RESUMEN
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.
Asunto(s)
Arterivirus , Fiebres Hemorrágicas Virales , Animales , Arterivirus/fisiología , Fiebres Hemorrágicas Virales/veterinaria , Fiebres Hemorrágicas Virales/virología , Humanos , Macaca , Primates , Zoonosis Virales , Internalización del Virus , Replicación ViralRESUMEN
Rift Valley fever phlebovirus (RVFV) infects humans and a wide range of ungulates and historically has caused devastating epidemics in Africa and the Arabian Peninsula. Lesions of naturally infected cases of Rift Valley fever (RVF) have only been described in detail in sheep with a few reports concerning cattle and humans. The most frequently observed lesion in both ruminants and humans is randomly distributed necrosis, particularly in the liver. Lesions supportive of vascular endothelial injury are also present and include mild hydropericardium, hydrothorax and ascites; marked pulmonary congestion and oedema; lymph node congestion and oedema; and haemorrhages in many tissues. Although a complete understanding of RVF pathogenesis is still lacking, antigen-presenting cells in the skin are likely the early targets of the virus. Following suppression of type I IFN production and necrosis of dermal cells, RVFV spreads systemically, resulting in infection and necrosis of other cells in a variety of organs. Failure of both the innate and adaptive immune responses to control infection is exacerbated by apoptosis of lymphocytes. An excessive pro-inflammatory cytokine and chemokine response leads to microcirculatory dysfunction. Additionally, impairment of the coagulation system results in widespread haemorrhages. Fatal outcomes result from multiorgan failure, oedema in many organs (including the lungs and brain), hypotension, and circulatory shock. Here, we summarize current understanding of RVF cellular tropism as informed by lesions caused by natural infections. We specifically examine how extant knowledge informs current understanding regarding pathogenesis of the haemorrhagic fever form of RVF, identifying opportunities for future research.
Asunto(s)
Fiebres Hemorrágicas Virales/fisiopatología , Fiebres Hemorrágicas Virales/veterinaria , Fiebre del Valle del Rift/fisiopatología , Virus de la Fiebre del Valle del Rift/patogenicidad , Tropismo Viral , Animales , Bovinos , Fiebres Hemorrágicas Virales/virología , Humanos , Hígado/patología , Hígado/virología , Fiebre del Valle del Rift/virología , Ovinos , Zoonosis Virales/fisiopatologíaRESUMEN
BACKGROUND: Severe fever with thrombocytopenia syndrome virus (SFTSV) causes severe hemorrhagic fever in humans and cats. Clinical symptoms of SFTS-infected cats resemble those of SFTS patients, whereas SFTS-contracted cats have high levels of viral RNA loads in the serum and body fluids. Due to the risk of direct infection from SFTS-infected cats to human, it is important to diagnose SFTS-suspected animals. In this study, a reverse transcription polymerase chain reaction (RT-PCR) was newly developed to diagnose SFTS-suspected animals without non-specific reactions. METHODOLOGY/PRINCIPLE FINDINGS: Four primer sets were newly designed from consensus sequences constructed from 108 strains of SFTSV. A RT-PCR with these four primer sets successfully and specifically detected four clades of SFTSV. Their limits of detection are 1-10 copies/reaction. Using this RT-PCR, 5 cat cases among 56 SFTS-suspected animal cases were diagnosed as SFTS. From these cats, IgM or IgG against SFTSV were detected by enzyme-linked immunosorbent assay (ELISA), but not neutralizing antibodies by plaque reduction neutralization titer (PRNT) test. This phenomenon is similar to those of fatal SFTS patients. CONCLUSION/SIGNIFICANCE: This newly developed RT-PCR could detect SFTSV RNA of several clades and from SFTS-suspected animals. In addition to ELISA and PRNT test, the useful laboratory diagnosis systems of SFTS-suspected animals has been made in this study.
