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Article ; Online: A Glimpse into the Past: What Ancient Viral Genomes Reveal About Human History.

Guzmán-Solís, Axel A / Navarro, Miguel Alejandro / Ávila-Arcos, María C / Blanco-Melo, Daniel

2023 Volume 10, Issue 1, Page(s) 49–75

Abstract: Humans have battled viruses for millennia. However, directly linking the symptomatology of disease outbreaks to specific viral pathogens was not possible until the twentieth century. With the advent of the genomic era and the development of advanced ... ...

Abstract	Humans have battled viruses for millennia. However, directly linking the symptomatology of disease outbreaks to specific viral pathogens was not possible until the twentieth century. With the advent of the genomic era and the development of advanced protocols for isolation, sequencing, and analysis of ancient nucleic acids from diverse human remains, the identification and characterization of ancient viruses became feasible. Recent studies have provided invaluable information about past epidemics and made it possible to examine assumptions and inferences on the origin and evolution of certain viral families. In parallel, the study of ancient viruses also uncovered their importance in the evolution of the human lineage and their key roles in shaping major events in human history. In this review, we describe the strategies used for the study of ancient viruses, along with their limitations, and provide a detailed account of what past viral infections have revealed about human history.
MeSH term(s)	Humans ; Genomics ; Virus Diseases/genetics ; Viruses/genetics ; Disease Outbreaks ; Genome, Viral
Language	English
Publishing date	2023-06-02
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2764224-0
ISSN	2327-0578 ; 2327-056X
ISSN (online)	2327-0578
ISSN	2327-056X
DOI	10.1146/annurev-virology-111821-123859
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Article ; Online: Archaeal Kink-Turn Binding Protein Mediates Inhibition of Orthomyxovirus Splicing Biology.

Oishi, Kohei / Blanco-Melo, Daniel / Kurland, Andrew P / Johnson, Jeffrey R / tenOever, Benjamin R

Journal of virology

2023 Volume 97, Issue 4, Page(s) e0181322

Abstract: Despite lacking a DNA intermediate, orthomyxoviruses complete their replication cycle in the nucleus and generate multiple transcripts by usurping the host splicing machinery. This biology results in dynamic changes of relative viral transcripts over ... ...

Abstract	Despite lacking a DNA intermediate, orthomyxoviruses complete their replication cycle in the nucleus and generate multiple transcripts by usurping the host splicing machinery. This biology results in dynamic changes of relative viral transcripts over time and dictates the replicative phase of the infection. Here, we demonstrate that the family of archaeal L7Ae proteins uniquely inhibit the splicing biology of influenza A virus, influenza B virus, and Salmon isavirus, revealing a common strategy utilized by
MeSH term(s)	Archaeal Proteins/genetics ; Archaeal Proteins/metabolism ; Orthomyxoviridae/physiology ; RNA Splicing/physiology ; Humans ; Animals ; Dogs ; Vero Cells ; Chlorocebus aethiops ; A549 Cells ; HEK293 Cells ; Host Microbial Interactions ; Orthomyxoviridae Infections/genetics ; Orthomyxoviridae Infections/virology
Chemical Substances	Archaeal Proteins
Language	English
Publishing date	2023-03-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/jvi.01813-22
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Article: Modulation of Influenza A virus NS1 expression reveals prioritization of host response antagonism at single-cell resolution.

Yang, Qing / Elz, Anna E / Panis, Maryline / Liu, Ting / Nilsson-Payant, Benjamin E / Blanco-Melo, Daniel

Frontiers in microbiology

2023 Volume 14, Page(s) 1267078

Abstract: Influenza A virus (IAV) is an important human respiratory pathogen that causes significant seasonal epidemics and potential devastating pandemics. As part of its life cycle, IAV encodes the multifunctional protein NS1, that, among many roles, prevents ... ...

Abstract	Influenza A virus (IAV) is an important human respiratory pathogen that causes significant seasonal epidemics and potential devastating pandemics. As part of its life cycle, IAV encodes the multifunctional protein NS1, that, among many roles, prevents immune detection and limits interferon (IFN) production. As distinct host immune pathways exert different selective pressures against IAV, as replication progresses, we expect a prioritization in the host immune antagonism by NS1. In this work, we profiled bulk transcriptomic differences in a primary bronchial epithelial cell model facing IAV infections at distinct NS1 levels. We further demonstrated that, at single cell level, the intracellular amount of NS1 in-part shapes the heterogeneity of the host response. We found that modulation of NS1 levels reveal a ranking in its inhibitory roles: modest NS1 expression is sufficient to inhibit immune detection, and thus the expression of pro-inflammatory cytokines (including IFNs), but higher levels are required to inhibit IFN signaling and ISG expression. Lastly, inhibition of chaperones related to the unfolded protein response requires the highest amount of NS1, often associated with later stages of viral replication. This work demystifies some of the multiple functions ascribed to IAV NS1, highlighting the prioritization of NS1 in antagonizing the different pathways involved in the host response to IAV infection.
Language	English
Publishing date	2023-10-09
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2587354-4
ISSN	1664-302X
ISSN	1664-302X
DOI	10.3389/fmicb.2023.1267078
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Article ; Online: Reconstruction of a replication-competent ancestral murine endogenous retrovirus-L.

