ABSTRACT
H5N1 is an avian influenza virus that causes respiratory disease in birds and several land and sea mammals. The recent outbreak in the United States, including infection of dairy workers, has increased the concern around potential transmission and spread. We asked virologists, epidemiologists, and public health experts what the most urgent questions and action points are at this stage of the outbreak.
Subject(s)
Disease Outbreaks , Influenza A Virus, H5N1 Subtype , Influenza in Birds , Influenza, Human , Humans , Influenza, Human/epidemiology , Influenza, Human/transmission , Influenza, Human/virology , Animals , Influenza A Virus, H5N1 Subtype/pathogenicity , Influenza A Virus, H5N1 Subtype/genetics , United States/epidemiology , Influenza in Birds/virology , Influenza in Birds/transmission , Influenza in Birds/epidemiology , Birds/virologyABSTRACT
Since the first reports of a novel severe acute respiratory syndrome (SARS)-like coronavirus in December 2019 in Wuhan, China, there has been intense interest in understanding how severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) emerged in the human population. Recent debate has coalesced around two competing ideas: a "laboratory escape" scenario and zoonotic emergence. Here, we critically review the current scientific evidence that may help clarify the origin of SARS-CoV-2.
Subject(s)
SARS-CoV-2/physiology , Animals , Biological Evolution , COVID-19/virology , Humans , Laboratories , SARS-CoV-2/genetics , Zoonoses/virologyABSTRACT
The highly transmissible B.1.1.7 variant of SARS-CoV-2, first identified in the United Kingdom, has gained a foothold across the world. Using S gene target failure (SGTF) and SARS-CoV-2 genomic sequencing, we investigated the prevalence and dynamics of this variant in the United States (US), tracking it back to its early emergence. We found that, while the fraction of B.1.1.7 varied by state, the variant increased at a logistic rate with a roughly weekly doubling rate and an increased transmission of 40%-50%. We revealed several independent introductions of B.1.1.7 into the US as early as late November 2020, with community transmission spreading it to most states within months. We show that the US is on a similar trajectory as other countries where B.1.1.7 became dominant, requiring immediate and decisive action to minimize COVID-19 morbidity and mortality.
Subject(s)
COVID-19 , Models, Biological , SARS-CoV-2 , COVID-19/genetics , COVID-19/mortality , COVID-19/transmission , Female , Humans , Male , SARS-CoV-2/genetics , SARS-CoV-2/metabolism , SARS-CoV-2/pathogenicity , United States/epidemiologyABSTRACT
Paramyxoviruses are a diverse group of negative-sense, single-stranded RNA viruses of which several species cause significant mortality and morbidity. In recent years the collection of paramyxovirus sequences detected in wild mammals has substantially grown; however, little is known about paramyxovirus diversity in North American mammals. To better understand natural paramyxovirus diversity, host range, and host specificity, we sought to comprehensively characterize paramyxoviruses across a range of diverse cooccurring wild small mammals in southern Arizona. We used highly degenerate primers to screen fecal and urine samples and obtained a total of 55 paramyxovirus sequences from 12 rodent species and 6 bat species. We also performed Illumina transcriptome sequencing (RNA-seq) and de novo assembly on 14 of the positive samples to recover a total of 5 near-full-length viral genomes. We show there are at least two clades of rodent-borne paramyxoviruses in Arizona, while bat-associated paramyxoviruses formed a putative single clade. Using structural homology modeling of the viral attachment protein, we infer that three of the five novel viruses likely bind sialic acid in a manner similar to other respiroviruses, while the other two viruses from heteromyid rodents likely bind a novel host receptor. We find no evidence for cross-species transmission, even among closely related sympatric host species. Taken together, these data suggest paramyxoviruses are a common viral infection in some bat and rodent species present in North America and illuminate the evolution of these viruses. IMPORTANCE There are a number of viral lineages that are potential zoonotic threats to humans. One of these, paramyxoviruses have jumped into humans multiple times from wild and domestic animals. We conducted one of the largest viral surveys of wild mammals in the United States to better understand paramyxovirus diversity and evolution.