Asunto(s)
Phlebovirus/genética , Síndrome de Trombocitopenia Febril Grave/diagnóstico , Síndrome de Trombocitopenia Febril Grave/veterinaria , Animales , Anticuerpos Antivirales/inmunología , Infecciones por Bunyaviridae/virología , Gatos/virología , Pruebas Diagnósticas de Rutina/métodos , Perros , Ensayo de Inmunoadsorción Enzimática/métodos , Femenino , Fiebre/diagnóstico , Fiebres Hemorrágicas Virales/diagnóstico , Fiebres Hemorrágicas Virales/veterinaria , Fiebres Hemorrágicas Virales/virología , Inmunoglobulina G/inmunología , Inmunoglobulina M/inmunología , Japón , Masculino , Phlebovirus/metabolismo , ARN Viral/sangre , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa/métodos , Síndrome de Trombocitopenia Febril Grave/virología , Trombocitopenia/diagnósticoRESUMEN
Severe fever with thrombocytopenia syndrome (SFTS) is an emerging hemorrhagic fever caused by the SFTS phlebovirus (SFTSV). SFTS patients were first reported in China, followed by Japan and South Korea. In 2017, cats were diagnosed with SFTS for the first time, suggesting that these animals are susceptible to SFTSV. To confirm whether or not cats were indeed susceptible to SFTSV, animal subjects were experimentally infected with SFTSV. Four of the six cats infected with the SPL010 strain of SFTSV died, all showing similar or more severe symptoms than human SFTS patients, such as a fever, leukocytopenia, thrombocytopenia, weight loss, anorexia, jaundice and depression. High levels of SFTSV RNA loads were detected in the serum, eye swab, saliva, rectal swab and urine, indicating a risk of direct human infection from SFTS-infected animals. Histopathologically, acute necrotizing lymphadenitis and hemophagocytosis were prominent in the lymph nodes and spleen. Severe hemorrhaging was observed throughout the gastrointestinal tract. B cell lineage cells with MUM-1 and CD20, but not Pax-5 in the lesions were predominantly infected with SFTSV. The present study demonstrated that cats were highly susceptible to SFTSV. The risk of direct infection from SFTS-infected cats to humans should therefore be considered.
Asunto(s)
Enfermedades de los Gatos/virología , Fiebres Hemorrágicas Virales/veterinaria , Phlebovirus/fisiología , Animales , Biomarcadores , Biopsia , Enfermedades de los Gatos/diagnóstico , Enfermedades de los Gatos/mortalidad , Enfermedades de los Gatos/transmisión , Gatos , Susceptibilidad a Enfermedades , Evaluación de SíntomasRESUMEN
Simian hemorrhagic fever virus (SHFV) causes a fulminant and typically lethal viral hemorrhagic fever (VHF) in macaques (Cercopithecinae: Macaca spp.) but causes subclinical infections in patas monkeys (Cercopithecinae: Erythrocebus patas). This difference in disease course offers a unique opportunity to compare host responses to infection by a VHF-causing virus in biologically similar susceptible and refractory animals. Patas and rhesus monkeys were inoculated side-by-side with SHFV. Unlike the severe disease observed in rhesus monkeys, patas monkeys developed a limited clinical disease characterized by changes in complete blood counts, serum chemistries, and development of lymphadenopathy. Viral RNA was measurable in circulating blood 2 days after exposure, and its duration varied by species. Infectious virus was detected in terminal tissues of both patas and rhesus monkeys. Varying degrees of overlap in changes in serum concentrations of interferon (IFN)-γ, monocyte chemoattractant protein (MCP)-1, and interleukin (IL)-6 were observed between patas and rhesus monkeys, suggesting the presence of common and species-specific cytokine responses to infection. Similarly, quantitative immunohistochemistry of livers from terminal monkeys and whole blood flow cytometry revealed varying degrees of overlap in changes in macrophages, natural killer cells, and T-cells. The unexpected degree of overlap in host response suggests that relatively small subsets of a host's response to infection may be responsible for driving hemorrhagic fever pathogenesis. Furthermore, comparative SHFV infection in patas and rhesus monkeys offers an experimental model to characterize hostâ»response mechanisms associated with viral hemorrhagic fever and evaluate pan-viral hemorrhagic fever countermeasures.
