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1.
Cell ; 187(19): 5468-5482.e11, 2024 Sep 19.
Artículo en Inglés | MEDLINE | ID: mdl-39303692

RESUMEN

Zoonotic spillovers of viruses have occurred through the animal trade worldwide. The start of the COVID-19 pandemic was traced epidemiologically to the Huanan Seafood Wholesale Market. Here, we analyze environmental qPCR and sequencing data collected in the Huanan market in early 2020. We demonstrate that market-linked severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) genetic diversity is consistent with market emergence and find increased SARS-CoV-2 positivity near and within a wildlife stall. We identify wildlife DNA in all SARS-CoV-2-positive samples from this stall, including species such as civets, bamboo rats, and raccoon dogs, previously identified as possible intermediate hosts. We also detect animal viruses that infect raccoon dogs, civets, and bamboo rats. Combining metagenomic and phylogenetic approaches, we recover genotypes of market animals and compare them with those from farms and other markets. This analysis provides the genetic basis for a shortlist of potential intermediate hosts of SARS-CoV-2 to prioritize for serological and viral sampling.


Asunto(s)
Animales Salvajes , COVID-19 , Filogenia , SARS-CoV-2 , Animales , COVID-19/epidemiología , COVID-19/virología , SARS-CoV-2/genética , SARS-CoV-2/aislamiento & purificación , Animales Salvajes/virología , Humanos , Pandemias
2.
Cell ; 184(19): 4848-4856, 2021 09 16.
Artículo en Inglés | MEDLINE | ID: mdl-34480864

RESUMEN

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.


Asunto(s)
SARS-CoV-2/fisiología , Animales , Evolución Biológica , COVID-19/virología , Humanos , Laboratorios , SARS-CoV-2/genética , Zoonosis/virología
3.
Cell ; 182(4): 794-795, 2020 08 20.
Artículo en Inglés | MEDLINE | ID: mdl-32697970

RESUMEN

In this issue of Cell, Korber et al. found that a SARS-CoV-2 variant in the spike protein D614G rapidly became dominant around the world. Although clinical and in vitro data suggest that D614G changes the virus phenotype, the impact of the mutation on transmission, disease, and vaccine and therapeutic development are largely unknown.


Asunto(s)
Betacoronavirus , Infecciones por Coronavirus , Pandemias , Neumonía Viral , COVID-19 , Humanos , Mutación , SARS-CoV-2
4.
Nature ; 586(7830): 509-515, 2020 10.
Artículo en Inglés | MEDLINE | ID: mdl-32967005

RESUMEN

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the aetiological agent of coronavirus disease 2019 (COVID-19), an emerging respiratory infection caused by the introduction of a novel coronavirus into humans late in 2019 (first detected in Hubei province, China). As of 18 September 2020, SARS-CoV-2 has spread to 215 countries, has infected more than 30 million people and has caused more than 950,000 deaths. As humans do not have pre-existing immunity to SARS-CoV-2, there is an urgent need to develop therapeutic agents and vaccines to mitigate the current pandemic and to prevent the re-emergence of COVID-19. In February 2020, the World Health Organization (WHO) assembled an international panel to develop animal models for COVID-19 to accelerate the testing of vaccines and therapeutic agents. Here we summarize the findings to date and provides relevant information for preclinical testing of vaccine candidates and therapeutic agents for COVID-19.


Asunto(s)
Infecciones por Coronavirus/tratamiento farmacológico , Infecciones por Coronavirus/prevención & control , Modelos Animales de Enfermedad , Pandemias/prevención & control , Neumonía Viral/tratamiento farmacológico , Neumonía Viral/prevención & control , Animales , Betacoronavirus/efectos de los fármacos , Betacoronavirus/inmunología , COVID-19 , Vacunas contra la COVID-19 , Infecciones por Coronavirus/inmunología , Hurones/virología , Humanos , Mesocricetus/virología , Ratones , Neumonía Viral/inmunología , Primates/virología , SARS-CoV-2 , Vacunas Virales/inmunología
5.
J Virol ; 98(1): e0179123, 2024 Jan 23.
Artículo en Inglés | MEDLINE | ID: mdl-38168672

RESUMEN

In the United States (US), biosafety and biosecurity oversight of research on viruses is being reappraised. Safety in virology research is paramount and oversight frameworks should be reviewed periodically. Changes should be made with care, however, to avoid impeding science that is essential for rapidly reducing and responding to pandemic threats as well as addressing more common challenges caused by infectious diseases. Decades of research uniquely positioned the US to be able to respond to the COVID-19 crisis with astounding speed, delivering life-saving vaccines within a year of identifying the virus. We should embolden and empower this strength, which is a vital part of protecting the health, economy, and security of US citizens. Herein, we offer our perspectives on priorities for revised rules governing virology research in the US.


