate a non-human primate reservoir host into the model, providing a more comprehensive representation of the disease spread. Our results reveal the importance of utilizing a nonstandard finite difference (NSFD) scheme to simulate the disease's dynamics accurately. This NSFD scheme ensures the positivity of the solution and captures the correct asymptotic behavior, addressing a crucial limitation of standard solvers like the Runge-Kutta Fehlberg method (ode45). The numerical simulations vividly demonstrate the advantages of our approach, particularly in terms of positivity preservation, offering a more reliable depiction of Zika virus transmission dynamics. From these findings, we draw the conclusion that considering a non-human primate reservoir host and employing an NSFD scheme significantly enhances the accuracy and reliability of modeling Zika virus transmission. Researchers and policymakers can use these insights to develop more effective strategies for disease control and prevention.

Monkey Business – Host Viral Load and Vector Infection Reveals Heterogeneity of Dengue Type 2 and Zika Virus Transmission in Native and Novel Non-Human Primate Hosts

Monkey Business – Host Viral Load and Vector Infection Reveals Heterogeneity of Dengue Type 2 and Zika Virus Transmission in Native and Novel Non-Human Primate Hosts

High temporal resolution Nanopore sequencing dataset of SARS-CoV-2 and host cell RNAs.

BackgroundRecent studies have disclosed the genome, transcriptome, and epigenetic compositions of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the effect of viral infection on gene expression of the host cells. It has been demonstrated that, besides the major canonical transcripts, the viral genome also codes for noncanonical RNA molecules. While the structural characterizations have revealed a detailed transcriptomic architecture of the virus, the kinetic studies provided poor and often misleading results on the dynamics of both the viral and host transcripts due to the low temporal resolution of the infection event and the low virus/cell ratio (multiplicity of infection [MOI] = 0.1) applied for the infection. It has never been tested whether the alteration in the host gene expressions is caused by aging of the cells or by the viral infection.FindingsIn this study, we used Oxford Nanopore's direct cDNA and direct RNA sequencing methods for the generation of a high-coverage, high temporal resolution transcriptomic dataset of SARS-CoV-2 and of the primate host cells, using a high infection titer (MOI = 5). Sixteen sampling time points ranging from 1 to 96 hours with a varying time resolution and 3 biological replicates were used in the experiment. In addition, for each infected sample, corresponding noninfected samples were employed. The raw reads were mapped to the viral and to the host reference genomes, resulting in 49,661,499 mapped reads (54,62 Gbs). The genome of the viral isolate was also sequenced and phylogenetically classified.ConclusionsThis dataset can serve as a valuable resource for profiling the SARS-CoV-2 transcriptome dynamics, the virus–host interactions, and the RNA base modifications. Comparison of expression profiles of the host gene in the virally infected and in noninfected cells at different time points allows making a distinction between the effect of the aging of cells in culture and the viral infection. These data can provide useful information for potential novel gene annotations and can also be used for studying the currently available bioinformatics pipelines.

Primate hemorrhagic fever-causing arteriviruses are poised for spillover to humans.

Simian arteriviruses are endemic in some African primates and can cause fatal hemorrhagic fevers when they cross into primate hosts of new species. We find that CD163 acts as an intracellular receptor for simian hemorrhagic fever virus (SHFV; a simian arterivirus), a rare mode of virus entry that is shared with other hemorrhagic fever-causing viruses (e.g., Ebola and Lassa viruses). Further, SHFV enters and replicates in human monocytes, indicating full functionality of all of the human cellular proteins required for viral replication. Thus, simian arteriviruses in nature may not require major adaptations to the human host. Given that at least three distinct simian arteriviruses have caused fatal infections in captive macaques after host-switching, and that humans are immunologically naive to this family of viruses, development of serology tests for human surveillance should be a priority.

Population genetics study of Strongyloides fuelleborni and phylogenetic considerations on primate-infecting species of Strongyloides based on their mitochondrial genome sequences

Strongyloides is a genus of parasitic nematodes of vertebrates comprising approximately 50 documented species, each with various host ranges. Among these, three species (S. stercoralis, S. fuelleborni, and S. cebus) are known to infect primate hosts. S. fuelleborni typically infects non-human primates in the Old World. To complement the existing information on the global genetic structure of this species, we conducted a genotyping study of S. fuelleborni samples collected from rhesus macaques in Myanmar, Japanese macaques in Japan, and some zoo-kept primates. This study identified a novel haplotype group in isolates from the Myanmar rhesus macaques. Subsequently, we obtained the complete or nearly complete mitochondrial genome sequences of S. fuelleborni, S. cebus (Strongyloides of New World monkeys), and S. vituli (Strongyloides of cattle). Phylogenetic analysis based on concatenated mitochondrial protein sequences of various Strongyloides species indicated a close relationship between S. fuelleborni, S. vituli and S. papillosus (Strongyloides in sheep and cattle). S. cebus is quite distantly related to both S. fuelleborni and S. stercoralis, which led to the hypothesis that the three primate Strongyloides species evolved independently as parasites of primates.

Population genomics of ancient and modern Trichuris trichiura

The neglected tropical disease trichuriasis is caused by the whipworm Trichuris trichiura, a soil-transmitted helminth that has infected humans for millennia. Today, T. trichiura infects as many as 500 million people, predominantly in communities with poor sanitary infrastructure enabling sustained faecal-oral transmission. Using whole-genome sequencing of geographically distributed worms collected from human and other primate hosts, together with ancient samples preserved in archaeologically-defined latrines and deposits dated up to one thousand years old, we present the first population genomics study of T. trichiura. We describe the continent-scale genetic structure between whipworms infecting humans and baboons relative to those infecting other primates. Admixture and population demographic analyses support a stepwise distribution of genetic variation that is highest in Uganda, consistent with an African origin and subsequent translocation with human migration. Finally, genome-wide analyses between human samples and between human and non-human primate samples reveal local regions of genetic differentiation between geographically distinct populations. These data provide insight into zoonotic reservoirs of human-infective T. trichiura and will support future efforts toward the implementation of genomic epidemiology of this globally important helminth.