Asunto(s)
Infecciones por Arterivirus/veterinaria , Arterivirus/patogenicidad , Fiebres Hemorrágicas Virales/veterinaria , Interacciones Huésped-Patógeno , Enfermedades de los Monos/inmunología , Animales , Anticuerpos Antivirales/sangre , Arterivirus/inmunología , Infecciones por Arterivirus/inmunología , Citocinas/sangre , Erythrocebus , Femenino , Fiebres Hemorrágicas Virales/inmunología , Macaca , Macrófagos/virología , Masculino , Enfermedades de los Monos/virología , ARN Viral , Replicación ViralRESUMEN
UNLABELLED: Simian hemorrhagic fever (SHF) is a highly lethal disease in captive macaques. Three distinct arteriviruses are known etiological agents of past SHF epizootics, but only one, simian hemorrhagic fever virus (SHFV), has been isolated in cell culture. The natural reservoir(s) of the three viruses have yet to be identified, but African nonhuman primates are suspected. Eleven additional divergent simian arteriviruses have been detected recently in diverse and apparently healthy African cercopithecid monkeys. Here, we report the successful isolation in MARC-145 cell culture of one of these viruses, Kibale red colobus virus 1 (KRCV-1), from serum of a naturally infected red colobus (Procolobus [Piliocolobus] rufomitratus tephrosceles) sampled in Kibale National Park, Uganda. Intramuscular (i.m.) injection of KRCV-1 into four cynomolgus macaques (Macaca fascicularis) resulted in a self-limiting nonlethal disease characterized by depressive behavioral changes, disturbance in coagulation parameters, and liver enzyme elevations. In contrast, i.m. injection of SHFV resulted in typical lethal SHF characterized by mild fever, lethargy, lymphoid depletion, lymphoid and hepatocellular necrosis, low platelet counts, increased liver enzyme concentrations, coagulation abnormalities, and increasing viral loads. As hypothesized based on the genetic and presumed antigenic distance between KRCV-1 and SHFV, all four macaques that had survived KRCV-1 injection died of SHF after subsequent SHFV injection, indicating a lack of protective heterotypic immunity. Our data indicate that SHF is a disease of macaques that in all likelihood can be caused by a number of distinct simian arteriviruses, although with different severity depending on the specific arterivirus involved. Consequently, we recommend that current screening procedures for SHFV in primate-holding facilities be modified to detect all known simian arteriviruses. IMPORTANCE: Outbreaks of simian hemorrhagic fever (SHF) have devastated captive Asian macaque colonies in the past. SHF is caused by at least three viruses of the family Arteriviridae: simian hemorrhagic fever virus (SHFV), simian hemorrhagic encephalitis virus (SHEV), and Pebjah virus (PBJV). Nine additional distant relatives of these three viruses were recently discovered in apparently healthy African nonhuman primates. We hypothesized that all simian arteriviruses are potential causes of SHF. To test this hypothesis, we inoculated cynomolgus macaques with a highly divergent simian arterivirus (Kibale red colobus virus 1 [KRCV-1]) from a wild Ugandan red colobus. Despite being only distantly related to red colobuses, all of the macaques developed disease. In contrast to SHFV-infected animals, KRCV-1-infected animals survived after a mild disease presentation. Our study advances the understanding of an important primate disease. Furthermore, our data indicate a need to include the full diversity of simian arteriviruses in nonhuman primate SHF screening assays.
Asunto(s)
Infecciones por Arterivirus/veterinaria , Arterivirus/aislamiento & purificación , Arterivirus/patogenicidad , Colobus/virología , Fiebres Hemorrágicas Virales/veterinaria , Macaca fascicularis/virología , Enfermedades de los Monos/virología , Animales , Arterivirus/genética , Arterivirus/crecimiento & desarrollo , Infecciones por Arterivirus/inmunología , Infecciones por Arterivirus/fisiopatología , Infecciones por Arterivirus/virología , Línea Celular , Fiebres Hemorrágicas Virales/inmunología , Fiebres Hemorrágicas Virales/fisiopatología , Fiebres Hemorrágicas Virales/virología , Hígado/química , Hígado/enzimología , Masculino , Enfermedades de los Monos/inmunología , Enfermedades de los Monos/fisiopatología , Uganda , Carga ViralRESUMEN
Favipiravir is approved in Japan to treat novel or re-emerging influenza viruses, and is active against a broad spectrum of RNA viruses, including Ebola. Ribavirin is the only other licensed drug with activity against multiple RNA viruses. Recent studies show that ribavirin and favipiravir act synergistically to inhibit bunyavirus infections in cultured cells and laboratory mice, likely due to their different mechanisms of action. Convalescent immune globulin is the only approved treatment for Argentine hemorrhagic fever caused by the rodent-borne Junin arenavirus. We previously reported that favipiravir is highly effective in a number of small animal models of Argentine hemorrhagic fever. We now report that addition of low dose of ribavirin synergistically potentiates the activity of favipiravir against Junin virus infection of guinea pigs and another arenavirus, Pichinde virus infection of hamsters. This suggests that the efficacy of favipiravir against hemorrhagic fever viruses can be further enhanced through the addition of low-dose ribavirin.