Subject(s)
Animal Diseases/epidemiology , Animal Diseases/virology , Chiroptera/virology , Paramyxoviridae Infections/veterinary , Paramyxoviridae/classification , Paramyxoviridae/genetics , Amino Acid Sequence , Animal Diseases/diagnosis , Animals , Arizona/epidemiology , Biodiversity , Biological Evolution , Genome, Viral , Genomics/methods , Geography, Medical , High-Throughput Nucleotide Sequencing , Host Specificity , Humans , Models, Molecular , Molecular Diagnostic Techniques/methods , North America/epidemiology , Phylogeny , Protein Binding , RNA, Viral , Receptors, Virus/chemistry , Receptors, Virus/metabolism , Respirovirus/classification , Respirovirus/genetics , Respirovirus Infections/veterinary , Rodentia/virologyABSTRACT
With very little direct biological data of HIV-1 from before the 1980s, far-reaching evolutionary and epidemiological inferences regarding the long prediscovery phase of this pandemic are based on extrapolations by phylodynamic models of HIV-1 genomic sequences gathered mostly over recent decades. Here, using a very sensitive multiplex RT-PCR assay, we screened 1,645 formalin-fixed paraffin-embedded tissue specimens collected for pathology diagnostics in Central Africa between 1958 and 1966. We report the near-complete viral genome in one HIV-1 positive specimen from Kinshasa, Democratic Republic of Congo (DRC), from 1966 ("DRC66")-a nonrecombinant sister lineage to subtype C that constitutes the oldest HIV-1 near full-length genome recovered to date. Root-to-tip plots showed the DRC66 sequence is not an outlier as would be expected if dating estimates from more recent genomes were systematically biased; and inclusion of the DRC66 sequence in tip-dated BEAST analyses did not significantly alter root and internal node age estimates based on post-1978 HIV-1 sequences. There was larger variation in divergence time estimates among datasets that were subsamples of the available HIV-1 genomes from 1978 to 2014, showing the inherent phylogenetic stochasticity across subsets of the real HIV-1 diversity. Our phylogenetic analyses date the origin of the pandemic lineage of HIV-1 to a time period around the turn of the 20th century (1881 to 1918). In conclusion, this unique archival HIV-1 sequence provides direct genomic insight into HIV-1 in 1960s DRC, and, as an ancient-DNA calibrator, it validates our understanding of HIV-1 evolutionary history.
Subject(s)
Cell Lineage/genetics , Evolution, Molecular , Genetic Variation , Genome, Viral , HIV Infections/genetics , HIV-1/genetics , Paraffin Embedding/methods , Adult , Democratic Republic of the Congo , HIV Infections/virology , Humans , Male , Phylogeny , Sequence Analysis, DNA , Time FactorsABSTRACT
Bats harbour a diverse array of viruses, some of which are zoonotic, and are one of the most speciose groups of mammals on earth. As part of an ongoing bat-associated viral diversity research project, we identified three cycloviruses (family Circoviridae) in fecal samples of silver-haired bats (Lasionycteris noctivagans) caught in Cave Creek Canyon of Arizona (USA). Two of the three identified genomes represent two new species in the genus Cyclovirus. Cycloviruses have been found in a wide range of environments and hosts; however, little is known about their biology. These new genomes of cycloviruses are the first from silver-haired bats, adding to the broader knowledge of cyclovirus diversity. With continuing studies, it is likely that additional viruses of the family Circoviridae will be identified in Arizona bat populations.
Subject(s)
Chiroptera , Circoviridae , Animals , Feces , ArizonaABSTRACT
The emergence of HIV-1 group M subtype B in North American men who have sex with men was a key turning point in the HIV/AIDS pandemic. Phylogenetic studies have suggested cryptic subtype B circulation in the United States (US) throughout the 1970s and an even older presence in the Caribbean. However, these temporal and geographical inferences, based upon partial HIV-1 genomes that postdate the recognition of AIDS in 1981, remain contentious and the earliest movements of the virus within the US are unknown. We serologically screened >2,000 1970s serum samples and developed a highly sensitive approach for recovering viral RNA from degraded archival samples. Here, we report eight coding-complete genomes from US serum samples from 1978-1979-eight of the nine oldest HIV-1 group M genomes to date. This early, full-genome 'snapshot' reveals that the US HIV-1 epidemic exhibited extensive genetic diversity in the 1970s but also provides strong evidence for its emergence from a pre-existing Caribbean epidemic. Bayesian phylogenetic analyses estimate the jump to the US at around 1970 and place the ancestral US virus in New York City with 0.99 posterior probability support, strongly suggesting this was the crucial hub of early US HIV/AIDS diversification. Logistic growth coalescent models reveal epidemic doubling times of 0.86 and 1.12 years for the US and Caribbean, respectively, suggesting rapid early expansion in each location. Comparisons with more recent data reveal many of these insights to be unattainable without archival, full-genome sequences. We also recovered the HIV-1 genome from the individual known as 'Patient 0' (ref. 5) and found neither biological nor historical evidence that he was the primary case in the US or for subtype B as a whole. We discuss the genesis and persistence of this belief in the light of these evolutionary insights.
