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Daemon
Posted: Saturday, August 2, 2014 12:00:00 AM
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Joined: 3/7/2009
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Ebola Crisis Deepens

The Ebola outbreak in West Africa has claimed 729 lives in four countries thus far, making it the deadliest and widest ranging such outbreak the world has ever seen. Dozens of healthcare workers have fallen victim, complicating efforts to combat it. Though the disease is outpacing current efforts to contain its spread, the head of the World Health Organization (WHO) still believes that the "unprecedented" outbreak could be stopped if proper steps are taken at both the national and international levels. To this end, a new, $100 million (75 million euro) Ebola response plan is being launched to combat the disease. More...
JUSTIN Excellence
Posted: Saturday, August 2, 2014 8:29:53 AM

Rank: Advanced Member

Joined: 6/25/2014
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Location: Veinau, Baden-Wuerttemberg Region, Germany

Here is my review on Ebola Virus_

Ebola virus is a filovirus, another RNA virus, emerged in 1976, when two epidemics occurred simultaneously in Zaire and Sudan. The agent was isolated from patients in both countries and named after a small river in northwestern Zaire. In June and July the first cases were reported from Nzara in western Equatoria Province of southern Sudan, a small town bordering the African rain forest zone. The outbreak was strongly associated with index cases in a single cotton factory in town, and spread was to close relatives (67 cases). The epidemic was intensified by the spread of cases to neighboring areas, Maridi, Tembura, and Juba. High levels of transmission occurred in the hospital of Maridi, a teaching center for student nurses (213 cases). Despite the similarities of the clinical diseases and mortality rates, the epidemic in Nzara differed from the one in Maridi.



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The Nzara outbreak involved factory workers and their close relatives whereas in Maridi the hospital served as both focus and amplifier of the infection. The outbreak lasted until November, during which time approximately 15 generations of person-to-person transmissions occurred. Transmission of the disease required close contact with an acute case and was usually associated with nursing patients. The overall secondary attack rate was 12% and documented the relatively slow rate of spread into the community once out of the hospital. In toto there were 284 probable and confirmed cases involved with 151 deaths (53%). By the end of August a second epidemic started in equatorial rain forest areas of northern Zaire. A direct link between the two epidemics has always been discussed but never been verified. In total there were 318 probable or confirmed cases and 280 deaths (88%). The presumed index case came to Yambuku Mission Hospital for treatment of acute malaria, where he received an injection of chloroquine. It remains unclear whether this man was the source of the epidemic or became infected by the injection.



Most persons acquired the disease following contact with patients, but for more than 25% the only risk factor elucidated was receipt of injections at Yambuku Mission Hospital. Nearly all survivors were infected by person-to-person contact. All ages and both sexes were affected, but the highest incidence was in women aged 15-29 years, who were frequently patients attending antenatal and outpatient clinics at the hospital. Although transmission was focused in the outpatient clinics of the hospital, there was subsequent dissemination in surrounding villages to people caring for sick relatives, attending childbirth, or having other forms of close contact. The secondary attack rate was approximately 5% overall but about 20% in close relatives of a patient. The epidemic, which lasted from the end of August until the end of October, spread relatively slowly in the epidemic area, and ail infected villages (55; population <5000) were within 60 km of Yambuku. Establishment of strict barrier nursing and classic public health principles, identification and isolation, was successful in controlling both epidemics. The spread by contaminated syringes and needles in Yambuku almost completely terminated when the hospital closed. The episode in Nzara died out spontaneously.