Asunto(s)
Amidas/farmacología , Antivirales/farmacología , Fiebres Hemorrágicas Virales/tratamiento farmacológico , Pirazinas/farmacología , Virus ARN/efectos de los fármacos , Ribavirina/farmacología , Animales , Arenavirus/efectos de los fármacos , Chlorocebus aethiops , Cricetinae , Virus del Dengue/efectos de los fármacos , Modelos Animales de Enfermedad , Sinergismo Farmacológico , Femenino , Cobayas , Orthohantavirus/efectos de los fármacos , Virus de la Fiebre Hemorrágica de Crimea-Congo/efectos de los fármacos , Fiebre Hemorrágica Americana/tratamiento farmacológico , Fiebre Hemorrágica Ebola/tratamiento farmacológico , Fiebres Hemorrágicas Virales/sangre , Fiebres Hemorrágicas Virales/veterinaria , Fiebres Hemorrágicas Virales/virología , Virus Junin/efectos de los fármacos , Masculino , Mesocricetus , Ratones , Células VeroRESUMEN
Simian hemorrhagic fever (SHF) is lethal for macaques. Based on clinical presentation and serological diagnosis, all reported SHF outbreaks were thought to be caused by different strains of the same virus, simian hemorrhagic fever virus (SHFV; Arteriviridae). Here we show that the SHF outbreaks in Sukhumi in 1964 and in Alamogordo in 1989 were caused not by SHFV but by two novel divergent arteriviruses. Our results indicate that multiple divergent simian arteriviruses can cause SHF.
Asunto(s)
Infecciones por Arterivirus/veterinaria , Arterivirus/aislamiento & purificación , Fiebres Hemorrágicas Virales/veterinaria , Macaca/virología , Enfermedades de los Primates/virología , Secuencia de Aminoácidos , Animales , Arterivirus/clasificación , Arterivirus/genética , Arterivirus/fisiología , Infecciones por Arterivirus/historia , Infecciones por Arterivirus/virología , Evolución Molecular , Fiebres Hemorrágicas Virales/historia , Fiebres Hemorrágicas Virales/virología , Historia del Siglo XX , Humanos , Datos de Secuencia Molecular , Filogenia , Enfermedades de los Primates/historia , Homología de Secuencia de Aminoácido , Proteínas Virales/química , Proteínas Virales/genéticaRESUMEN
Simian hemorrhagic fever virus is an arterivirus that naturally infects species of African nonhuman primates causing acute or persistent asymptomatic infections. Although it was previously estimated that 1% of baboons are SHFV-positive, more than 10% of wild-caught and captive-bred baboons tested were SHFV positive and the infections persisted for more than 10 years with detectable virus in the blood (100-1000 genomes/ml). The sequences of two baboon SHFV isolates that were amplified by a single passage in primary macaque macrophages had a high degree of identity to each other as well as to the genome of SHFV-LVR, a laboratory strain isolated in the 1960s. Infection of Japanese macaques with 100PFU of a baboon isolate consistently produced high level viremia, pro-inflammatory cytokines, elevated tissue factor levels and clinical signs indicating coagulation defects. The baboon virus isolate provides a reliable BSL2 model of viral hemorrhagic fever disease in macaques.