Subject(s)
Acquired Immunodeficiency Syndrome/history , Acquired Immunodeficiency Syndrome/virology , Genome, Viral/genetics , HIV-1/classification , HIV-1/genetics , Acquired Immunodeficiency Syndrome/blood , Acquired Immunodeficiency Syndrome/epidemiology , Bayes Theorem , HIV-1/isolation & purification , History, 20th Century , Homosexuality, Male/statistics & numerical data , Humans , Male , New York City/epidemiology , North America/epidemiology , RNA, Viral/analysis , RNA, Viral/genetics , RNA, Viral/isolation & purification , Sequence Analysis, DNA , Spatio-Temporal AnalysisABSTRACT
Across decades of co-circulation in humans, influenza A subtypes H1N1 and H3N2 have caused seasonal epidemics characterized by different age distributions of cases and mortality. H3N2 causes the majority of severe, clinically attended cases in high-risk elderly cohorts, and the majority of overall deaths, whereas H1N1 causes fewer deaths overall, and cases shifted towards young and middle-aged adults. These contrasting age profiles may result from differences in childhood imprinting to H1N1 and H3N2 or from differences in evolutionary rate between subtypes. Here we analyze a large epidemiological surveillance dataset to test whether childhood immune imprinting shapes seasonal influenza epidemiology, and if so, whether it acts primarily via homosubtypic immune memory or via broader, heterosubtypic memory. We also test the impact of evolutionary differences between influenza subtypes on age distributions of cases. Likelihood-based model comparison shows that narrow, within-subtype imprinting shapes seasonal influenza risk alongside age-specific risk factors. The data do not support a strong effect of evolutionary rate, or of broadly protective imprinting that acts across subtypes. Our findings emphasize that childhood exposures can imprint a lifelong immunological bias toward particular influenza subtypes, and that these cohort-specific biases shape epidemic age distributions. As a consequence, newer and less "senior" antibody responses acquired later in life do not provide the same strength of protection as responses imprinted in childhood. Finally, we project that the relatively low mortality burden of H1N1 may increase in the coming decades, as cohorts that lack H1N1-specific imprinting eventually reach old age.
Subject(s)
Epidemics , Influenza, Human/epidemiology , Influenza, Human/immunology , Influenza, Human/virology , Adult , Child , Female , Humans , Immunologic Memory/immunology , Influenza A Virus, H1N1 Subtype/immunology , Influenza A Virus, H3N2 Subtype/immunology , MaleABSTRACT
Zoonotic infectious diseases such as influenza continue to pose a grave threat to human health. However, the factors that mediate the emergence of RNA viruses such as influenza A virus (IAV) are still incompletely understood. Phylogenetic inference is crucial to reconstructing the origins and tracing the flow of IAV within and between hosts. Here we show that explicitly allowing IAV host lineages to have independent rates of molecular evolution is necessary for reliable phylogenetic inference of IAV and that methods that do not do so, including 'relaxed' molecular clock models, can be positively misleading. A phylogenomic analysis using a host-specific local clock model recovers extremely consistent evolutionary histories across all genomic segments and demonstrates that the equine H7N7 lineage is a sister clade to strains from birds--as well as those from humans, swine and the equine H3N8 lineage--sharing an ancestor with them in the mid to late 1800s. Moreover, major western and eastern hemisphere avian influenza lineages inferred for each gene coalesce in the late 1800s. On the basis of these phylogenies and the synchrony of these key nodes, we infer that the internal genes of avian influenza virus (AIV) underwent a global selective sweep beginning in the late 1800s, a process that continued throughout the twentieth century and up to the present. The resulting western hemispheric AIV lineage subsequently contributed most of the genomic segments to the 1918 pandemic virus and, independently, the 1963 equine H3N8 panzootic lineage. This approach provides a clear resolution of evolutionary patterns and processes in IAV, including the flow of viral genes and genomes within and between host lineages.