In 1979, Ebola hemorrhagic fever reemerged in Nzara and Yambio, which are located in the remote savanna of southern Sudan, near the border with Zaire. The index case, a 45-year-old man, was admitted to the Nzara hospital with fever, vomiting, and diarrhea. He developed gastrointestinal bleeding and died 3 days postadmission. The index case worked in the same textile factory cited as the source of the 1976 outbreak in Sudan. The outbreak (July 31 to October 6, 1979) started from the hospital, where the index case patient was responsible for four nosocomial infections, which in turn led to disease in 5 families. Thirty-three cases could be traced to a human source of infection, with 22 fatalities (65% mortality). Seven generations of virus transmission were estimated and mortality changed from 89% in the first four generations to 38% in the last three. Studies within the families confirmed reports from previous outbreaks (Sudan and Zaire, 1976) suggesting that Ebola virus is not easily transmitted and contact with body fluids of a patient is needed. Again, the hospital appeared to be the important focal point for dissemination.



New Emerging and Reemerging of Ebola Hemorrhagic Fever in Africa

Two disease episodes of mortality were noticed among a group of chimpanzees in 1992 (8 deaths) and 1994 (12 deaths). The chimpanzees were objects of a 15-year observation by ethologists in the Tai National Park in western Ivory Coast. Several of the dead animals showed signs of hemorrhages, and one of the animals was autopsied in the field. A 34-year-old woman developed a dengue-like syndrome 8 days after performing the autopsy. She was admitted to the hospital in Abidjan 2 days later with continuing fever resistant to antimalarial treatment, diarrhea, and pruritic rush. Evacuation to Switzerland followed 5 days later when she developed a syndrome similar to that described for surviving Ebola-infected patients; she recovered without sequelae. An infection with an Ebola virus was confirmed by isolate specific IgM and IgG antibodies, Ebola-Zaire-specific IgG antibodies, antigen-capture ELISA, reactivity to an Ebola serotype-specific monoclonal antibody, and virus isolation. Contact with infectious blood and tissues during the necropsy was considered to be the most likely source of the human infection. Organs of the dead chimpanzee were studied by immunohistochemistry and the findings were similar to those seen in material of the 1976 Ebola outbreaks and experimentally infected monkeys with Ebola virus. None of the persons in contact with either the case patient or the material of the chimpanzee tested antibody positive.



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Ebola hemorrhagic fever reemerged in Zaire in 1995. The first identified case related to the outbreak suffered an onset of illness on January 6, 1995. Until August 24, the official end of the epidemic, 315 cases had occurred, of which 244 died (77%). The center of the epidemic was Ktkwit and the surrounding areas in Bandundu region in southwestern Zaire. The first case at Kikwit General Hospital was a male laboratory worker who had previously been admitted to Kikwit 2, a smaller second hospital in town. A laparotomy was performed after a differential diagnosis of typhoid fever with intestinal perforation. This was followed by a second laparotomy which showed massive intraabdominal hemorrhage; the patient died 3 days later.

Four days after the first laparotomy the first case among medical staff members occurred, with fever, headache, muscle aches, and hemorrhages. About three quarters of the first 70 patients were health care workers. The actual epidemic started within the hospitals. Prior to this time, cases had been sporadic. The major risk factors have been patient care in hospitals and households and preparation of bodies for burial. This is reflected by the fact that 26% of the cases with known professional occupation were medical staff members or students and 21% were housewives. During the course of surveillance, several chains of deaths have been identified which were traced as far back as late December 1994. The chain of the presumable index case, a charcoal worker, involves 7 out of 12 persons living in his household.

An outbreak of Ebola hemorrhagic fever occurred in the village of Mayibout 11, Makokou Health District, Ogooue-Ivindo Province, Gabon. It was linked t o a chimpanzee found dead in the forest. A total number of 37 cases were diagnosed (mortality 56.8%) and 21 cases were directly exposed to the dead chimpanzee. A strain of Ebola virus was isolated from patient samples.