Asunto(s)
Infecciones por Arterivirus/veterinaria , Arterivirus/aislamiento & purificación , Arterivirus/patogenicidad , Fiebres Hemorrágicas Virales/veterinaria , Enfermedades de los Monos/virología , Papio/virología , Animales , Arterivirus/genética , Infecciones por Arterivirus/patología , Infecciones por Arterivirus/virología , Citocinas/sangre , Genoma Viral , Fiebres Hemorrágicas Virales/patología , Fiebres Hemorrágicas Virales/virología , Interacciones Huésped-Patógeno , Macaca , Enfermedades de los Monos/inmunología , Enfermedades de los Monos/patología , Especificidad de Órganos , Viremia/veterinaria , Viremia/virologíaRESUMEN
BACKGROUND: Lassa virus and Marburg virus are two causative agents of viral hemorrhagic fever. Their diagnosis is difficult because patients infected with either pathogen present similar nonspecific symptoms early after infection. Current diagnostic tests are based on detecting viral proteins or nucleic acids in the blood, but these cannot be found during the early stages of disease, before the virus starts replicating in the blood. Using the transcriptional response of the host during infection can lead to earlier diagnoses compared to those of traditional methods. RESULTS: In this study, we use RNA sequencing to obtain a high-resolution view of the in vivo transcriptional dynamics of peripheral blood mononuclear cells (PBMCs) throughout both types of infection. We report a subset of host mRNAs, including heat-shock proteins like HSPA1B, immunoglobulins like IGJ, and cell adhesion molecules like SIGLEC1, whose differences in expression are strong enough to distinguish Lassa infection from Marburg infection in non-human primates. We have validated these infection-specific expression differences by using microarrays on a larger set of samples, and by quantifying the expression of individual genes using RT-PCR. CONCLUSIONS: These results suggest that host transcriptional signatures are correlated with specific viral infections, and that they can be used to identify highly pathogenic viruses during the early stages of disease, before standard detection methods become effective.
Asunto(s)
Fiebres Hemorrágicas Virales/veterinaria , Interacciones Huésped-Patógeno/genética , Virus Lassa , Marburgvirus , Enfermedades de los Monos/genética , Transcripción Genética , Animales , Femenino , Perfilación de la Expresión Génica , Regulación de la Expresión Génica/efectos de los fármacos , Interferón Tipo I/farmacología , Leucocitos Mononucleares/metabolismo , Leucocitos Mononucleares/virología , Macaca fascicularis , Masculino , Enfermedades de los Monos/diagnóstico , Enfermedades de los Monos/virología , Reproducibilidad de los Resultados , Análisis de Secuencia de ARNRESUMEN
To ascertain the role played by the various liver monocyte-macrophage populations in the course of a viral hemorrhagic fever, fifteen pigs were inoculated intramuscularly with the highly virulent isolate of African Swine Fever Virus (ASFV) España-70 and slaughtered at 1-7 days post-inoculation (dpi). Samples of liver were fixed in different solutions and routinely processed for morphological, immunohistochemical and ultrastructural studies. Viral antigen (vp73) was detected from 3 dpi onward, mainly in circulating monocytes of sinusoid and Kupffer's cells (KC), as well as in portal macrophages and hepatocytes from 5 dpi. Anti-SWC3 immunolabelled cells were increased from 1 dpi, peaking between 3 and 5 dpi, thereafter declining until the end of the experiment. The significant increase in the number of sinusoidal circulating monocytes and KC expressing IL-1alpha, TNFalpha and IL-6 from 1 dpi, confirmed the secretory activation of these cells. The results show that in the course of an ASFV-induced hemorrhagic syndrome, hepatic macrophage populations undergo major quantitative and biosynthetic changes prior to virus detection, suggesting the existence of a mechanism by which the virus concentrates infectable cells, which subsequently spread the virus around the body.
Asunto(s)
Virus de la Fiebre Porcina Africana/fisiología , Fiebres Hemorrágicas Virales/veterinaria , Macrófagos del Hígado/patología , Hígado/patología , Enfermedades de los Porcinos/patología , Animales , Antígenos Virales/metabolismo , Apoptosis , Recuento de Células , Citocinas/metabolismo , Femenino , Técnica del Anticuerpo Fluorescente Directa , Fiebres Hemorrágicas Virales/metabolismo , Fiebres Hemorrágicas Virales/patología , Técnicas para Inmunoenzimas , Macrófagos del Hígado/metabolismo , Macrófagos del Hígado/virología , Masculino , Monocitos/metabolismo , Monocitos/patología , Monocitos/virología , Porcinos , Enfermedades de los Porcinos/metabolismoRESUMEN
Few diseases generate such alarm among the general population and health professionals as viral hemorrhagic fevers (VHFs). VHFs are acute infections with high associated mortality that are difficult to clinically diagnose and differentiate. Reliable laboratory diagnosis is required for proper patient support and to limit the risk of transmission and the development of secondary cases. Even today many factors related to origin, pathogenesis, treatment and control of these diseases remain uncertain.
