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At least 19 recordsLinked to original sources
PubMed1986

A century of progress in combating yellow fever.

Yellow fever was responsible for several epidemics among the settlers in tropical areas of the Americas and Africa during the 17th to the 19th centuries. Scientific research into its cause and epidemiology was started at the beginning of the present century and progressed well ahead of other viral disease research. However, epidemics still occur and the worst one ever recorded was in Ethiopia in 1960-62. Epidemiological research has recently provided new findings on the ecology of the virus and the risk of epidemics. Recent breakthroughs in the molecular study of the virus should provide new tools for further progress in treatment and control of the disease. Meanwhile, the risk of urbanization of the disease, deficiencies in treatment, limitations in vector control, and erratic policies in preventive immunization present real problems.

Africa↗
PubMedDate not supplied

1987 yellow fever epidemics in Oyo State, Nigeria: a survey for yellow fever virus haemagglutination inhibiting antibody in residents of two communities before and after the epidemics.

A survey for yellow fever haemagglutination inhibiting antibody was carried out before and after the 1987 yellow fever epidemics in Nigeria in two localities in Oyo State, namely: Ibadan and Ogbomosho. A total of 129 sera were collected from the two localities before the epidemic. The overall prevalence of yellow fever HI antibody was 37%. A breakdown of positive sera showed that 30/100 and 18/29 sera tested in Ibadan and Ogbomosho respectively were positive. There was a higher prevalence of HI antibody in males (43%) than in females (32%). Of the 48 yellow fever positive sera 23(47%) contained HI antibody to West Nile and 26(52%) to Potiskum viruses. Following the epidemic and the subsequent mass vaccination campaign with the 17D yellow fever vaccine, 200 sera were randomly collected from the same localities. The overall prevalence of yellow fever HI antibody was 67%. The percentage of positive sera in the individual locality was 63% in Ibadan and 73% in Ogbomosho. No statistical difference was observed in the prevalence of yellow fever antibody in both sexes following the yellow fever vaccination campaign (P greater than 0.05). Tests on yellow fever HI antibody positive sera collected after the vaccination campaign showed that 74% and 82% were positive for West Nile and Potiskum HI antibody respectively. Results of this study showed that despite the massive antiyellow fever vaccination campaign there was still a high percentage of seronegative persons in the two communities.

Age Factors↗
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↗
PubMed1985

[Use of stabilized yellow fever vaccine 17D at the time of the yellow fever epidemic in Burkina Faso in 1983].

During the 1983 yellow fever epidemic in Burkina Faso, vaccinations were performed with a stabilized yellow fever 17D vaccine. Samples of vaccine were collected in different places during the vaccination campaigns. The virus titers of these samples were compared with those of vaccine samples of the same batches stored at--20 degree C in the Institut Pasteur in Dakar. There was no significant decrease of the titer when the vaccine had been stored in the conditions recommended by the expanded programme on immunization. The results confirm the experimental data on the stability of this vaccine. A serological survey carried out in young children showed that about 90% have hemagglutination inhibition antibodies following the vaccination.

Burkina Faso↗
PubMed1990

Protection of mice against yellow fever virus encephalitis by immunization with a vaccinia virus recombinant encoding the yellow fever virus non-structural proteins, NS1, NS2a and NS2b.

Recent evidence of a protective immune response to the flavivirus non-structural protein, NS1, has suggested its incorporation into possible recombinant vaccines. The region of the 17D yellow fever virus (YFV) genome encoding the C terminus of envelope glycoprotein and extending to the N terminus of non-structural protein NS3 (NS1-NS2a-NS2b; nucleotides 2030 to 4940) was expressed in vaccinia virus and physical and immunogenic properties of the NS1 moiety were studied. Recombinant NS1 protein, and native YFV NS1, was detected at the surface of infected cells by immunofluorescence and by immune cytolysis after treatment with anti-NS1 antibody and complement. NS1 was also detected in the extracellular medium as a secreted form. Recombinant NS1 was immunoprecipitated as a single protein of approximately the same size as native 17D YFV NS1. Unboiled, both recombinant and native NS1 formed polymers of high Mr. Immunization of mice with this recombinant vaccinia virus stimulated production of non-neutralizing, complement-fixing cytolytic antibody and conferred partial protection against lethal intracerebral inoculation of mice with live 17D YFV.

Animals↗
PubMed1986

Lethal 17D yellow fever encephalitis in mice. I. Passive protection by monoclonal antibodies to the envelope proteins of 17D yellow fever and dengue 2 viruses.