Asunto(s)
Investigación Biomédica , Contención de Riesgos Biológicos , Virología , Humanos , COVID-19 , Estados Unidos , Virus , Investigación Biomédica/normas
6.
PLoS Pathog ; 17(12): e1009678, 2021 12.
Artículo en Inglés | MEDLINE | ID: mdl-34855915

RESUMEN

Kyasanur Forest disease virus (KFDV) and the closely related Alkhurma hemorrhagic disease virus (AHFV) are emerging flaviviruses that cause severe viral hemorrhagic fevers in humans. Increasing geographical expansion and case numbers, particularly of KFDV in southwest India, class these viruses as a public health threat. Viral pathogenesis is not well understood and additional vaccines and antivirals are needed to effectively counter the impact of these viruses. However, current animal models of KFDV pathogenesis do not accurately reproduce viral tissue tropism or clinical outcomes observed in humans. Here, we show that pigtailed macaques (Macaca nemestrina) infected with KFDV or AHFV develop viremia that peaks 2 to 4 days following inoculation. Over the course of infection, animals developed lymphocytopenia, thrombocytopenia, and elevated liver enzymes. Infected animals exhibited hallmark signs of human disease characterized by a flushed appearance, piloerection, dehydration, loss of appetite, weakness, and hemorrhagic signs including epistaxis. Virus was commonly present in the gastrointestinal tract, consistent with human disease caused by KFDV and AHFV where gastrointestinal symptoms (hemorrhage, vomiting, diarrhea) are common. Importantly, RNAseq of whole blood revealed that KFDV downregulated gene expression of key clotting factors that was not observed during AHFV infection, consistent with increased severity of KFDV disease observed in this model. This work characterizes a nonhuman primate model for KFDV and AHFV that closely resembles human disease for further utilization in understanding host immunity and development of antiviral countermeasures.


Asunto(s)
Modelos Animales de Enfermedad , Virus de la Encefalitis Transmitidos por Garrapatas/patogenicidad , Encefalitis Transmitida por Garrapatas/virología , Fiebres Hemorrágicas Virales/virología , Macaca nemestrina , Animales , Chlorocebus aethiops , Citocinas/sangre , Virus de la Encefalitis Transmitidos por Garrapatas/genética , Virus de la Encefalitis Transmitidos por Garrapatas/inmunología , Encefalitis Transmitida por Garrapatas/inmunología , Encefalitis Transmitida por Garrapatas/patología , Femenino , Células HEK293 , Fiebres Hemorrágicas Virales/inmunología , Fiebres Hemorrágicas Virales/patología , Humanos , Ganglios Linfáticos/virología , Células Vero , Viremia
7.
Clin Infect Dis ; 75(1): e1195-e1201, 2022 08 24.
Artículo en Inglés | MEDLINE | ID: mdl-34651164

RESUMEN

The relationship between severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) dose, infection, and coronavirus disease 2019 (COVID-19) outcomes remains poorly understood. This review summarizes the existing literature regarding this issue, identifies gaps in current knowledge, and suggests opportunities for future research. In humans, host characteristics, including age, sex, comorbidities, smoking, and pregnancy, are associated with severe COVID-19. Similarly, in animals, host factors are strong determinants of disease severity, although most animal infection models manifest clinically with mild to moderate respiratory disease. The influence of variants of concern as it relates to infectious dose, consequence of overall pathogenicity, and disease outcome in dose-response remains unknown. Epidemiologic data suggest a dose-response relationship for infection contrasting with limited and inconsistent surrogate-based evidence between dose and disease severity. Recommendations include the design of future infection studies in animal models to investigate inoculating dose on outcomes and the use of better proxies for dose in human epidemiology studies.