Asunto(s)
Fiebres Hemorrágicas Virales , Animales , Vectores Arácnidos/virología , Arenaviridae/fisiología , Bunyaviridae/fisiología , Dengue/diagnóstico , Dengue/tratamiento farmacológico , Dengue/epidemiología , Dengue/transmisión , Diagnóstico Diferencial , Filoviridae/fisiología , Flaviviridae/fisiología , Fiebres Hemorrágicas Virales/diagnóstico , Fiebres Hemorrágicas Virales/tratamiento farmacológico , Fiebres Hemorrágicas Virales/epidemiología , Fiebres Hemorrágicas Virales/transmisión , Fiebres Hemorrágicas Virales/veterinaria , Fiebres Hemorrágicas Virales/virología , Humanos , Insectos Vectores/virología , Guías de Práctica Clínica como Asunto , Enfermedades de los Primates/virología , Primates , Enfermedades de los Roedores/virología , Roedores , Garrapatas/virologíaRESUMEN
This work reports preliminary data on the application of a novel method, ultrasound, for the DNA vaccination of rainbow trout. First, the best formulations were selected that increased the transfer by immersion of a plasmid coding for the green fluorescent protein (GFP) gene into trout fry. Quantification of GFP expression by fluorescence in the fin cells was used to study time course, DNA concentration dependence and comparison of different formulations. The best GFP expression results were obtained with short pulses of ultrasound, DOTAP liposomes and recombinant bacteria or bactofection. Other liposomes or microencapsulation formulations resulted in a GFP fluorescence similar to background values. Second, DNA immersion-vaccination of immunocompetent fingerling trout with the selected formulations was performed by using a plasmid coding for the glycoprotein G gene of the viral haemorrhagic septicaemia virus (VHSV). The immunization of fingerling trout was estimated by measuring humoral antibody, lymphoproliferation and VHSV challenge responses. Short pulses of low intensity ultrasound were the only method by which both humoral antibody responses and survival after VHSV challenge were obtained. Immersion DNA-vaccination using short pulses of ultrasound could eventually lead to a practical way to vaccinate small fish.
Asunto(s)
Enfermedades de los Peces/prevención & control , Fiebres Hemorrágicas Virales/veterinaria , Oncorhynchus mykiss/inmunología , Oncorhynchus mykiss/virología , Infecciones por Rhabdoviridae/veterinaria , Rhabdoviridae/inmunología , Vacunas de ADN/administración & dosificación , Vacunas Virales/administración & dosificación , Animales , Anticuerpos Antivirales/sangre , Escherichia coli/genética , Enfermedades de los Peces/inmunología , Enfermedades de los Peces/virología , Proteínas Fluorescentes Verdes , Fiebres Hemorrágicas Virales/inmunología , Fiebres Hemorrágicas Virales/prevención & control , Fiebres Hemorrágicas Virales/virología , Inmersión , Liposomas , Proteínas Luminiscentes/genética , Activación de Linfocitos , Oncorhynchus mykiss/crecimiento & desarrollo , Rhabdoviridae/genética , Infecciones por Rhabdoviridae/inmunología , Infecciones por Rhabdoviridae/prevención & control , Infecciones por Rhabdoviridae/virología , Ultrasonido , Vacunas de ADN/genética , Vacunas Virales/genéticaRESUMEN
Hantaviruses and arenaviruses are naturally occurring viruses of rodents. Four South American hemorrhagic fevers caused by arenaviruses have emerged in the last 5 decades. All have similar clinical manifestations, with a case-fatality rate as high as 15% to 30%. Hantavirus infections have been increasingly recognized in South America since the description in 1993 of Hantavirus pulmonary syndrome. Given the diversity of rodent species in the region, it can be foreseen that many other viruses will be discovered, and some of them will be causing human illnesses of high public health impact.