Blanco-Melo, Daniel / Gifford, Robert J / Bieniasz, Paul D

Retrovirology

2018 Volume 15, Issue 1, Page(s) 34

Abstract: Background: About 10% of the mouse genome is composed of endogenous retroviruses (ERVs) that represent a molecular fossil record of past retroviral infections. One such retrovirus, murine ERV-L (MuERV-L) is an env-deficient ERV that has undergone ... ...

Abstract	Background: About 10% of the mouse genome is composed of endogenous retroviruses (ERVs) that represent a molecular fossil record of past retroviral infections. One such retrovirus, murine ERV-L (MuERV-L) is an env-deficient ERV that has undergone episodic proliferation, with the most recent amplification occurring ~ 2 million years ago. MuERV-L related sequences have been co-opted by mice for antiretroviral defense, and possibly as promoters for some genes that regulate totipotency in early mouse embryos. However, MuERV-L sequences present in modern mouse genomes have not been observed to replicate. Results: Here, we describe the reconstruction of an ancestral MuERV-L (ancML) sequence through paleovirological analyses of MuERV-L elements in the modern mouse genome. The resulting MuERV-L (ancML) sequence was synthesized and a reporter gene embedded. The reconstructed MuERV-L (ancML) could replicate in a manner that is dependent on reverse transcription and generated de novo integrants. Notably, MuERV-L (ancML) exhibited a narrow host range. Interferon-α could reduce MuERV-L (ancML) replication, suggesting the existence of interferon-inducible genes that could inhibit MuERV-L replication. While mouse APOBEC3 was able to restrict the replication of MuERV-L (ancML), inspection of endogenous MuERV-L sequences suggested that the impact of APOBEC3 mediated hypermutation on MuERV-L has been minimal. Conclusion: The reconstruction of an ancestral MuERV-L sequence highlights the potential for the retroviral fossil record to illuminate ancient events and enable studies of the impact of retroviral elements on animal evolution.
MeSH term(s)	Amino Acid Sequence ; Animals ; Base Sequence ; CHO Cells ; Cell Line ; Computational Biology/methods ; Cricetulus ; Cytidine Deaminase ; Disease Resistance/genetics ; Disease Resistance/immunology ; Endogenous Retroviruses/classification ; Endogenous Retroviruses/physiology ; Evolution, Molecular ; Host-Pathogen Interactions/genetics ; Host-Pathogen Interactions/immunology ; Immunity, Innate ; Mice ; Phylogeny ; RNA-Directed DNA Polymerase/genetics ; RNA-Directed DNA Polymerase/metabolism ; Retroviridae Infections/immunology ; Retroviridae Infections/metabolism ; Retroviridae Infections/virology ; Virus Integration ; Virus Replication
Chemical Substances	RNA-Directed DNA Polymerase (EC 2.7.7.49) ; Apobec3 protein, mouse (EC 3.5.4.5) ; Cytidine Deaminase (EC 3.5.4.5)
Language	English
Publishing date	2018-05-02
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2142602-8
ISSN	1742-4690 ; 1742-4690
ISSN (online)	1742-4690
ISSN	1742-4690
DOI	10.1186/s12977-018-0416-3
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Article ; Online: Delayed engagement of host defenses enables SARS-CoV-2 viremia and productive infection of distal organs in the hamster model of COVID-19.

Carrau, Lucia / Frere, Justin J / Golynker, Ilona / Fajardo, Alvaro / Rivera, Cristobal F / Horiuchi, Shu / Roonprapunt, Tyler / Minkoff, Judith M / Blanco-Melo, Daniel / TenOever, Benjamin

Science signaling

2023 Volume 16, Issue 789, Page(s) eadg5470

Abstract: Clinical presentations that develop in response to infection result from interactions between the pathogen and host defenses. SARS-CoV-2, the etiologic agent of COVID-19, directly antagonizes these defenses, leading to delayed immune engagement in the ... ...