Asunto(s)
COVID-19 , SARS-CoV-2 , Animales , Comorbilidad , Femenino , Humanos , Embarazo
8.
BMC Infect Dis ; 21(1): 710, 2021 Jul 27.
Artículo en Inglés | MEDLINE | ID: mdl-34315427

RESUMEN

Scientists across disciplines, policymakers, and journalists have voiced frustration at the unprecedented polarization and misinformation around coronavirus disease 2019 (COVID-19) pandemic. Several false dichotomies have been used to polarize debates while oversimplifying complex issues. In this comprehensive narrative review, we deconstruct six common COVID-19 false dichotomies, address the evidence on these topics, identify insights relevant to effective pandemic responses, and highlight knowledge gaps and uncertainties. The topics of this review are: 1) Health and lives vs. economy and livelihoods, 2) Indefinite lockdown vs. unlimited reopening, 3) Symptomatic vs. asymptomatic severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, 4) Droplet vs. aerosol transmission of SARS-CoV-2, 5) Masks for all vs. no masking, and 6) SARS-CoV-2 reinfection vs. no reinfection. We discuss the importance of multidisciplinary integration (health, social, and physical sciences), multilayered approaches to reducing risk ("Emmentaler cheese model"), harm reduction, smart masking, relaxation of interventions, and context-sensitive policymaking for COVID-19 response plans. We also address the challenges in understanding the broad clinical presentation of COVID-19, SARS-CoV-2 transmission, and SARS-CoV-2 reinfection. These key issues of science and public health policy have been presented as false dichotomies during the pandemic. However, they are hardly binary, simple, or uniform, and therefore should not be framed as polar extremes. We urge a nuanced understanding of the science and caution against black-or-white messaging, all-or-nothing guidance, and one-size-fits-all approaches. There is a need for meaningful public health communication and science-informed policies that recognize shades of gray, uncertainties, local context, and social determinants of health.


Asunto(s)
COVID-19 , SARS-CoV-2 , Control de Enfermedades Transmisibles , Humanos , Salud Pública , Reinfección
9.
12.
Annu Rev Genomics Hum Genet ; 17: 333-51, 2016 08 31.
Artículo en Inglés | MEDLINE | ID: mdl-27147086

RESUMEN

Ebola virus (EBOV) emerged in West Africa in 2014 to devastating effect, and demonstrated that infection can cause a broad range of severe disease manifestations. As the virus itself was genetically similar to other Zaire ebolaviruses, the spectrum of pathology likely resulted from variable responses to infection in a large and genetically diverse population. This review comprehensively summarizes current knowledge of the host response to EBOV infection, including pathways hijacked by the virus to facilitate replication, host processes that contribute directly to pathogenesis, and host-pathogen interactions involved in subverting or antagonizing host antiviral immunity.


Asunto(s)
Ebolavirus/genética , Fiebre Hemorrágica Ebola/genética , Interacciones Huésped-Patógeno/genética , Replicación Viral/genética , Animales , Modelos Animales de Enfermedad , Vacunas contra el Virus del Ébola/genética , Vacunas contra el Virus del Ébola/uso terapéutico , Ebolavirus/patogenicidad , Fiebre Hemorrágica Ebola/prevención & control , Humanos , Ratones , Factores de Riesgo
13.
Curr Top Microbiol Immunol ; 419: 113-150, 2018.
Artículo en Inglés | MEDLINE | ID: mdl-28710692

RESUMEN

Ebola virus (EBOV) is a highly pathogenic emerging virus that represents a serious threat to global public health and a major priority for biodefense. The 2014 West African outbreak demonstrated the potential of EBOV to cause an epidemic affecting thousands of people. The severity of disease and high case fatality rate of EBOV is largely due to the host response elicited by the virus. EBOV infection hijacks a number of host pathways to carry out replication and stimulate potent inflammatory responses, while simultaneously subverting the host antiviral immune response. Together, these events trigger a complex, systemic, often lethal febrile disease characterized by high levels of inflammatory cytokines, acute hepatitis and liver dysfunction, immune antagonism, gastrointestinal distress, and, in some cases, hemorrhage caused by coagulopathy and vascular leakage. This review presents current knowledge about the particular host responses induced and disrupted by EBOV infection and how these contribute to virus replication, immune evasion, pathogenesis, and disease outcome.