Asunto(s)
Infecciones por Arenaviridae/epidemiología , Infecciones por Hantavirus/epidemiología , Fiebres Hemorrágicas Virales/epidemiología , Enfermedades de los Roedores/virología , Zoonosis/epidemiología , Animales , Infecciones por Arenaviridae/terapia , Infecciones por Arenaviridae/veterinaria , Infecciones por Arenaviridae/virología , Arenavirus , Orthohantavirus , Infecciones por Hantavirus/terapia , Infecciones por Hantavirus/veterinaria , Infecciones por Hantavirus/virología , Fiebres Hemorrágicas Virales/terapia , Fiebres Hemorrágicas Virales/veterinaria , Fiebres Hemorrágicas Virales/virología , Humanos , Enfermedades de los Roedores/transmisión , América del Sur/epidemiologíaRESUMEN
A viral haemorrhagic syndrome was induced in 14 pigs by inoculation with an African swine fever (ASF) virus strain of moderate virulence, to determine changes in megakaryocyte (MK) numbers and morphology and thus to assess the role of these cells in the thrombocytopenia characteristic of subacute ASF. The strain tested induced changes in the proportion of different types of MK (typical nucleated MKs, apoptotic MKs and immature MKs); it also caused subcellular lesions over the first 7 days post-inoculation (dpi). At 7 dpi, severe thrombocytopenia was observed. There was a statistically significant increase in apoptotic MK numbers. The MKs showed three stages in the course of the disease: a compensatory stage, represented by cytoplasmic projections, a hypermaturity stage, represented by apoptotic MKs, and a regenerative stage, represented by clusters of immature MKs. These changes, especially the presence of numerous apoptotic MKs, may explain the early and transitory thrombocytopenia detected in subacute ASF. The large number of apoptotic MKs observed may be associated with the accelerated maturation of these cells, resulting from the action of cytokines, or peripheral platelet consumption, or both.
Asunto(s)
Virus de la Fiebre Porcina Africana/patogenicidad , Fiebre Porcina Africana/patología , Apoptosis , Fiebres Hemorrágicas Virales/veterinaria , Megacariocitos/patología , Trombocitopenia/patología , Trombocitopenia/veterinaria , Fiebre Porcina Africana/sangre , Animales , Recuento de Células/veterinaria , Femenino , Fiebres Hemorrágicas Virales/sangre , Fiebres Hemorrágicas Virales/patología , Masculino , Megacariocitos/ultraestructura , Recuento de Plaquetas/veterinaria , Porcinos , Síndrome , Trombocitopenia/sangre , VirulenciaRESUMEN
To help determine specific vectors of epizootic hemorrhagic disease (EHD) and bluetongue (BT) viruses for white-tailed deer, Odocoileus virginianus Zimmermann, in the southeastern United States, Culicoides sp. midges were collected during epizootics of hemorrhagic disease among captive white-tailed deer in Georgia, Mississippi, and North Carolina. Culicoides variipennis (Coquillett), a confirmed vector of EHD and BT viruses, was present in low numbers in light-trap collections made at all sites. Collections from deer made in Georgia and North Carolina yielded only a single specimen of C. variipennis. Other Culicoides species present in far greater numbers during the epizootics included C. lahillei Lutz, C. paraensis (Goeldi), and C. stellifer (Coquillett) C. lahillei warrants particular attention as a potential vector because its readily feeds on white-tailed deer and was by far the predominant species collected from deer during the epizootics.
Asunto(s)
Virus de la Lengua Azul/aislamiento & purificación , Ceratopogonidae/virología , Ciervos/parasitología , Virus de la Enfermedad Hemorrágica Epizoótica/aislamiento & purificación , Fiebres Hemorrágicas Virales/veterinaria , Insectos Vectores/virología , Animales , Línea Celular , Ceratopogonidae/clasificación , Cricetinae , Ciervos/virología , Brotes de Enfermedades/veterinaria , Femenino , Fiebres Hemorrágicas Virales/transmisión , Masculino , Infecciones por Reoviridae/transmisión , Infecciones por Reoviridae/veterinaria , Infecciones por Reoviridae/virologíaRESUMEN
Most of the viral hemorrhagic fevers (VHFs) are caused by viruses that are handled in high containment laboratories in Europe and the United States because of their high pathogenicity and their aerosol infectivity. Special precautions should be taken when caring for patients infected with these viruses, but most hospitals can safely provide high-quality care. The major danger is parenteral inoculation of a staff member. Fomites and droplets must be considered as well. The role of small particle aerosols in inter-human transmission continues to be controversial. We believe that the aerosol infectivity observed for these viruses in the laboratory and the rare clinical situations that suggest aerosol spread dictate caution, but the many instances in which no transmission occurs provide a framework in which a measured approach is possible. The major challenge is in early recognition by an educated medical staff and rapid specific etiological diagnosis.
