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At least 19 recordsLinked to original sources
PubMed1992

Recombinant vaccinia virus producing the prM and E proteins of yellow fever virus protects mice from lethal yellow fever encephalitis.

Four recombinant vaccinia viruses were constructed for expression of different portions of the 17D yellow fever virus (YFV-17D) open reading frame. A recombinant, vP869, expressing prM and E induced high titers of neutralizing and hemagglutination inhibiting antibodies in mice and was protective against intracranial challenge with the French neurotropic strain of YFV. Levels of protection were equivalent to those achieved by immunization with the YFV-17D vaccine virus. Recombinant vaccinia viruses expressing E and NS1, C prM, E, NS1, or only NS1 failed to protect mice against challenge with YFV despite eliciting antibodies to NS1. The vP869-infected HeLa cells produced a particulate extracellular hemagglutinin (HA) similar to that produced by YFV-infected cells, supporting previous studies with Japanese encephalitis virus (Mason et al., 1991), suggesting that the ability of recombinant vaccinia virus to produce extracellular HA particles is important for effective flavivirus immunity.

Animals↗
PubMed1992

Unto the least of these: the Howard Association and yellow fever.

Epidemics of yellow fever in mid-19th century America caused, in the port cities of the South, devastation and death almost unequalled in this country's history. In response to this horror, a benevolent organization of young men was formed to minister to the unfortunate victims through visitations, nursing care, supplies, and compassion. The group adopted the name Howard Association in honor of the British philanthropist and reformer, John Howard. This paper is an attempt to introduce this little-known society to 20th century readers by taking a brief look at some of the records of Howard Associations in several southern cities: New Orleans, Memphis, Norfolk, and Charleston.

Disease Outbreaks↗
PubMedDate not supplied

[Serological and entomological study on yellow fever in Sierra Leone].

In a serological and entomological survey on yellow fever carried out in Sierra-Leone in 1972, altogether 899 sera from children 0 to 14 years were tested with 12 antigens by haemagglutination-inhibition and complement fixation tests. Mouse neutralization test with yellow fever, West-Nile and Zika viruses were also performed on selected sera. Generally speaking, the incidence of arboviruses is low but the prevalence of antibodies for some viruses was found to vary considerably between different areas. As regards yellow fever, the virus has recently been in circulation in only two areas: Bafodia and Lalehun-Labour Camp and there is no risk for a yellow fever outbreak to occur in the near future. Due to the shortness of the survey, entomological prospections were confined to a search for Ae. aegypti larvae in and around dwellings: no breeding places are found in houses and Breteau indices are usually low, especially in forest villages. On the other hand, in urban settlements in the mining areas, breeding places around houses are numerous and are bound to increase in number. All the conditions necessary for the outbreak of an epidemic would be present within few years: such a situation would appear in Labour Camp where yellow fever virus has been circulating, where most of the population has no immunity and where Breteau indice goes as high as 34.4. As regards the other arboviruses, Zika virus is active in most areas and Chikungunya virus is particularly active in the plateau and savanna zones, in the North-East.

Aedes↗
PubMed2026

Identification of an unannotated early embryonic single-minded transcript in the yellow fever mosquito Aedes aegypti.

The yellow fever mosquito, Aedes aegypti , is a cosmopolitan species that serves as the vector of multiple disease causing agents including dengue, chikungunya, Zika, and yellow fever viruses. The genome of Ae. aegypti has been characterized at the chromosome level, but further manual refinement is required for genes and isoforms with transient expression or low abundance. Here we report on the identification of an early embryonic transcript for the single-minded (sim ) gene in Ae. aegypti , and present the putative promoter for the transcript. The identification of an early-driven transcript is consistent with the annotation for sim in Drosophila melanogaster.

Journal Article↗
PubMed1977

A yellow fever epizootic in Zika forest, Uganda, during 1972: Part 1: Virus isolation and sentinel monkeys.

The results of the yellow fever immunity survey of Central and East Africa reported by SAWYER & WHITMAN in 1936 prompted scientists to undertake well-planned epidemiological studies on yellow fever in eastern Africa. A Yellow Fever Research Institute (the present East African Virus Research Institute) was established at Entebbe in 1936 for this purpose. One of the areas where much work has been carried out is a strip of typical tropical forest, the Zika Forest, 12 kilometres from the Institute. Routine surveillance work, particularly on the biting activity of the yellow fever vector mosquitoes, has been going on since 1946. It was during one of these studies in 1972 that the first yellow fever virus strain was isolated from Aedes africanus collected from the Zika and Sisa forests and one strain was isolated from Coquillettidia fuscopennata, also from the Zika Forest. Three sentinel rhesus monkeys, nomimmune to YF, which were kept in the Zika Forest during the time of the epizootic died of YF disease. The present observations indicate that YF is still present in Africa, and as such it still remains a potential menace to the human population. The epidemiological implications are discussed.