Asunto(s)
Ebolavirus/crecimiento & desarrollo , Fiebre Hemorrágica Ebola/metabolismo , Fiebre Hemorrágica Ebola/virología , Interacciones Huésped-Patógeno/fisiología , Replicación Viral , Citocinas/metabolismo , Ebolavirus/inmunología , Ebolavirus/patogenicidad , Fiebre Hemorrágica Ebola/inmunología , Fiebre Hemorrágica Ebola/patología , Humanos , Evasión Inmune
15.
J Virol ; 91(11)2017 06 01.
Artículo en Inglés | MEDLINE | ID: mdl-28331091

RESUMEN

Ebola virus (EBOV) and Reston virus (RESTV) are members of the Ebolavirus genus which greatly differ in their pathogenicity. While EBOV causes a severe disease in humans characterized by a dysregulated inflammatory response and elevated cytokine and chemokine production, there are no reported disease-associated human cases of RESTV infection, suggesting that RESTV is nonpathogenic for humans. The underlying mechanisms determining the pathogenicity of different ebolavirus species are not yet known. In this study, we dissected the host response to EBOV and RESTV infection in primary human monocyte-derived macrophages (MDMs). As expected, EBOV infection led to a profound proinflammatory response, including strong induction of type I and type III interferons (IFNs). In contrast, RESTV-infected macrophages remained surprisingly silent. Early activation of IFN regulatory factor 3 (IRF3) and NF-κB was observed in EBOV-infected, but not in RESTV-infected, MDMs. In concordance with previous results, MDMs treated with inactivated EBOV and Ebola virus-like particles (VLPs) induced NF-κB activation mediated by Toll-like receptor 4 (TLR4) in a glycoprotein (GP)-dependent manner. This was not the case in cells exposed to live RESTV, inactivated RESTV, or VLPs containing RESTV GP, indicating that RESTV GP does not trigger TLR4 signaling. Our results suggest that the lack of immune activation in RESTV-infected MDMs contributes to lower pathogenicity by preventing the cytokine storm observed in EBOV infection. We further demonstrate that inhibition of TLR4 signaling abolishes EBOV GP-mediated NF-κB activation. This finding indicates that limiting the excessive TLR4-mediated proinflammatory response in EBOV infection should be considered as a potential supportive treatment option for EBOV disease.IMPORTANCE Emerging infectious diseases are a major public health concern, as exemplified by the recent devastating Ebola virus (EBOV) outbreak. Different ebolavirus species are associated with widely varying pathogenicity in humans, ranging from asymptomatic infections for Reston virus (RESTV) to severe disease with fatal outcomes for EBOV. In this comparative study of EBOV- and RESTV-infected human macrophages, we identified key differences in host cell responses. Consistent with previous data, EBOV infection is associated with a proinflammatory signature triggered by the surface glycoprotein (GP), which can be inhibited by blocking TLR4 signaling. In contrast, infection with RESTV failed to stimulate a strong host response in infected macrophages due to the inability of RESTV GP to stimulate TLR4. We propose that disparate proinflammatory host signatures contribute to the differences in pathogenicity reported for ebolavirus species and suggest that proinflammatory pathways represent an intriguing target for the development of novel therapeutics.


Asunto(s)
Ebolavirus/inmunología , Ebolavirus/patogenicidad , Interacciones Huésped-Patógeno , Macrófagos/virología , Receptor Toll-Like 4/metabolismo , Animales , Línea Celular , Quimiocinas/inmunología , Quimiocinas/metabolismo , Chlorocebus aethiops , Citocinas/inmunología , Células Dendríticas/inmunología , Células Dendríticas/virología , Ebolavirus/fisiología , Perfilación de la Expresión Génica , Humanos , Factor 3 Regulador del Interferón/genética , Factor 3 Regulador del Interferón/inmunología , Interferones/inmunología , Macrófagos/inmunología , Macrófagos/metabolismo , Subunidad p50 de NF-kappa B/genética , Subunidad p50 de NF-kappa B/metabolismo , Receptor Toll-Like 4/genética , Receptor Toll-Like 4/inmunología , Células Vero , Virulencia
17.
J Virol ; 89(20): 10399-406, 2015 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-26246577