Monoclonal antibodies to the envelope proteins (E) of the 17D vaccine strain of yellow fever virus (17D YF) and to dengue 2 virus were examined for their ability to confer passive protection against lethal 17D YF encephalitis in mice. All 13 IgG anti-17D YF antibodies, regardless of neutralizing capacity, conferred solid protection when given in a relatively high dose prior to intracerebral inoculation of virus. Three antibodies with high in vitro neutralizing titres were all protective at a low dose as were several non-neutralizing antibodies. One flavivirus group-reactive antibody to dengue 2 virus conferred similar protection at low dose. Protection was also observed when antibodies were given several days after virus inoculation when peak infectious virus titres and histopathological evidence of infection were present in brains. The ability of a non-neutralizing antibody to protect could not be attributed to complement-dependent lysis of virus-infected cells and did not correlate with avidity or with proximity of its binding site to a critical neutralizing epitope of the E protein. Some antibodies, characterized as non-neutralizing by plaque reduction assay on Vero cells, inhibited the growth of virus in a mouse neuroblastoma cell line, suggesting one possible mechanism of protection. These results may be relevant to the design of prospective flavivirus vaccines and support the possibility of conferring broadened protection among flaviviruses by stimulating the antibody response to appropriate epitopes of the E protein.

Animals↗
PubMed1989

Association of IDDM and attenuated response of 2',5'-oligoadenylate synthetase to yellow fever vaccine.

Basal and yellow fever vaccination-induced 2',5'-oligoadenylate synthetase (2',5'A) activity was determined in blood mononuclear cells (peripheral blood lymphocytes [PBLs]) from insulin-dependent diabetes mellitus (IDDM) and matched control subjects. The live attenuated yellow fever vaccine represented a primary stimulus in all subjects. First, basal 2',5'A activity increased severalfold in response to yellow fever vaccination. In IDDM subjects, this increase was significantly lower (P = .025). Second, the 2',5'A activity increased proportionately to the higher basal 2',5'A activity in IDDM subjects. In control subjects, the increase in 2',5'A activity was not dependent on the basal activity. There was no relationship between basal or stimulated 2',5'A activity and age, sex, duration of IDDM, age at onset of IDDM, metabolic control, or HLA-DQ beta-chain gene polymorphism. There is a direct relationship between 2',5'A activity and latent viral infections associated with the presence of double-stranded RNA and with cellular interferons (IFNs) formed in response to viral infections. The higher basal 2',5'A activity (P = .05) in relation to the stimulated activity may therefore signify a latent infection or the presence of double-stranded RNA in PBLs of IDDM subjects. In vitro stimulation of PBLs showed increased IFN sensitivity in IDDM subjects. Analysis of 2',5'A activity is proposed to be a sensitive measure of the activation of the IFN system and the level of latent infectivity.

2',5'-Oligoadenylate Synthetase↗
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

The thermal stability of yellow fever vaccines.

The assessment of yellow fever vaccine thermostability both in lyophilized form and after reconstitution were analyzed. Two commercial yellow fever vaccines were assayed for their thermal stability. Vaccines were exposed to test temperatures in the range of 8 degrees C to 45 degrees C. Residual infectivity was measured by a plaque assay using Vero cells. The titre values were used in an accelerated degradation test that follows the Arrhenius equation and the minimum immunizing dose was assumed to be 10(3) particles forming unit (pfu)/dose. Some of the most relevant results include that (i) regular culture medium show the same degradation pattern of a reconstituted 17D-204 vaccine; (ii) reconstituted YF-17D-204 showed a predictable half life of more than six days if kept at 0 degrees C; (iii) there are differences in thermostability between different products that are probably due to both presence of stabilizers in the preparation and the modernization in the vaccine production; (iv) it is important to establish a proper correlation between the mouse infectivity test and the plaque assay since the last appears to be more simple, economical, and practical for small laboratories to assess the potency of the vaccine, and (v) the accelerated degradation test appears to be the best procedure to quantify the thermostability of biological products.

Drug Stability↗
PubMed1990

[The quality standardization of a national vaccine against yellow fever].