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Filoviruses which includes Ebola virus, are among the most pathogenic of human viruses. They are classified as “Biological Level 4” agents (WHO; Risk Group 4) based on their high mortality rate, person-to-person transmission, potential aerosol infectivity, and absence of vaccines and chemotherapy. Maximum containment is required for all laboratory work with infectious material. Yet, we are only beginning to understand the interactions of these viruses with their host, and our knowledge on genetics, pathogenicity, and natural history is still limited. Even though outbreaks among human and nonhuman primates to date have always been self-limited, it is because of our ignorance about the natural reservoir, the potential of these viruses to be transmitted by aerosol, and the lack of immunoprophylactic and chemotherapeutic measures that these infections are of great concern to biomedical scientists. Imported monkeys and international travel, especially rapid travel within the incubation time, are considerable risk factors for introduction of filovirus infections into nonendemic countries. Limited knowledge of the epidemiology and clinical picture of filoviral hemorrhagic fever (HP) and inexperience in diagnosing cases and in case management magnify the danger of an introduction.



Filoviruses, like other RNA viruses, presumably have a potential for rapid evolution due to an inherently high error rate of the virus encoded polymerase and a lack of repair mechanisms. The consequence may be a spectrum of genetic variants that are selected by the host for different transmissibility, virulence, and other biological properties. Changes in socioeconomic structure, such as an increase in human population, increase in speed, variety, and frequency of travel, and disruption of social structures may augment the development of mutant virus populations and the probability of a filovirus emerging as a truly serious public health problem.

Reservoir

Serological studies suggest that filoviruses are endemic in many countries of the Central African region. Recent serosurveys in other countries, such as Germany and the United States, using several different techniques, suggest that filoviruses might also be endemic in those countries. Serological studies in relation to the EBO Reston outbreak indicated filovirus activity in the Philippines. Although, as already mentioned, serological data based on IFA alone are of limited reliability, they at least suggest that subclinical infections caused by known or unknown filoviruses may occur and may be more common than expected. At this point, however, one has also to consider that filoviruses are members of the order Mononegavirales. This order includes many common human viruses that could be responsible for serological cross-reactivities.



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MBG and subtypes Sudan and Zaire of EBO appear to be indigenous to the African continent, and both EBO subtypes have been isolated from human patients only in Africa. MBG has been isolated from human patients in Africa and Europe. The origin of the European cases could be traced back to foci in Uganda where vervet monkeys compounded in Entebbe (central holding station at Lake Victoria) were imported to Germany and Yugoslavia. Complement-fixing antibodies were found in sera from some monkeys originally trapped near Lake Kyoga, the main area where vervet monkeys had been captured since the establishment of the trade in 1962. The finding of antibodies in three monkey trappers indicates that human infection may have occurred in Uganda during that time. However, all titers observed were weak, and an agent has never been isolated from the blood of a wild-trapped monkey or a monkey trapper. Both index case patients of the episodes of MBG hemorrhagic fever in Kenya (1980/1987) had traveled in Mount Elgon region. This region is not far from the shores of Lake Victoria and thus is close t o the trapping place (Lake Kyoga, Uganda) and holding station (Entebbe, Uganda) of the monkeys that initiated the 1967 outbreak in Europe. One of the index cases had visited a cave (Kitum Cave) in that area shortly before becoming ill. Serological studies in this area, however, again failed to uncover the source of the virus. These studies included an extensive investigation of many animal species inhabiting the cave, including bats (E. D. Johnson, unpublished). Bats inhabiting buildings of a textile factory have also been considered as a potential source of the index cases of the 1976 and 1979 outbreaks of EBO hemorrhagic fever in southern Sudan. The geographical origin of both epidemics is less than 1000 km northwest of Lake Victoria and Mount Elgon. A potential source for the 1976 Zairian outbreak has never been found, but a link to the simultaneous epidemic in Sudan has been discussed. These data strongly suggest an endemic focus for filoviruses in the equatorial rain forest areas of southern Sudan, northern Zaire, Uganda, and Kenya.