Aedes↗
PubMed1978

An epidemic of yellow fever in central Brazil. 1972-1973. I. Epidemiological studies.

An epidemic of jungle yellow fever occurred in Goiás State, Brazil, between December 1972 and March 1973. Laboratory confirmed cases were observed in 36 counties located in the central and southern parts of the State. Seventy-one cases were proved, of which 44 were fatal. The diagnosis was made on the basis of pathology, serology, and virus isolation. Besides yellow fever, malaria and viral hepatitis were present, and in two fatal cases there was malarial pigment in the liver in addition to the specific lesions associated with yellow fever virus infection. The fact that male patients strikingly outnumbered females (9:1) and that young adults were predominantly affected indicates that transmission occurred mainly inside or adjacent to the forests. The lack of cases in urban areas can be attributed to the absence of Aedes aegypti in these areas. Yellow fever complement-fixing antibody in high titers was found in 18 of 1,201 (1.4%) persons living in eight counties of the affected area. This finding suggests that at least 21,000 persons out of the 1.5 million rural inhabitants of the three districts where the epidemic occurred had been infected by the virus. The epidemic subsided following an intensive vaccination campaign, and the last four cases were observed in March 1973.

Adolescent↗
PubMed1991

[A new combined vaccine against yellow fever and measles in infants aged 6 to 24 months in Mali].

In a rural area in Mali, 453 children were randomly enrolled in a study comparing the safety and the immunogenicity of a combined yellow-fever-measles freeze dried vaccine with each yellow-fever and measles separate administration. Children were divided in 2 populations 4-8 and 12-24 month old. 249 were controlled for measles (inhibition of hemagglutination) and yellow-fever (seroneutralization) antibodies. Seroconversion rates for measles were 82% when administrated before 9 months and 100% when given in 12-24 months period. Measles GMT is similar whatever the schedule or the age group; so, early vaccination does not impair the immunogenetic response. Moreover, 96% of the children vaccinated before 9 months still have detectable measles protective antibodies 8 months after. Among the initially seronegative children, the yellow-fever response is satisfactory with 92 to 96% seroconversion rate and post-immunization GMT ranging 16.5 to 29.5 without any statistical difference between the vaccine and age groups. The safety of the combined yellow-fever-measles vaccine is assessed by the rare number of reactions which are equivalent with the normally expected reactions with each vaccine administered separately. The results demonstrate the satisfactory immunogenicity and safety of the combined yellow-fever-measles vaccine. Combine yellow-fever-measles vaccination could help to improve the feasibility of EPI.

Age Factors↗
PubMed1975

Concurrent and consecutive infection and immunisation with yellow fever and UGMP-359 viruses.

Concurrent and consecutive infection and immunisation with yellow fever virus and UGMP-359 virus was investigated in mice, using identical doses of both viruses. In double infection it was shown that both viruses could multiply independently of one another, when both were inoculated simultaneously by the intracerebral route. On the other hand, there was mutual exclusion between them when the inoculation of one antedated the other, by the same intracerebral route. Both viruses multiplied to similar titres, in single infection, in the target organ (brain). By the intraperitoneal route, the outcome was influenced byhe relative sensitivity of this route of inoculation to support and sustain the replication of either virus. Thus, because yellow fever virus replicated more than UGMP-359 after intraperitoneal inoculation, the latter is always excluded, even when the inoculation ofUGMP-359 preceded that of yellow fever. In the double immunization studies it was shown that comparative specific antibody titres to both viruses were obtained either when both viruses, as immunogens, were given simultaneously, or when the inoculation of one was alternated, at weekly intervals, with the other.

Animals↗
PubMedDate not supplied

[A comparison of the serological effects of classical cholera vaccine and of purified fraction vaccine, with or without simultaneous yellow fever vaccine (author's transl)].