One of the commercial lots of yellow fever vaccine has been attested as the National Branch Standard (NBS) of yellow fever vaccine. This NBS has been studied in all tests required by the regulations for standard vaccines. The NBS has been found to meet the necessary requirements in all its characteristics. The study of the thermostability of the NBS at temperatures of 4-10 degrees C, 20-22 degrees C, 37 degrees C during storage for 24 hours to 1 year has revealed the rapid loss of the infectious capacity of the virus at the above temperatures and its high stability during storage at -20 degrees C. Thus, the NBS has been found to retain the required level of immunizing potency for 3 months at a temperature of 4-10 degrees C, for 1 month at 20-22 degrees C and for 2 weeks (the term of observation) at 37 degrees C. The heat resistance of the NBS of yellow fever vaccine corresponds to the WHO requirements. The newly developed NBS has been used as the standard preparation for controlling 27 lots of commercial yellow fever vaccine.

Animals↗
PubMed1988

Epidemic yellow fever in eastern Nigeria, 1986.

An epidemic of yellow fever occurred in the eastern part of Nigeria during the second half of 1986. Oju, in Benue State, was the most heavily affected region, but yellow fever also occurred in surrounding areas, particularly Ogoja, in Cross River State. In Oju, the mean attack and mortality rates were 4.9% and 2.8%, respectively. Sex and age specific rates were highest in males and in the 20-29 yr age group. The overall case fatality rate was approximately 50%. Diagnosis was confirmed by IgM capture enzyme-linked immunosorbent assay (ELISA) and complement fixation (CF) tests. Entomological investigations implicated Aedes africanus as the epidemic vector. Oju alone probably had about 9800 cases of yellow fever with jaundice, and some 5600 deaths. Outbreaks of this nature could be prevented by inclusion of yellow fever in the Expanded Programme on Immunisation, in areas subject to recurrent epidemics.

Adolescent↗
PubMed1990

Yellow fever haemagglutination-inhibiting, neutralising and IgM antibodies in vaccinated and unvaccinated residents of Ibadan, Nigeria.

A survey for yellow fever virus haemagglutination inhibiting (HI) and neutralising (N) and IgM antibodies was carried out in unvaccinated people in Ibadan and in those immunised with the yellow fever 17-D vaccine. A total of 207 people were tested for HI antibody to yellow fever and two other flaviviruses namely: Wesselsbron and Uganda S. viruses. Prevalence of HI antibody to each flavivirus antigen was as follows: Yellow fever 26%, Wesselsbron 18% and Uganda S 33%. Of the 207 people, 37 (18%) had yellow fever N antibody. There was a higher prevalence of N antibody to yellow fever virus in adults than children. Twenty-one people vaccinated with 17-D yellow fever vaccine donated post-vaccination sera; 10 (48%) had no prevaccination HI antibody, 7 (33%) had HI antibody to one flavivirus and 4 (19%) to two or more flaviviruses. Ninety percent of seronegative people and all those with prevaccination flavivirus antibodies developed HI or N antibody, following vaccination. A total of 58 unvaccinated people were tested for yellow fever IgM antibody by an enzyme linked immunosorbent assay, 2 (3%) were positive; suggesting that active yellow fever transmission was in progress at the time of survey.

Adolescent↗
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↗
PubMedDate not supplied

Replication, tissue tropisms and transmission of yellow fever virus in Aedes albopictus.

Experimental studies undertaken to ascertain the dynamics of yellow fever virus replication in an introduced strain (Houston) of the Asian mosquito, Aedes albopictus (Skuse), indicate that this species is an efficient vector of yellow fever virus. Replication of virus in Ae. albopictus could be detected 3 d after feeding on a suspension containing 7.2 log10 Vero cell plaque forming units (PFU) per ml of virus; peak titres (3.5 log10 PFU/mosquito) occurred 7 d after exposure. Viral antigen, visualized by immunofluorescence, was first detected in midgut cells 4 d after exposure and appeared in fat cells 7 d after exposure. The only other mosquito tissues revealing viral antigen were the salivary glands, brain, and occasionally cells of the suboesophageal ganglion. Viral antigen was not detected in any of the tissues of the reproductive tract, nor could viral genomic ribonucleic acid (RNA) be detected in these tissues by RNA-RNA molecular hybridization in situ. We detected no vertical transmission of yellow fever virus in 6180 F1 adult progeny produced from infected females. The extrinsic incubation period at 26.7 degrees C was 9 d. We conclude that the Houston strain of Ae. albopictus is a competent vector of yellow fever virus and can serve as bridging vector between the jungle yellow fever cycle and the urban cycle in New World ecosystems.

Adipose Tissue↗