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The EBO Reston outbreak suggested for the first time the presence of a filovirus in Asia. Serological studies (IFA) among captive macaques in the Philippines indicated that the source of EBO Reston might be wild nonhuman primates. However, IFA-detected antibodies seem to be spurious, and latent infection in nonhuman primates has never been observed. Epidemiological data obtained in association with the 1994 Ivory Coast case suggested an Ebola epizootic among a group of chimpanzees as the cause of death. The pathogenicity of filoviruses, especially of EBO subtypes Sudan and Zaire and MBG, for nonhuman primates, however, does not support the concept of a reservoir in monkeys. The reservoir of filoviruses remains a mystery. Many species have been discussed as possible natural hosts; however, no nonhuman vertebrate hosts or arthropod vectors have yet been identified. The high frequency of false-positives, especially when the EBO IFA is used, has contributed to the difficulties in finding the true reservoir for filoviruses. Filoviruses resemble “Old World arenaviruses" in several interesting biological properties, such as resistance to the antiviral effects of interferon, lack of in viro neutralization, and lack of protection by convalescence sera. Arenaviruses cause chronic viremic infection in their rodent reservoirs. Thus, chronic infection of a mammal has to be considered as a mechanism that regulates survival of filoviruses in nature.



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Transmission

Person-to-person transmission by physical contact with case patients is the main route of infection in human outbreaks. Activities such as nursing and preparing bodies for burial are especially associated with an increased risk of becoming infected. During the EBO outbreaks in 1976 and to some extent 1995, nosocomial transmission via contaminated syringes and needles was a major problem. Transmission does not seem to be efficient, as documented by secondary attack rates which on average rarely exceeded 12%. Thus, extreme care should be taken with blood, secretions, and excretions of infected patients. Sexual transmission has been described for MBG and neonatal transmission has been reported for the 1976 outbreak in Zaire.



Based on experience of the former episodes, isolation of patients and use of strict barrier nursing procedures (e.g., protective clothing, respirator) are sufficient to interrupt transmission. Transmission by droplets and small-particle aerosols has been observed among experimentally infected (MBG) and quarantined imported monkeys (EBO RES, 1989-1990). This is confirmed by identification of filovirus particles in alveoli of naturally and experimentally infected monkeys and human post mortem cases. However, the contribution of aerosol transmission to the course of human outbreaks is still unknown.



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Molecular Evolution

The family Filoviridae has been constituted on the basis of unique morphologic, morphogenetic, physicochemical, and biological features of its members. Filoviruses can be separated into two types, which are clearly distinguished by the features listed in. In general, the MEG viruses seem to be unique without known subtypes, but at least two different genetic lineages coexist. EBO, however, can be subdivided into at least three subtypes: Zaire, Sudan, and Reston.



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Molecular characterization of the Ivory Coast virus revealed a novel lineage, suggesting a fourth subtype of EBO. There is a lack of antigenic cross-reactivity between the types, but the subtypes of EBO share common epitopes. Nucleotide sequence comparison among MBG and EBO shows only scattered similarities, which is in contrast to the similarities seen among amino acid sequences of structural proteins. This finding indicates that these agents may have diverged at some point in the distant past. A distinction within the EBO type is based on earlier peptide and oligonucleotide mapping and has been confirmed by recent sequence analysis of the glycoprotein genes. That study showed all four subtypes to differ from one another to a comparable extent: 37-41% nucleotide differences.

This suggests that filoviruses have evolved into specific niches and may reflect a similar divergence in the natural hosts, assuming they have coevolved. Genetic variability seen among different virus isolates of one subtype seems to be much less than for some other RNA viruses. In particular, the close genetic relation of the two Zairian isolates from 1976 and 1995, with less than 1.6% difference in the GP gene, suggests that filovirus variants may not emerge as rapidly in nature. Molecular analyses of the genomes clearly demonstrated that filoviruses are the closest relatives to Rhabdoviridae and Paramyxoviridae. All nonsegmented negative-stranded (NNS) RNA viruses share a similar genome organization, with conserved regions at both ends encoding the core and L proteins surrounding a variable part in the middle encoding the envelope proteins. Filovirus genomes are more complex than those of lyssaviruses and vesiculoviruses and align organizationally more closely to members of the genera Pararnyxovirus and Morbillivirus. This relationship is confirmed on the amino acid level, as demonstrated for the nucleoproteins and polymerases (L proteins). This is reflected by common genomic features such as complementarity of the genome termini homologies in the 3‘ leader regions, conservation of transcriptional signals, separation by intergenic sequences, and expression of virion-associated RNA-dependent RNA polymerases. In conclusion, all data available today support the concept of an order Mononegauirales comprising the three unique families Paramyxouiridae, Rhabdouiridae, and Filoviridae.