In order to test whether simultaneously administered cholera vaccine has a depressive effect on yellow fever vaccine, a controlled trial was undertaken on school-age children in the South-Central Province of Cameroun. In addition to this principle objective, the study also permitted a comparison of the serological response in subjects vaccinated with classical cholera vaccine and in those vaccinated with a purified fraction vaccine, either with or without simultaneous yellow fever vaccine. The evaluation was measured by changes in vibriocidal antibodies and cholera agglutinins 30 days after vaccination. Only subjects without cholera antibodies prior to the study, were included. 1) Results obtained by assay of vibriocidal antibodies. It was confirmed that, no matter which cholera vaccine was used, the simultaneous administration of yellow fever vaccine had no influence on the percentage of subjects showing a significant rise in vibriocidal antibodies (4-fold increase in titre) following vaccination. In addition, in this study the purified fraction vaccine resulted in a significantly higher rate of seroconversion than did the classical vaccine. However, in comparison to other studies using classical cholera vaccine, our figures for seroconversion after purified fraction vaccine show very little, if any, differences. 2) Results obtained by assay of agglutinating antibodies. When measured by this method, there was a high frequency of non-reactors to the vaccines. This may be attributed to the date of the post vaccination blood speciment (30th day after vaccination). It has been shown that agglutinins decay rapidly after the 15th day following clinical cholera. Thus, the late date of the second speciment after vaccination could explain why we were unable to show any difference in the level of agglutinin after either classical or purified cholera vaccination. The simultaneous administration of the yellow fever vaccine did not influence the titre of agglutinins induced by the classic cholera vaccine. On the other hand, using the association, the seroconversion rate as observed on the 30th day post vaccination was significantly higher than that observed when the fraction was administered alone. If one accepts the generally admitted specificity of the agglutination reaction after clinical disease, two hypotheses can be considered: a) the yellow fever vaccine has an adjuvant effect for the production of antibodies induced by the purified fraction vaccine, or b) the addition of yellow fever vaccine has a retarding effect on the elimination of the agglutinins which, in the natural disease, are rapidly eliminated. Further studies to verify these hypothesis should be undertaken.

Adolescent↗
PubMed1992

Human fatal yellow fever. Immunohistochemical detection of viral antigens in the liver, kidney and heart.

An immunohistochemical method to detect yellow fever antigen was developed using immune sera from rabbits and hamsters and hyperimmune ascitic fluid from mice. A search for the antigen was carried out in liver, kidney and heart in three fatal cases of yellow fever. In the liver it was present in the cytoplasm of hepatocytes, Councilman bodies and Kupffer cells. Yellow fever antigen was also detected in renal tubular epithelium and in groups of myocardial fibers. These findings suggest that viral replication occurs at sites other than the liver. Since yellow fever shares many features with other haemorrhagic fevers the use of immunohistochemistry can impart a significant improvement in the accuracy of its histopathological diagnosis.

Adult↗
PubMed1992

Yellow fever epidemics and mortality in the United States, 1693-1905.

Yellow fever epidemics struck the United States repeatedly in the 18th and 19th centuries. The disease was not indigenous; epidemics were imported by ship from the Caribbean. Prior to 1822, yellow fever attacked cities as far north as Boston, but after 1822 it was restricted to the south. Port cities were the primary targets, but the disease occasionally spread up the Mississippi River system in the 1800s. New Orleans, Mobile, Savannah, and Charleston were major targets; Memphis suffered terribly in 1878. Yellow fever epidemics caused terror, economic disruption, and some 100,000-150,000 deaths. Recent white immigrants to southern port cities were the most vulnerable; local whites and blacks enjoyed considerable resistance.

Disease Outbreaks↗
PubMed1978

[Isolation in east Senegal of a yellow fever virus strain from a pool of Aedes belonging to the subgenus Diceromyia].

During an epidemiological survey of yellow fever in Eastern Senegal, one strain of yellow fever virus was isolated in December 1976 from wild Mosquitoes. This first isolate obtained in nature from Aedes subgenus Diceromyia shows the primordial part these vectors may have in the area studied. It corroborates the existence of a selvatic focus of yellow fever in this region. It also gives information on the transmission cycle in a dry area.

Aedes↗
PubMedDate not supplied

Use of MAC-ELISA for evaluation of yellow fever vaccination.

An evaluation of the IgM antibody immune response against yellow fever using strain 17D was carried out by MAC-ELISA and PRNT. The results showed an agreement of 97% between both tests and the authors conclude that MAC-ELISA can be used as a specific and sensitive assay to replace the PRNT for detecting yellow fever antibodies in human sera, after vaccination programs.

Antibodies, Viral↗
PubMed1979

Transovarial transmission of yellow fever virus by mosquitoes (Aedes aegypti).

Female Aedes aegypti mosquitoes infected with yellow fever virus by intrathoracic inoculation transmitted the virus to a small percentage of their F1 progeny. Infected offspring were obtained from surface-sterilized as well as from untreated eggs, indicating that the virus was transovarially transmitted. Vertical transmission of yellow fever virus in mosquitoes may be an alternative mechanism for biological survival of the virus during adverse periods or in the absence of susceptible vertebrate hosts.