Abstract	Clinical presentations that develop in response to infection result from interactions between the pathogen and host defenses. SARS-CoV-2, the etiologic agent of COVID-19, directly antagonizes these defenses, leading to delayed immune engagement in the lungs that materializes only as cells succumb to infection and are phagocytosed. Leveraging the golden hamster model of COVID-19, we sought to understand the dynamics between SARS-CoV-2 infection in the airways and the systemic host response that ensues. We found that early SARS-CoV-2 replication was largely confined to the respiratory tract and olfactory system and, to a lesser extent, the heart and gastrointestinal tract but generated a host antiviral response in every organ as a result of circulating type I and III interferons. Moreover, we showed that diminishing the response in the airways by immunosuppression or administration of SARS-CoV-2 intravenously resulted in decreased immune priming, viremia, and increased viral tropism, including productive infection of the liver, kidney, spleen, and brain. Last, we showed that productive infection of the airways was required for mounting an effective and system-wide antiviral response. Together, these data illustrate how COVID-19 can result in diverse clinical presentations in which disease outcomes can be a by-product of the speed and strength of immune engagement. These studies provide additional evidence for the mechanistic basis of the diverse clinical presentations of COVID-19 and highlight the ability of the respiratory tract to generate a systemic immune defense after pathogen recognition.
MeSH term(s)	Animals ; Cricetinae ; COVID-19 ; SARS-CoV-2 ; Viremia ; Antiviral Agents ; Brain
Chemical Substances	Antiviral Agents
Language	English
Publishing date	2023-06-13
Publishing country	United States
Document type	Journal Article
ZDB-ID	2417226-1
ISSN	1937-9145 ; 1945-0877
ISSN (online)	1937-9145
ISSN	1945-0877
DOI	10.1126/scisignal.adg5470
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Article ; Online: Co-option of an endogenous retrovirus envelope for host defense in hominid ancestors.

Blanco-Melo, Daniel / Gifford, Robert J / Bieniasz, Paul D

eLife

2017 Volume 6

Abstract: Endogenous retroviral sequences provide a molecular fossil record of ancient infections whose analysis might illuminate mechanisms of viral extinction. A close relative of gammaretroviruses, HERV-T, circulated in primates for ~25 million years (MY) ... ...

Abstract	Endogenous retroviral sequences provide a molecular fossil record of ancient infections whose analysis might illuminate mechanisms of viral extinction. A close relative of gammaretroviruses, HERV-T, circulated in primates for ~25 million years (MY) before apparent extinction within the past ~8 MY. Construction of a near-complete catalog of HERV-T fossils in primate genomes allowed us to estimate a ~32 MY old ancestral sequence and reconstruct a functional envelope protein (ancHTenv) that could support infection of a pseudotyped modern gammaretrovirus. Using ancHTenv, we identify monocarboxylate transporter-1 (MCT-1) as a receptor used by HERV-T for attachment and infection. A single HERV-T provirus in hominid genomes includes an
MeSH term(s)	Animals ; Endogenous Retroviruses/genetics ; Gammaretrovirus/genetics ; Gammaretrovirus/growth & development ; Gene Products, env/genetics ; Hominidae/genetics ; Hominidae/virology ; Monocarboxylic Acid Transporters/metabolism ; Receptors, Virus/metabolism ; Symporters/metabolism ; Virus Attachment ; Virus Internalization
Chemical Substances	Gene Products, env ; Monocarboxylic Acid Transporters ; Receptors, Virus ; Symporters ; monocarboxylate transport protein 1
Language	English
Publishing date	2017-04-11
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.22519
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Article ; Online: Origins and Evolution of tetherin, an Orphan Antiviral Gene.

Blanco-Melo, Daniel / Venkatesh, Siddarth / Bieniasz, Paul D

Cell host & microbe

2016 Volume 20, Issue 2, Page(s) 189–201

Abstract: Tetherin encodes an interferon-inducible antiviral protein that traps a broad spectrum of enveloped viruses at infected cell surfaces. Despite the absence of any clearly related gene or activity, we describe possible scenarios by which tetherin arose ... ...