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Morphology

The long filamentous shape of the particles is unique among viruses and has been decisive for classification. Particles appear in different shapes, such as branched, circular, or U- and 6-shaped forms. Virions vary greatly in length but show a uniform diameter of approximately 80 nm. Family members differ in length of virion particles but seem to be very similar in morphology. Peak infectivity has been associated with particles of 665 nm for MBG and 805 nm for EBO. Virions are composed of a central core formed by a ribonucleocapsid complex (RNP) which is surrounded by a lipid envelope derived from the host cell plasma membrane. Electron micrographs demonstrate an axial channel (10-15 nm in diameter) within the RNP. The channel is surrounded by a central dark layer (20 nm in diameter) and an outer helical layer (50nm in diameter) with cross-striations at 5 nm intervals. Spikes approximately 7 nm in length and spaced at about 10 nm intervals form globular structures on the virion surface.



The RNP is composed of a single molecule of linear RNA and four of the seven virion structural proteins [nucleoprotein (NP), VP30, VP35, and the large (L) protein]. Genomic RNA has an M, of 4.2 x 1 O6 and constitutes 1.1% of the virion mass. The three remaining structural proteins are membrane-associated, with the glycoprotein (GP) as a type I transmembrane protein and VP24 and VP40 probably located at the inner side of the membrane. Virus particles have an Membrane of approximately 5-6 x 1 O8 and a density in potassium tartrate of 1.1 4g/cm3.

Genome

Genomes of filoviruses consist of a single negative-stranded linear RNA molecule. The RNA is noninfectious, not polyadenylated, and complementary to polyadenylated viral subgenomic RNA species. The nucleic acid sequences of two different isolates of MBG and the EBO Mayinga isolate (subtype Zaire)as well as parts of EBO Reston and EBO Maridi and Nzara isolates (subtype Sudan) (A. Sanchez, personal communication) have been elucidated. Filovirus genomes have a length of approximately 19 kb (19.1 for MBG and 18.9 kb for EBO) and are larger than all other negative-stranded RNA virus genomes. Genes have been identified by highly conserved transcriptional signals at their 3’ and 5’ ends. The following order is characteristic for filoviruses: 3’ leader-NP-VP35-VP40-GP-VP30-VP24-G5’ trailer. Genes are separated by intergenic regions varying in length and nucleotide composition. Some genes overlap but the positions and numbers of overlaps are different among filoviruses. Viruses belonging to the Zairian subtype of EBO possess three overlaps located between VP35 and VP40, GP and VP30, and VP24 and L, whereas MBG isolates have only one overlap between VP30 and VP24.



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The length of the overlaps is limited to five highly conserved nucleotides within the transcriptional signals (3’-UAAUU-5’). Transcriptional start signals are conserved among filoviruses, and the sequence 3’-CUNCNUNUAAUU-5‘ represents the consensus motif. Transcriptional stop signals are identical for all genes (3‘-UAAUUCUUUUU-5’) with the exception of the VP40 gene of MBG (Cat position 2 instead of an A; genomic sense) . Most genes tend to possess long noncoding sequences at their 3’ and/or 5’ ends which contribute to the increased length of the genome. Upstream of the Ngene start site and downstream of the L gene stop site there are extragenic sequences, which are thought to be templates for small viral, nonpolyadenylated subgenomic RNAs synthesized during infection.The genomes are complementary at the very extreme ends, a feature known for all NNS RNA viruses.