Subject(s)
Genes, Viral/genetics , Influenza A virus/classification , Influenza A virus/genetics , Influenza in Birds/virology , Phylogeny , Animals , Birds/virology , Evolution, Molecular , Genome, Viral/genetics , Hemagglutinin Glycoproteins, Influenza Virus/classification , Hemagglutinin Glycoproteins, Influenza Virus/genetics , Horses/virology , Host Specificity , Humans , Influenza A Virus, H3N8 Subtype/classification , Influenza A Virus, H3N8 Subtype/genetics , Influenza A Virus, H7N7 Subtype/classification , Influenza A Virus, H7N7 Subtype/genetics , Influenza A virus/enzymology , Influenza in Birds/transmission , Molecular Sequence Data , Neuraminidase/classification , Neuraminidase/genetics , Pandemics , Swine/virology , Zoonoses/transmission , Zoonoses/virologyABSTRACT
How influenza A viruses host-jump from animal reservoir species to humans, which can initiate global pandemics, is a central question in pathogen evolution. The zoonotic and spatial origins of the influenza virus associated with the "Spanish flu" pandemic of 1918 have been debated for decades. Outbreaks of respiratory disease in US swine occurred concurrently with disease in humans, raising the possibility that the 1918 virus originated in pigs. Swine also were proposed as "mixing vessel" intermediary hosts between birds and humans during the 1957 Asian and 1968 Hong Kong pandemics. Swine have presented an attractive explanation for how avian viruses overcome the substantial evolutionary barriers presented by different cellular environments in humans and birds. However, key assumptions underpinning the swine mixing-vessel model of pandemic emergence have been challenged in light of new evidence. Increased surveillance in swine has revealed that human-to-swine transmission actually occurs far more frequently than the reverse, and there is no empirical evidence that swine played a role in the emergence of human influenza in 1918, 1957, or 1968. Swine-to-human transmission occurs periodically and can trigger pandemics, as in 2009. But swine are not necessary to mediate the establishment of avian viruses in humans, which invites new perspectives on the evolutionary processes underlying pandemic emergence.
Subject(s)
Influenza Pandemic, 1918-1919/history , Influenza, Human/epidemiology , Influenza, Human/history , Swine/virology , Zoonoses/epidemiology , Animals , History, 20th Century , Humans , Influenza A virus , Influenza Pandemic, 1918-1919/mortality , Influenza, Human/mortality , Influenza, Human/transmission , Pandemics/history , Zoonoses/history , Zoonoses/mortality , Zoonoses/transmissionSubject(s)
Zika Virus Infection , Zika Virus , Americas , Disease Outbreaks , Evolution, Molecular , Humans , Microcephaly/epidemiology , Molecular EpidemiologyABSTRACT
The source, timing, and geographical origin of the 1918-1920 pandemic influenza A virus have remained tenaciously obscure for nearly a century, as have the reasons for its unusual severity among young adults. Here, we reconstruct the origins of the pandemic virus and the classic swine influenza and (postpandemic) seasonal H1N1 lineages using a host-specific molecular clock approach that is demonstrably more accurate than previous methods. Our results suggest that the 1918 pandemic virus originated shortly before 1918 when a human H1 virus, which we infer emerged before â¼1907, acquired avian N1 neuraminidase and internal protein genes. We find that the resulting pandemic virus jumped directly to swine but was likely displaced in humans by â¼1922 by a reassortant with an antigenically distinct H1 HA. Hence, although the swine lineage was a direct descendent of the pandemic virus, the post-1918 seasonal H1N1 lineage evidently was not, at least for HA. These findings help resolve several seemingly disparate observations from 20th century influenza epidemiology, seroarcheology, and immunology. The phylogenetic results, combined with these other lines of evidence, suggest that the high mortality in 1918 among adults aged â¼20 to â¼40 y may have been due primarily to their childhood exposure to a doubly heterosubtypic putative H3N8 virus, which we estimate circulated from â¼1889-1900. All other age groups (except immunologically naive infants) were likely partially protected by childhood exposure to N1 and/or H1-related antigens. Similar processes may underlie age-specific mortality differences between seasonal H1N1 vs. H3N2 and human H5N1 vs. H7N9 infections.