RESUMEN

UNLABELLED: Ebola virus (EBOV) initially targets monocytes and macrophages, which can lead to the release of proinflammatory cytokines and chemokines. These inflammatory cytokines are thought to contribute to the development of circulatory shock seen in fatal EBOV infections. The VP40 matrix protein is a key viral structural protein that is critical for virion egress. Physical and functional interactions between VP40 and host proteins such as Tsg101 and Nedd4 facilitate efficient release of VP40-driven virus-like particles (VLPs) and infectious virus. Here, we show that host suppressor of cytokine signaling 3 (SOCS3) can also bind to EBOV VP40, leading to enhanced ubiquitinylation and egress of VP40. Indeed, titers of infectious EBOV derived from SOCS3 knockout mouse embryonic fibroblasts (MEFs) were significantly reduced compared to those from wild-type (WT) MEFs at 24 and 48 h postinfection. Importantly, this reduced virus yield could be rescued back to WT levels by exogenously expressing SOCS3. Lastly, we show that SOCS3 expression is induced by EBOV glycoprotein (GP) expression and that VLPs containing EBOV VP40 and GP induced production of proinflammatory cytokines, which induced SOCS3 for negative-feedback regulation. These data indicate that host innate immune protein SOCS3 may play an important role in budding and pathogenesis of EBOV. IMPORTANCE: The VP40 matrix protein is a key structural protein critical for Ebola virus budding. Physical and functional interactions between VP40 and host proteins such as Tsg101 and Nedd4 facilitate efficient release of VLPs and infectious virus. We reported that host TLR4 is a sensor for Ebola GP on VLPs and that the resultant TLR4 signaling pathways lead to the production of proinflammatory cytokines. Host SOCS3 regulates the innate immune response by controlling and limiting the proinflammatory response through negative-feedback inhibition of cytokine receptors. We present evidence that Ebola virus VLPs stimulate induction of SOCS3 as well as proinflammatory cytokines, and that expression of human SOCS3 enhances budding of Ebola VLPs and infectious virus via a mechanism linked to the host ubiquitinylation machinery.


Asunto(s)
Fibroblastos/metabolismo , Regulación Viral de la Expresión Génica , Macrófagos/metabolismo , Nucleoproteínas/metabolismo , Proteínas Supresoras de la Señalización de Citocinas/metabolismo , Proteínas del Núcleo Viral/metabolismo , Liberación del Virus/genética , Animales , Línea Celular , Proteínas de Unión al ADN/genética , Proteínas de Unión al ADN/metabolismo , Ebolavirus/genética , Ebolavirus/metabolismo , Complejos de Clasificación Endosomal Requeridos para el Transporte/genética , Complejos de Clasificación Endosomal Requeridos para el Transporte/metabolismo , Retroalimentación Fisiológica , Fibroblastos/virología , Glicoproteínas/genética , Glicoproteínas/metabolismo , Células HEK293 , Interacciones Huésped-Patógeno , Humanos , Macrófagos/virología , Ratones , Ratones Endogámicos C57BL , Ubiquitina-Proteína Ligasas Nedd4 , Nucleoproteínas/genética , Transducción de Señal , Proteína 3 Supresora de la Señalización de Citocinas , Proteínas Supresoras de la Señalización de Citocinas/genética , Receptor Toll-Like 4/genética , Receptor Toll-Like 4/metabolismo , Factores de Transcripción/genética , Factores de Transcripción/metabolismo , Ubiquitina-Proteína Ligasas/genética , Ubiquitina-Proteína Ligasas/metabolismo , Ubiquitinación , Proteínas del Núcleo Viral/genética , Virión/genética , Virión/metabolismo
18.
J Virol ; 89(5): 2543-52, 2015 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-25520505

RESUMEN

UNLABELLED: To identify host factors associated with arenavirus virulence, we used a cynomolgus macaque model to evaluate the pathogenesis of Lujo virus (LUJV), a recently emerged arenavirus that caused an outbreak of severe viral hemorrhagic fever in southern Africa. In contrast to human cases, LUJV caused mild, nonlethal illness in macaques. We then compared this to contrasting clinical outcomes during arenavirus infection, specifically to samples obtained from macaques infected with three highly pathogenic lines of Lassa virus (LASV), the causative agent of Lassa fever (LF). We assessed gene expression in peripheral blood mononuclear cells (PBMC) and determined genes that significantly changed expression relative to that in uninfected animals over the course of infection. We detected a 72-h delay in the induction of host responses to infection during LUJV infection compared to that of the animals infected with LASV. This included genes associated with inflammatory and antiviral responses and was particularly apparent among groups of genes promoting cell death. We also observed early differential expression of a subset of genes specific to LUJV infection that accounts for the delayed inflammatory response. Cell type enrichment analysis suggested that host response induction delay and an LUJV-specific profile are due to a different proportion of natural killer cells responding in LUJV infection than that in the LASV-infected animals. Together, these data indicate that delayed proinflammatory and proapoptotic host responses to arenavirus infection could ameliorate disease severity. This conclusion provides insight into the cellular and molecular mechanisms of arenaviral hemorrhagic fever and suggests potential strategies for therapeutic development. IMPORTANCE: Old World arenaviruses are significant human pathogens that often are associated with high mortality. However, mechanisms underlying disease severity and virulence in arenavirus hemorrhagic fever are largely unknown, particularly regarding host responses that contribute to pathogenicity. This study describes a comparison between Lujo and Lassa virus infection in cynomolgus macaques. Lujo virus-infected macaques developed only mild illness, while Lassa virus-infected macaques developed severe illness consistent with Lassa fever. We determined that mild disease is associated with a delay in host expression of genes linked to virulence, such as those causing inflammation and cell death, and with distinct cell types that may mediate this delay. This is the first study to associate the timing and directionality of gene expression with arenaviral pathogenicity and disease outcome and evokes new potential approaches for developing effective therapeutics for treating these deadly emerging pathogens.