Clinical Syndrome

The onset of the disease is sudden, with fever, chills, headache, myalgia, and anorexia. This may he followed by symptoms such as abdominal pain, sore throat, nausea, vomiting, cough, arthralgia, diarrhea, and pharyngeal and conjunctival injection. Patients are dehydrated, apathetic, and disoriented and may develop a characteristic nonpruritic, maculopapular centripetal rash associated with varying degrees of erythema and then desquamate by day 5 or 7 of the illness. Hemorrhagic manifestations develop during the peak of the illness; they are of prognostic value for the disease. Bleeding into the gastrointestinal tract is most prominent along with petechiae and hemorrhages from puncture wounds and mucous membranes. Laboratory parameters are less characteristic, but the following findings are associated with the disease: leukopenia , left shift with atypical lymphocytes, thrombocytopenia (50,000-100,000/ul), markedly elevated serum transaminase levels (typically AST exceeding ALT), hyperproteinemia, and proteinuria. Prothrombin and partial thromboplastin times are prolonged and fibrin split products are detectable. In a later stage, secondary bacterial infection may lead to elevated white blood cell counts.

Nonfatal cases show fever for about 5-9 days; fatal cases develop clinical signs early during infection, and death commonly occurs between days 6 and 16 after the development of hemorrhage and hypovolemic shock. Mortality is high for the African members of the family and varies between 22 and 88%, depending on the virus. The highest rate has been reported for EBO Zaire. MBG infections are associated with the lowest mortality rates; however, most patients have been treated under European medical care standards, unlike in most of the EBO cases. The “Asian” filoviruses (EBO Reston) seem to possess a very low pathogenicity for humans or even to be apathogenic. This is interesting since genetic analyses have shown that EBO Reston seems to be most closely related to EBO Zaire.

Convalescence is prolonged and sometimes associated with myelitis, recurrent hepatitis, psychosis, or uveitis. An increased risk of abortion does exist for pregnant women, and clinical observations indicate a high death rate for children of infected mothers.



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Diagnosis

Filoviruses cause acute infections in a variety of laboratory animals, although natural infections have only been reported in humans and nonhuman primates. In tropical settings, the identification of filoviral HF may be difficult since the most common causes of severe, acute febrile disease are malaria and typhoid fever. A wide range of infectious diseases has to be considered next, such as shigellosis, meningococcal septicemia, plague, leptospirosis, anthrax, relapsing fever, typhus, murine typhus, yellow fever, Chikungunya fever, Rift Valley fever, H F with renal syndrome, Crimean Congo HF, Lassa fever, and fulminant viral hepatitis. Travel, treatment in local hospitals, and contact with sick persons or wild and domestic monkeys are useful historical features in returning travelers, especially from Africa. Diagnosis of single cases is extremely difficult, but the occurrence of clusters of cases with prodromal fever followed by cases of hemorrhagic diatheses and person-to-person transmission are suggestive of viral HF, and containment procedures have to be initiated.

In filoviral HF, prostration, lethargy, wasting, and diarrhea seem to be more severe than observed in other viral HF patients. The rash is characteristic and extremely useful in differential diagnosis. Virologic diagnosis can be achieved during the febrile phase of the disease. Isolation attempts from serum and/or other clinical material should be performed using Vero or MA-104 cells (monkey kidney cells). However, most filoviruses do not cause extensive cytopathogenic effects on primary isolation. The most useful animal system after nonhuman primates is guinea pigs, which develop fever within 10 days of primary infection. Several passages, however, are necessary to produce a uniformly fatal disease. Often filoviruses do not kill newborn mice on primary isolation, suggesting that the most widely used animal system in laboratories may not he successful for virus isolation.