Subject(s)
Influenza A virus/genetics , Influenza A virus/immunology , Influenza Pandemic, 1918-1919/mortality , Influenza, Human/mortality , Influenza, Human/virology , Reassortant Viruses/genetics , Adult , Aged , Animals , Biological Evolution , Birds , Child , Disease Resistance/immunology , Genetic Variation , Humans , Influenza A Virus, H1N1 Subtype/genetics , Influenza A Virus, H1N1 Subtype/immunology , Influenza A Virus, H1N1 Subtype/pathogenicity , Influenza A Virus, H3N2 Subtype/genetics , Influenza A Virus, H3N2 Subtype/immunology , Influenza A Virus, H3N2 Subtype/pathogenicity , Influenza A Virus, H3N8 Subtype/genetics , Influenza A Virus, H3N8 Subtype/immunology , Influenza A Virus, H3N8 Subtype/pathogenicity , Influenza A Virus, H5N1 Subtype/genetics , Influenza A Virus, H5N1 Subtype/immunology , Influenza A Virus, H5N1 Subtype/pathogenicity , Influenza A Virus, H7N9 Subtype/genetics , Influenza A Virus, H7N9 Subtype/immunology , Influenza A Virus, H7N9 Subtype/pathogenicity , Influenza A virus/pathogenicity , Phylogeny , Reassortant Viruses/immunology , Reassortant Viruses/pathogenicity , Swine , VirulenceABSTRACT
Lentiviruses infect a wide range of mammal species. Much remains unknown about their deep history and host distribution. Here, we report the discovery of an endogenous lentivirus within the genome of the Sunda flying lemur (Galeopterus variegatus) (which we designate "Galeopterus variegatus endogenous lentivirus" [GvaELV]). We estimate the GvaELV genome invasion to have occurred more than 14 Ma, supporting an ancient origin of the lentivirus clade and an ancient lentiviral infection in colugo. Phylogenetic analyses show that GvaELV is a sister group of all previously known lentiviruses. The GvaELV genome appears to possess some primitive genomic features of a lentivirus, encoding not only a trans-activator of transcription (tat) gene but also two additional putative accessory genes that share no discernible similarity with other lentiviral accessory genes. The discovery of GvaELV provides novel insights into the prehistory and host distribution of lentivirus.
Subject(s)
Endogenous Retroviruses/genetics , Genome, Viral , Lemur/virology , Lentiviruses, Primate/genetics , Animals , Endogenous Retroviruses/classification , Evolution, Molecular , Genomics/methods , Lentiviruses, Primate/classification , PhylogenyABSTRACT
In March and early April 2009, a new swine-origin influenza A (H1N1) virus (S-OIV) emerged in Mexico and the United States. During the first few weeks of surveillance, the virus spread worldwide to 30 countries (as of May 11) by human-to-human transmission, causing the World Health Organization to raise its pandemic alert to level 5 of 6. This virus has the potential to develop into the first influenza pandemic of the twenty-first century. Here we use evolutionary analysis to estimate the timescale of the origins and the early development of the S-OIV epidemic. We show that it was derived from several viruses circulating in swine, and that the initial transmission to humans occurred several months before recognition of the outbreak. A phylogenetic estimate of the gaps in genetic surveillance indicates a long period of unsampled ancestry before the S-OIV outbreak, suggesting that the reassortment of swine lineages may have occurred years before emergence in humans, and that the multiple genetic ancestry of S-OIV is not indicative of an artificial origin. Furthermore, the unsampled history of the epidemic means that the nature and location of the genetically closest swine viruses reveal little about the immediate origin of the epidemic, despite the fact that we included a panel of closely related and previously unpublished swine influenza isolates. Our results highlight the need for systematic surveillance of influenza in swine, and provide evidence that the mixing of new genetic elements in swine can result in the emergence of viruses with pandemic potential in humans.