Asunto(s)
Infecciones por Arenaviridae/patología , Infecciones por Arenaviridae/virología , Fiebres Hemorrágicas Virales/patología , Fiebres Hemorrágicas Virales/virología , Lujo virus/patogenicidad , Animales , Infecciones por Arenaviridae/inmunología , Muerte Celular , Modelos Animales de Enfermedad , Perfilación de la Expresión Génica , Fiebres Hemorrágicas Virales/inmunología , Inflamación/patología , Células Asesinas Naturales/inmunología , Fiebre de Lassa/patología , Fiebre de Lassa/virología , Virus Lassa/patogenicidad , Leucocitos Mononucleares/inmunología , Macaca fascicularis , Factores de Tiempo
19.
PLoS Pathog ; 10(8): e1004250, 2014 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-25144235

RESUMEN

The availability of a robust disease model is essential for the development of countermeasures for Middle East respiratory syndrome coronavirus (MERS-CoV). While a rhesus macaque model of MERS-CoV has been established, the lack of uniform, severe disease in this model complicates the analysis of countermeasure studies. Modeling of the interaction between the MERS-CoV spike glycoprotein and its receptor dipeptidyl peptidase 4 predicted comparable interaction energies in common marmosets and humans. The suitability of the marmoset as a MERS-CoV model was tested by inoculation via combined intratracheal, intranasal, oral and ocular routes. Most of the marmosets developed a progressive severe pneumonia leading to euthanasia of some animals. Extensive lesions were evident in the lungs of all animals necropsied at different time points post inoculation. Some animals were also viremic; high viral loads were detected in the lungs of all infected animals, and total RNAseq demonstrated the induction of immune and inflammatory pathways. This is the first description of a severe, partially lethal, disease model of MERS-CoV, and as such will have a major impact on the ability to assess the efficacy of vaccines and treatment strategies as well as allowing more detailed pathogenesis studies.


Asunto(s)
Infecciones por Coronavirus/patología , Modelos Animales de Enfermedad , Neumonía Viral/patología , Animales , Callithrix , Infecciones por Coronavirus/virología , Inmunohistoquímica , Masculino , Coronavirus del Síndrome Respiratorio de Oriente Medio , Neumonía Viral/virología , Reacción en Cadena en Tiempo Real de la Polimerasa
20.
Ann Intern Med ; 162(12): 860-5, 2015 Jun 16.
Artículo en Inglés | MEDLINE | ID: mdl-26075757

RESUMEN

The National Institutes of Health (NIH) Pathways to Prevention Workshop: Advancing the Research on Myalgic Encephalomyelitis/Chronic Fatigue Syndrome was cosponsored by the NIH Office of Disease Prevention and the Trans-NIH Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Research Working Group. A multidisciplinary working group developed the agenda, and an Evidence-based Practice Center prepared an evidence report through a contract with the Agency for Healthcare Research and Quality to facilitate the discussion. During the 1.5-day workshop, invited experts discussed the body of evidence and attendees had the opportunity to comment during open discussions. After weighing evidence from the evidence report, expert presentations, and public comments, an unbiased, independent panel prepared a draft report that identified research gaps and future research priorities. The report was posted on the NIH Office of Disease Prevention Web site for 4 weeks for public comment.


Asunto(s)
Investigación Biomédica , Encefalomielitis/terapia , Síndrome de Fatiga Crónica/terapia , Mialgia/terapia , Adulto , Niño , Educación Médica Continua , Encefalomielitis/diagnóstico , Encefalomielitis/epidemiología , Síndrome de Fatiga Crónica/diagnóstico , Síndrome de Fatiga Crónica/epidemiología , Femenino , Educación en Salud , Humanos , Incidencia , Masculino , Mialgia/diagnóstico , Mialgia/epidemiología , Grupo de Atención al Paciente , Prevalencia , Apoyo a la Investigación como Asunto , Estados Unidos/epidemiología
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