Aedes↗
PubMed1977

[A contribution to infection with yellow fever virus 17D in chick embryos (author's transl)].

During the production of yellow fever virus 17 D vaccine from chick embryos, few embryos die in the time between injection of the eggs and harvest of the embryos. In order to answer the question whether the death of the embryos is due to the infection or to the injury caused by the injection, it is necessary to examine the embryos macro- and microscopically for pathological changes. 8 and 9 days old chick embryos were inoculated into the amniotic cavity with different concentrations of yellow fever virus 17 D (table 1). The embryos were removed from the eggs between the 2nd and 7th day after inoculation. Heart, lung, kidney, brain, liver, and spleen were removed. Macroscopically observable pathological symptoms of the embryos and their organs were recorded. Sections of the organs were histologically investigated. Some embryos died soon after the infection, others on the 5th and 6th day of incubation (table 2). Their death was dependent on the dosage of the inoculum. Macroscopically, some embryos showed oedemas, petechiae on head and trunk, haemorrhages of liver and kidney, enlargement of liver and spleen, and a yellow discolouration of the liver (table 3). Microscopically, liver and brain showed the greatest pathological changes; heart and kidney were also affected, whereas lungs and spleen seemed to be unaffected. The following pathological changes were observed: slight fatty degeneration, oedemas, vascular inflammation, perivascular infiltrates, diffuse infiltrations, infiltrations in form of small nodules and necroses (table 3 and figures 1-12). the severity of the symptoms was evaluated using arbitrary units. These units are summarized on table 3 according to time of occurrence p.i., to virus dilution, to organ, and to type of symptom. An index of pathological changes was allived by dividing the sum of units by the number of organs. The maximum value of the index was demonstrable in liver and brain (table 4). Figure 13 adn table 5 show the development of the lesions during the infection. The maximum value of the index was reached on the 5th day p.i. The most significant pathological changes, as necrosis and perivascular infiltrate, were mainly observed from the 5th day p.i. on (table 6). The perivascular infiltrates were found in heart and brain, the necroses in brain and liver (table 7).

Animals↗
PubMed1977

A yellow fever epizootic in Zika Forest, Uganda, during 1972: Part 2: Monkey serology.

During the 1972 yellow fever epizootic in Zika Forest, Uganda, sera from 21 monkeys shot in a number of forests around the Entebbe area were tested for the presence of a number of arbovirus antibodies. All sera were tested for antibodies against Chikungunya (CHIK), O'nyong-nyong (ONN), Zika, yellow fever (YF) West Nile (WN) and Wesselsbron (WESS) by the haemagglutination-inhibition (HI) test. Because of the crossreaction within the flaviviruses (group B arboviruses) mouse protection test (PT) was also carried out on the sera against YF, WESS and Zika viruses. Serological studies carried out on monkey sera from different parts of Uganda, including the Entebbe area, during 1968 gave results which reflected a surprisingly low rate of YF immune monkeys (3%) throughout the country compared with the rate of over 40% immune monkeys obtained by Haddow et al. in 1951. 40% of the monkey sera collected during 1972 were immune to YF by the PT. Since no YF virus had been isolated between 1968 and 1972 the results indicate strongly that the monkeys in the Entebbe area were involved in the epizootic of 1972. No sick or dead monkeys were found in all the forests checked around Entebbe area during the epizootic. This indicates that the animal-to-animal cycle of the equatorial African forests involved the mild endemic infection characteristic of a virus in its natural habitat and infecting its natural host.

Animals↗
PubMed1992

Sowing the seeds of neo-imperialism: the Rockefeller Foundation's yellow fever campaign in Mexico.

The Rockefeller Foundation's campaign against yellow fever in Mexico sought to advance the economic and political interests of U.S. capitalism. The campaign was implemented at a time of strong anti-American sentiments on the part of the Mexican people. With no diplomatic relationships between Mexico and the United States, the Rockefeller Foundation presented its campaign as an international commitment. Thus, Foundation doctors became the most salient U.S. diplomats. At the same time they made sure that the Mexican yellow fever would not spread to the United States through the southern border. The by-products of the campaign went beyond the political arena. Special techniques to combat the vectors allowed the Rockefeller Foundation's brigades to change the anti-American sentiments of the people. When the campaign ended, the Foundation had already set in place the foundation for the modern Mexican health care system. Benefits from the campaign also accrued to President Obregón, who used the campaign to strengthen his position of power. Mexican doctors adopting a pro-American attitude also allied with the Rockefeller Foundation to gain reputation and power within the emerging Mexican State.

Cause of Death↗