Asunto(s)
Fiebres Hemorrágicas Virales/prevención & control , Fiebres Hemorrágicas Virales/transmisión , Aerosoles , Animales , Animales de Laboratorio , Arenaviridae/clasificación , Arenaviridae/patogenicidad , Bunyaviridae/clasificación , Bunyaviridae/patogenicidad , Europa (Continente) , Familia , Filoviridae/clasificación , Filoviridae/patogenicidad , Flaviviridae/clasificación , Flaviviridae/patogenicidad , Fiebres Hemorrágicas Virales/veterinaria , Humanos , Transmisión de Enfermedad Infecciosa de Paciente a Profesional/prevención & control , Laboratorios/normas , Ratones , Modelos Biológicos , Transporte de Pacientes/normas , Estados Unidos , ViremiaRESUMEN
We have isolated a new strain of Ebola virus from a non-fatal human case infected during the autopsy of a wild chimpanzee in the Côte-d'Ivoire. The wild troop to which this animal belonged has been decimated by outbreaks of haemorrhagic syndromes. This is the first time that a human infection has been connected to naturally-infected monkeys in Africa. Data from the long-term survey of this troop of chimpanzees could answer questions about the natural reservoir of the Ebola virus.
Asunto(s)
Ebolavirus/aislamiento & purificación , Adulto , Animales , Animales Salvajes , Anticuerpos Antivirales/análisis , Enfermedades del Simio Antropoideo/mortalidad , Enfermedades del Simio Antropoideo/transmisión , Enfermedades del Simio Antropoideo/virología , Autopsia/veterinaria , Côte d'Ivoire , Reservorios de Enfermedades/veterinaria , Ebolavirus/clasificación , Ebolavirus/inmunología , Ensayo de Inmunoadsorción Enzimática , Femenino , Fiebres Hemorrágicas Virales/mortalidad , Fiebres Hemorrágicas Virales/transmisión , Fiebres Hemorrágicas Virales/veterinaria , Fiebres Hemorrágicas Virales/virología , Humanos , Pan troglodytes , ZoonosisAsunto(s)
Enfermedades del Simio Antropoideo/virología , Brotes de Enfermedades/veterinaria , Ebolavirus , Fiebres Hemorrágicas Virales/veterinaria , Pan troglodytes/virología , Animales , Enfermedades del Simio Antropoideo/epidemiología , Enfermedades del Simio Antropoideo/transmisión , Côte d'Ivoire/epidemiología , Reservorios de Enfermedades , Fiebres Hemorrágicas Virales/epidemiología , Fiebres Hemorrágicas Virales/transmisión , Humanos , Estaciones del Año , ZoonosisRESUMEN
Following the detection of an Ebola-like virus in cynomolgus macaques recently imported into the United States from The Philippines, studies were initiated to document transmission at export facilities located in the latter country. At one export facility, 52.8% of 161 monkeys that died over a 2.5-month period were shown to be infected with this virus using an enzyme-linked immunosorbent assay to detect antigen in liver homogenates. A case fatality rate of 82.4% was documented for the infected monkeys. The initial anti-viral antibody prevalence among the captive macaques at this facility was 25.9% (indirect fluorescent antibody titer greater than or equal to 1:16). Followup documented infection of 24.4% of initially seronegative animals and 8.7% of initially seropositive monkeys. Being held in a gang cage versus a single cage was found to be a significant risk factor for subsequent virus infection, and the presence of IFA antibody was shown to predict protection. This study documents unequivocally for the first time the presence of an Ebola-related filovirus in Asia.