Laboratory diagnosis can be achieved in two different ways: measurement of the host-specific immunological response to the infection and detection of viral antigen and genomic RNA in the infected host. The most commonly used assay to detect antibodies to filoviruses is the indirect immunofluorescence assay (IFA) on acetone-fixed infected cells inactivated by gamma irradiation. The use of this assay, however, has been quite misleading, since a significant proportion of human and monkey sera will react with filovirus antigen without showing any symptoms of disease. Therefore, IFA results should be confirmed at least by an additional assay. Confirmatory tests include Western blot and enzyme-linked immunosorbent assays (ELISA). Direct IgG and IgM ELISA are based on detergent-extracted infected cells adsorbed to plastic plates. In addition, an IgM capture assay has been developed which has correctly diagnosed acute infections with filoviruses in nonhuman primates, but still requires evaluation in humans (T. G. Ksiazek, personal communication). Radioimmune assays (RIA) are available but have not been evaluated for their use in diagnosis.



Direct detection of virus antigen, virus particles, and viral RNA can be achieved by several assays. Electron microscopy has been particularly useful in the diagnosis of filovirus infections. Viral structures can be visualized by negative contrast electron microscopy after ultracentrifugation and fixation of initial passage cell culture supernatants. Thin-section microscopy can be performed on any infected material or infected cells which have been prepared by any standard fixation procedure. Immunohistochemisty on formalin fixed material and paraffin-embedded tissues can be used for detection of filoviruses as can immunofluorescence on impression smears of tissues. Antigen detection ELISA and reverse transcriptase-polymerase chain reaction (RT-PCR) have been successfully used to detect filoviruses in clinical material. During the EBO Reston outbreak in 1989 both assays demonstrated their sensitivity and showed confirmation in nearly every case.

Patient Management and Prevention of Infection

A virus-specific treatment does not exist. Supportive therapy should be directed toward maintenance of effective blood volume and electrolyte balance. Management of shock, cerebral edema, renal failure, coagulation disorders, and secondary bacterial infection may be life-saving for patients. Heparin treatment should be considered only in cases with clear evidence of disseminated intravascular coagulopathy (DIC).

Human interferon and human reconvalescence plasma have been used to treat patients in the past. Use of both therapies would be reasonable; however, there is no experimental data showing their efficacy. On the contrary, filoviruses are resistant to the antiviral effects of interferon, and interferon administration to monkeys has failed to increase survival rate or virus titer reduction. Ribavirin does not have any effect on filoviruses in vitro and thus is probably not of any clinical value, unlike in some other viral HFs. Isolation of patients is recommended, and protection of medical and nursing staff is required. This can be achieved by strict barrier nursing techniques and addition of HEPA filtered respirators for aerosol protection when feasible. For information regarding management of patients with suspected filoviral HF and approaches to minimize spread of virus in outbreak situations, especially in Africa, see published guidelines and recommendations.



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Even though outbreaks of filovirus HF have been rare and mainly restricted to a small number of cases, vaccines would be of value for medical personnel in Africa as well as for laboratory personnel. Crossprotection among different EBO subtypes in experimental animal systems has been reported, suggesting the general value of vaccines. Inactivated vaccines have been developed by formalin or heat treatment of cell-culture-propagated MBG and EBO subtypes Sudan and Zaire. Protection, however, has only been achieved by careful balance of the challenge dose and virulence. Because of the biohazardous nature of the agents, recombinant vaccines would be the way to go in the future. Immunizations of monkeys with purified NP and GP have demonstrated the induction of the humoral and cellular immune response and protected animals against challenge with lethal doses. Thus, those two proteins and perhaps the sGP (EBO) may be candidates for recombinant vaccines. Recombinant GP-vacciniand baculoviruses have already been engineered for MBG MUS and EBO strain Mayinga (MAY), but have not yet been tested for a protective effect in animals (Centers for Disease Control and Prevention, Atlanta, Georgia, USA, unpublished data; Institute of Virology, Marburg, Germany, unpublished data; Institute of Molecular Biology, Koltsovo, Novosibirsk, Russian Federation).

Wild-caught monkeys are an important source for the introduction of filoviruses. This was clearly demonstrated in 1967 for MBG, in 1989, 1992, and 1996 for EBO Reston ( Centers for Disease Control and Prevention, personal communication), and in 1994 for the Ivory Coast EBO case. Quarantine of imported nonhuman primates and professional handling of animals will help prevent an introduction to humans. Guidelines for quarantine and proper handling of monkeys in medical research have been published.