Abstract	Tetherin encodes an interferon-inducible antiviral protein that traps a broad spectrum of enveloped viruses at infected cell surfaces. Despite the absence of any clearly related gene or activity, we describe possible scenarios by which tetherin arose that exemplify how protein modularity, evolvability, and robustness can create and preserve new functions. We find that tetherin genes in various organisms exhibit no sequence similarity and share only a common architecture and location in modern genomes. Moreover, tetherin is part of a cluster of three potential sister genes encoding proteins of similar architecture, some variants of which exhibit antiviral activity while others can be endowed with antiviral activity by a simple modification. Only in slowly evolving species (e.g., coelacanths) does tetherin exhibit sequence similarity to one potential sister gene. Neofunctionalization, drift, and genetic conflict appear to have driven a near complete loss of sequence similarity among modern tetherin genes and their sister genes.
MeSH term(s)	Animals ; Antigens, CD/genetics ; Evolution, Molecular ; GPI-Linked Proteins/genetics ; Humans
Chemical Substances	Antigens, CD ; GPI-Linked Proteins
Language	English
Publishing date	2016-07-14
Publishing country	United States
Document type	Journal Article
ZDB-ID	2278004-X
ISSN	1934-6069 ; 1931-3128
ISSN (online)	1934-6069
ISSN	1931-3128
DOI	10.1016/j.chom.2016.06.007
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Article ; Online: Type I interferon response impairs differentiation potential of pluripotent stem cells.

Eggenberger, Julie / Blanco-Melo, Daniel / Panis, Maryline / Brennand, Kristen J / tenOever, Benjamin R

Proceedings of the National Academy of Sciences of the United States of America

2019 Volume 116, Issue 4, Page(s) 1384–1393

Abstract: Upon virus infection, pluripotent stem cells neither induce nor respond to canonical type I interferons (IFN-I). To better understand this biology, we characterized induced pluripotent stem cells (iPSCs) as well as their differentiated parental or ... ...

Abstract	Upon virus infection, pluripotent stem cells neither induce nor respond to canonical type I interferons (IFN-I). To better understand this biology, we characterized induced pluripotent stem cells (iPSCs) as well as their differentiated parental or rederived counterparts. We confirmed that only iPSCs failed to respond to viral RNA, IFN-I, or viral infection. This lack of response could be phenocopied in fibroblasts with the expression of a reprogramming factor which repressed the capacity to induce canonical antiviral pathways. To ascertain the consequences of restoring the antiviral response in the context of pluripotency, we engineered a system to engage these defenses in iPSCs. Inducible expression of a recombinant virus-activated transcription factor resulted in the successful reconstitution of antiviral defenses through the direct up-regulation of IFN-I-stimulated genes. Induction of the antiviral signature in iPSCs, even for a short duration, resulted in the dysregulation of genes associated with all three germ layers despite maintaining pluripotency markers. Trilineage differentiation of these same cells showed that engagement of the antiviral defenses compromised ectoderm and endoderm formation and dysregulated the development of mesodermal sublineages. In all, these data suggest that the temporal induction of the antiviral response primes iPSCs away from pluripotency and induces numerous aberrant gene products upon differentiation. Together these results suggest that the IFN-I system and pluripotency may be incompatible with each other and thus explain why stem cells do not utilize the canonical antiviral system.
MeSH term(s)	Antiviral Agents/pharmacology ; Biomarkers/metabolism ; Cell Differentiation/drug effects ; Cell Differentiation/physiology ; Cells, Cultured ; Cellular Reprogramming/physiology ; Ectoderm/drug effects ; Ectoderm/metabolism ; Ectoderm/physiology ; Ectoderm/virology ; Endoderm/drug effects ; Endoderm/metabolism ; Endoderm/physiology ; Endoderm/virology ; Fibroblasts/drug effects ; Fibroblasts/metabolism ; Fibroblasts/physiology ; Fibroblasts/virology ; Germ Layers/drug effects ; Germ Layers/metabolism ; Germ Layers/physiology ; Germ Layers/virology ; Humans ; Induced Pluripotent Stem Cells/drug effects ; Induced Pluripotent Stem Cells/metabolism ; Induced Pluripotent Stem Cells/physiology ; Induced Pluripotent Stem Cells/virology ; Interferon Type I/metabolism ; RNA, Viral/genetics ; Transcription Factors/metabolism ; Up-Regulation/drug effects ; Up-Regulation/physiology
Chemical Substances	Antiviral Agents ; Biomarkers ; Interferon Type I ; RNA, Viral ; Transcription Factors
Language	English
Publishing date	2019-01-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1812449116
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Article ; Online: The decline of human endogenous retroviruses: extinction and survival.

Magiorkinis, Gkikas / Blanco-Melo, Daniel / Belshaw, Robert

Retrovirology

2015 Volume 12, Page(s) 8

Abstract: Background: Endogenous Retroviruses (ERVs) are retroviruses that over the course of evolution have integrated into germline cells and eventually become part of the host genome. They proliferate within the germline of their host, making up ~5% of the ... ...