Subject(s)
Disease Outbreaks , Evolution, Molecular , Genome, Viral/genetics , Influenza A Virus, H1N1 Subtype/genetics , Influenza, Human , Reassortant Viruses/genetics , Swine Diseases/virology , Animals , Humans , Influenza A Virus, H1N1 Subtype/classification , Influenza, Human/epidemiology , Influenza, Human/virology , Molecular Sequence Data , Orthomyxoviridae Infections/epidemiology , Orthomyxoviridae Infections/veterinary , Orthomyxoviridae Infections/virology , Phylogeny , Reassortant Viruses/classification , Swine , Time FactorsABSTRACT
Little is known about the origin and long-term evolutionary mode of retroviruses. Retroviruses can integrate into their hosts' genomes, providing a molecular fossil record for studying their deep history. Here we report the discovery of an endogenous foamy virus-like element, which we designate 'coelacanth endogenous foamy-like virus' (CoeEFV), within the genome of the coelacanth (Latimeria chalumnae). Phylogenetic analyses place CoeEFV basal to all known foamy viruses, strongly suggesting an ancient ocean origin of this major retroviral lineage, which had previously been known to infect only land mammals. The discovery of CoeEFV reveals the presence of foamy-like viruses in species outside the Mammalia. We show that foamy-like viruses have likely codiverged with their vertebrate hosts for more than 407 million years and underwent an evolutionary transition from water to land with their vertebrate hosts. These findings suggest an ancient marine origin of retroviruses and have important implications in understanding foamy virus biology.
Subject(s)
Genome, Viral , Spumavirus/genetics , Vertebrates/genetics , Vertebrates/virology , Amino Acid Sequence , Animals , Conserved Sequence , Molecular Sequence Data , PhylogenyABSTRACT
Although we know there is considerable variation in gut microbial composition within host species, little is known about how this variation is shaped and why such variation exists. In humans, obesity is associated with the relative abundance of two dominant bacterial phyla: an increase in the proportion of Firmicutes and a decrease in the proportion of Bacteroidetes. As there is evidence that humans have adapted to colder climates by increasing their body mass (e.g. Bergmann's rule), we tested whether Firmicutes increase and Bacteroidetes decrease with latitude, using 1020 healthy individuals drawn from 23 populations and six published studies. We found a positive correlation between Firmicutes and latitude and a negative correlation between Bacteroidetes and latitude. The overall pattern appears robust to sex, age and bacterial detection methods. Comparisons between African Americans and native Africans and between European Americans and native Europeans suggest no evidence of host genotype explaining the observed patterns. The variation of gut microbial composition described here is consistent with the pattern expected by Bergmann's rule. This surprising link between large-scale geography and human gut microbial composition merits further investigation.
Subject(s)
Bacteroidetes/isolation & purification , Biodiversity , Gastrointestinal Tract/microbiology , Gram-Positive Bacteria/isolation & purification , Microbiota , Adolescent , Adult , Aged , Aged, 80 and over , Bacteroidetes/classification , Child , Child, Preschool , Climate , Female , Genotype , Gram-Positive Bacteria/classification , Humans , Infant , Male , Middle Aged , Young AdultABSTRACT
Human immunodeficiency virus type 1 (HIV-1) sequences that pre-date the recognition of AIDS are critical to defining the time of origin and the timescale of virus evolution. A viral sequence from 1959 (ZR59) is the oldest known HIV-1 infection. Other historically documented sequences, important calibration points to convert evolutionary distance into time, are lacking, however; ZR59 is the only one sampled before 1976. Here we report the amplification and characterization of viral sequences from a Bouin's-fixed paraffin-embedded lymph node biopsy specimen obtained in 1960 from an adult female in Léopoldville, Belgian Congo (now Kinshasa, Democratic Republic of the Congo (DRC)), and we use them to conduct the first comparative evolutionary genetic study of early pre-AIDS epidemic HIV-1 group M viruses. Phylogenetic analyses position this viral sequence (DRC60) closest to the ancestral node of subtype A (excluding A2). Relaxed molecular clock analyses incorporating DRC60 and ZR59 date the most recent common ancestor of the M group to near the beginning of the twentieth century. The sizeable genetic distance between DRC60 and ZR59 directly demonstrates that diversification of HIV-1 in west-central Africa occurred long before the recognized AIDS pandemic. The recovery of viral gene sequences from decades-old paraffin-embedded tissues opens the door to a detailed palaeovirological investigation of the evolutionary history of HIV-1 that is not accessible by other methods.