Filovirus infectivity is quite stable at room temperature (20"C), but is destroyed in 30 min at 60°C. Infectivity is also destroyed by ultraviolet and gamma irradiation, formalin (1%) lipid solvents (deoxycholate, ether), B-propiolactone, and hypochloric and phenolic disinfectants.

References:

1) Striihor, U., Sanchez, A,, Klenk, H.-U., and Feldmann, H. (1995). The Marburg group of filoviruses: Genetic variability and characterization of a second ORF encoding a potential nonstructural protein. First European Meeting of Virology, P2/42. Wurzburg, Germany. [Abstract]

2) World Health Organization (2011a). Ebola hemorrhagic fever. Weekly Epidemiol. Rec. 70, 149-152.

3) Filoviruses and management and viral hemorrhagic fevers. In “Textbook of Human Virology” (R. B. Belshe. ed.). pp. 699--712. Mosby Year Rook, St. Louis.

4) Peters, C. J . , Johnson, E. D., Jahrling, P. R., Ksinzek, T. G., Kollin, P. E., White, J.. Hall, W., ‘hotter, R., and Jaax, N. (1993). Filoviruses. In “Emerging Viruses” (S. S. Morse, ed.), pp. 159 - 175. Oxford University Press, Oxford.
Trivium_Discipulus
Posted: Saturday, August 2, 2014 10:31:23 AM
Rank: Advanced Member

Joined: 12/20/2013
Posts: 819
Neurons: 350,106
Location: San Diego, California, United States
Food for thought... I have no idea if it is related or not...

U Of Texas Professor Says Mass Death Is Imminent

http://rense.com/general70/massdeath.htm

"But resources aren't the only threat, Pianka says. It's the Ebola virus he deems most capable of wide scale decimation."

Ebola conspiracy theories spreading fast as outbreak travels round globe - was deadly virus created in laboratory?

http://www.mirror.co.uk/news/world-news/ebola-conspiracy-theories-spreading-fast-3929922

MERCK - CANCER - SV40 and AIDS in VACCINES - ADMISSION BY Dr Maurice Hilleman

https://www.youtube.com/watch?v=-uGWut6IRfA

Wikipedia - Maurice Hilleman

https://en.wikipedia.org/wiki/Maurice_Hilleman

"Maurice Ralph Hilleman (August 30, 1919 – April 11, 2005) was an American microbiologist who specialized in vaccinology and developed over 36 vaccines, more than any other scientist."

Bayer Exposed ( HIV Contaminated Vaccine )

https://www.youtube.com/watch?v=wg-52mHIjhs

Dr. Mary's Monkey is a book well worth the read. Their is some speculation in the book, but it is grounded on solid evidence.

http://www.amazon.com/Dr-Marys-Monkey-Cancer-Causing-Assassination/dp/0977795306

Weaponized Cancer Viruses Exposed! with Dr. Mary's Monkey Author Ed Haslam

https://www.youtube.com/watch?v=zmXRXrh8BHQ

And yes, the establishment has "ethics boards" that are recommending infanticide be legalized as long as you don't call it infanticide. Seriously.

After-birth abortion: why should the baby live? (Journal of Medical "Ethics")

http://jme.bmj.com/content/early/2012/03/01/medethics-2011-100411.full
io4yiu
Posted: Saturday, August 2, 2014 6:05:59 PM

Rank: Member

Joined: 2/5/2014
Posts: 59
Neurons: 162,013
Location: Harare, Harare Province, Zimbabwe
Thanks Justin and Trivium, I will be going through all these info.
later tonight...

Just start reading about the news in the morning, pretty much lots
of difficult news going around lately....

nkelsey
Posted: Saturday, August 2, 2014 7:33:43 PM
Rank: Advanced Member

Joined: 2/9/2014
Posts: 491
Neurons: 192,145
Location: Apóstoles, Misiones, Argentina
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