Abstract	Background: Endogenous Retroviruses (ERVs) are retroviruses that over the course of evolution have integrated into germline cells and eventually become part of the host genome. They proliferate within the germline of their host, making up ~5% of the human and mouse genome sequences. Several lines of evidence have suggested a decline in the rate of ERV integration into the human genome in recent evolutionary history but this has not been investigated quantitatively or possible causes explored. Results: By dating the integration of ERV loci in 40 mammal species, we show that the human genome and that of other hominoids (great apes and gibbons) have experienced an approximately four-fold decline in the ERV integration rate over the last 10 million years. A major cause is the recent extinction of one very large ERV lineage (HERV-H), which is responsible for most of the integrations over the last 30 million years. The decline however affects most other ERV lineages. Only about 10% of the decline might be attributed to an accompanying increase in body mass (a trait we have shown recently to be negatively correlated with ERV integration rate). Humans are unusual compared to related species - Old World monkeys, great apes and gibbons - in (a) having not acquired any new ERV lineages during the last 30 million years and (b) the possession of an old ERV lineage that has continued to replicate up until at least the last few hundred thousand years - the potentially medically significant HERVK(HML2). Conclusions: The human genome shares with the genome of other great apes and gibbons a recent decline in ERV integration that is not typical of other primates and mammals. The human genome differs from that of related species both in maintaining up until at least recently a replicating old ERV lineage and in not having acquired any new lineages. We speculate that the decline in ERV integration in the human genome has been exacerbated by a relatively low burden of horizontally-transmitted retroviruses and subsequent reduced risk of endogenization.
MeSH term(s)	Animals ; Endogenous Retroviruses/genetics ; Endogenous Retroviruses/physiology ; Evolution, Molecular ; Humans ; Primates ; Virus Integration ; Virus Replication
Language	English
Publishing date	2015-02-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1742-4690
ISSN (online)	1742-4690
DOI	10.1186/s12977-015-0136-x
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Article ; Online: Reduced Nucleoprotein Availability Impairs Negative-Sense RNA Virus Replication and Promotes Host Recognition.

Nilsson-Payant, Benjamin E / Blanco-Melo, Daniel / Uhl, Skyler / Escudero-Pérez, Beatriz / Olschewski, Silke / Thibault, Patricia / Panis, Maryline / Rosenthal, Maria / Muñoz-Fontela, César / Lee, Benhur / tenOever, Benjamin R

Journal of virology

2021 Volume 95, Issue 9

Abstract: Negative-sense RNA viruses (NSVs) rely on prepackaged viral RNA-dependent RNA polymerases (RdRp) to replicate and transcribe their viral genomes. Their replication machinery consists of an RdRp bound to viral RNA which is wound around a nucleoprotein (NP) ...

Abstract	Negative-sense RNA viruses (NSVs) rely on prepackaged viral RNA-dependent RNA polymerases (RdRp) to replicate and transcribe their viral genomes. Their replication machinery consists of an RdRp bound to viral RNA which is wound around a nucleoprotein (NP) scaffold, forming a viral ribonucleoprotein complex. NSV NP is known to regulate transcription and replication of genomic RNA; however, its role in maintaining and protecting the viral genetic material is unknown. Here, we exploited host microRNA expression to target NP of influenza A virus and Sendai virus to ascertain how this would impact genomic levels and the host response to infection. We find that in addition to inducing a drastic decrease in genome replication, the antiviral host response in the absence of NP is dramatically enhanced. Additionally, our data show that insufficient levels of NP prevent the replication machinery of these NSVs to process full-length genomes, resulting in aberrant replication products which form pathogen-associated molecular patterns in the process. These dynamics facilitate immune recognition by cellular pattern recognition receptors leading to a strong host antiviral response. Moreover, we observe that the consequences of limiting NP levels are universal among NSVs, including Ebola virus, Lassa virus, and measles virus. Overall, these results provide new insights into viral genome replication of negative-sense RNA viruses and highlight novel avenues for developing effective antiviral strategies, adjuvants, and/or live-attenuated vaccines.
MeSH term(s)	A549 Cells ; Animals ; Chlorocebus aethiops ; Dogs ; HEK293 Cells ; HeLa Cells ; Humans ; Influenza A Virus, H1N1 Subtype/physiology ; Influenza, Human/virology ; Madin Darby Canine Kidney Cells ; Nucleocapsid Proteins/physiology ; Respirovirus Infections/virology ; Sendai virus/physiology ; Vero Cells ; Viral Tropism ; Virus Replication
Chemical Substances	Nucleocapsid Proteins
Language	English
Publishing date	2021-04-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/JVI.02274-20
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