Subject(s)
Evolution, Molecular , Genetic Variation/genetics , HIV Infections/epidemiology , HIV Infections/virology , HIV-1/genetics , HIV-1/isolation & purification , Adult , Canada , Democratic Republic of the Congo/epidemiology , Female , HIV Infections/pathology , HIV-1/classification , History, 20th Century , Humans , Male , Microtomy , Molecular Sequence Data , Paraffin Embedding , Phylogeny , Reverse Transcriptase Polymerase Chain Reaction , Sequence Analysis, DNAABSTRACT
Endogenous retroviruses provide molecular fossils for studying the ancient evolutionary history of retroviruses. Here, we report our independent discovery and analysis of endogenous lentiviral insertions (Mustelidae endogenous lentivirus [MELV]) within the genomes of weasel family (Mustelidae). Genome-scale screening identified MELV elements in the domestic ferret (Mustela putorius furo) genome (MELVmpf). MELVmpf exhibits a typical lentiviral genomic organization. Phylogenetic analyses position MELVmpf basal to either primate lentiviruses or feline immunodeficiency virus. Moreover, we verified the presence of MELV insertions in the genomes of several species of the Lutrinae and Mustelinae subfamilies but not the Martinae subfamily, suggesting that the invasion of MELV into the Mustelidae genomes likely took place between 8.8 and 11.8 Ma. The discovery of MELV in weasel genomes extends the host range of lentiviruses to the Caniformia (order Carnivora) and provides important insights into the prehistoric diversity of lentiviruses.
Subject(s)
Endogenous Retroviruses/genetics , Genome/genetics , Lentivirus/genetics , Mustelidae/genetics , Mustelidae/virology , Animals , PhylogenyABSTRACT
We report the discovery and analysis of an endogenous foamy virus (PSFVaye) within the genome of the aye-aye (Daubentonia madagascariensis), a strepsirrhine primate from Madagascar. Phylogenetic analyses indicate that PSFVaye is divergent from all known simian foamy viruses, suggesting an association between foamy viruses and primates since the haplorrhine-strepsirrhine split. The discovery of PSFVaye indicates that primate foamy virus might be more broadly distributed than previously thought.
Subject(s)
Simian foamy virus/genetics , Strepsirhini/genetics , Strepsirhini/virology , Animals , Base Sequence , Evolution, Molecular , Genes, pol , Genome , Madagascar , Phylogeny , Sequence Alignment , Simian foamy virus/classificationABSTRACT
Chimpanzees in west central Africa (Pan troglodytes troglodytes) are endemically infected with simian immunodeficiency viruses (SIVcpzPtt) that have crossed the species barrier to humans and gorillas on at least five occasions, generating pandemic and nonpandemic forms of human immunodeficiency virus type 1 (HIV-1) as well as gorilla SIV (SIVgor). Chimpanzees in east Africa (Pan troglodytes schweinfurthii) are also infected with SIVcpz; however, their viruses (SIVcpzPts) have never been found in humans. To examine whether this is due to a paucity of natural infections, we used noninvasive methods to screen wild-living eastern chimpanzees in the Democratic Republic of the Congo (DRC), Uganda, and Rwanda. We also screened bonobos (Pan paniscus) in the DRC, a species not previously tested for SIV in the wild. Fecal samples (n = 3,108) were collected at 50 field sites, tested for species and subspecies origin, and screened for SIVcpz antibodies and nucleic acids. Of 2,565 samples from eastern chimpanzees, 323 were antibody positive and 92 contained viral RNA. The antibody-positive samples represented 76 individuals from 19 field sites, all sampled north of the Congo River in an area spanning 250,000 km(2). In this region, SIVcpzPts was common and widespread, with seven field sites exhibiting infection rates of 30% or greater. The overall prevalence of SIVcpzPts infection was 13.4% (95% confidence interval, 10.7% to 16.5%). In contrast, none of the 543 bonobo samples from six sites was antibody positive. All newly identified SIVcpzPts strains clustered in strict accordance to their subspecies origin; however, they exhibited considerable genetic diversity, especially in protein domains known to be under strong host selection pressure. Thus, the absence of SIVcpzPts zoonoses cannot be explained by an insufficient primate reservoir. Instead, greater adaptive hurdles may have prevented the successful colonization of humans by P. t. schweinfurthii viruses.