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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↗
PubMed1973

Arbovirus studies in Luanda, Angola. 1. Virological and serological studies during a yellow fever epidemic.

A yellow fever epidemic broke out in Luanda, Angola, in January 1971 and was halted in less than 3 months by prompt mass vaccination and intensive antimosquito measures. Nine strains of yellow fever virus were isolated from hospitalized cases, but attempts to isolate the virus from Aedes aegypti mosquitos failed. A serological survey for antibodies to arboviruses in 589 sera from unvaccinated persons showed that two arboviruses were circulating in the epidemic area: the yellow fever virus and the Chikungunya virus responsible for an outbreak of dengue-like disease that occurred shortly before the yellow fever epidemic.

Angola↗
PubMed1996

Use of the yellow fever virus vaccine strain 17D for the study of strategies for the treatment of yellow fever virus infections.

We have employed the attenuated vaccine strain 17D of yellow fever virus (YFV) to evaluate the inhibitory effect of a selected series of compounds on YFV in Vero cells. Use of the vaccine strain does not require high-level microbiological containment facilities and should allow extensive screening. In addition, YFV may serve as a model for other flaviviruses including hepatitis C virus (HCV), and thus strategies for the treatment of YFV infections may apply to flavivirus infections in general. In the present study, several compounds belonging to different classes of nucleoside analogues and polyanions were evaluated for their inhibitory effect on the replication of YFV. Compounds that are targeted at: (i) IMP dehydrogenase (ribavirin, EICAR, tiazofurin, selenazofurin and mycophenolic acid), (ii) OMP decarboxylase (pyrazofurin and 6-azauridine), (iii) CTP synthetase (carbodine and cyclopentenyl cytosine), (iv) dihydrofolate reductase (methotrexate) and the (v) sulfated polymers (dextran sulfate and PAVAS) proved inhibitory to the replication of YFV. Mycophenolic acid (EC50: 0.08 microgram/ml). EICAR (EC50: 0.8 microgram/ml) and methotrexate (EC50: 0.07 microgram/ml) were the most effective. The findings that EICAR and mycophenolic acid, despite their potent anti-YFV activity, had little or no effect on the replication of the bunyavirus Punta Toro or herpes simplex virus in Vero cells, indicates that their anti-YFV activity is rather specific and does not merely result from cytotoxicity. Inhibitors of S-adenosylhomocysteine hydrolase (SAH hydrolase) and thymidylate synthase were found to be devoid of anti-YFV activity.

Animals↗
PubMedDate not supplied

[Reflection on 2 current viral diseases: yellow fever and dengue].

Yellow fever and dengue are two current viral diseases induced by flaviviruses and usually transmitted by the same mosquito vector, Aedes aegypti. From 1987 to 1991, 18,753 cases of yellow fever, mainly from Africa, have been notified to WHO, leading to 4,522 deaths. On the other hand, WHO estimates that 2.5 billions individuals living in tropical areas are at risk to contract dengue fevers. In fact, 500,000 patients are hospitalized each year for dengue hemorrhagic fever/dengue shock syndrome and 90% of them are children. Nevertheless, the control of these two viral diseases would be reached easily in destroying mechanically the mosquito larval resting places. Although superficially similar, the two entities are in fact quite different. Relatively few is known about the pathogenesis of yellow fever whereas, for dengue fevers, it is difficult to integrate so many results accumulated to explain the occurrence of haemorrhagic phenomena according to the two main theories so far proposed which are not exclusive. The immunological one (S.B. Halstead) tries to explain the pathological events by the effect of anti-dengue enhancing antibodies acquired during a previous exposure to one of the dengue viruses, whereas that of increased virus virulence (L. Rosen) refers to fast passages between individuals during explosive epidemics.

Animals↗
PubMed2006

Live attenuated chimeric yellow fever dengue type 2 (ChimeriVax-DEN2) vaccine: Phase I clinical trial for safety and immunogenicity: effect of yellow fever pre-immunity in induction of cross neutralizing antibody responses to all 4 dengue serotypes.

A randomized double-blind Phase I Trial was conducted to evaluate safety, tolerability, and immunogenicity of a yellow fever (YF)-dengue 2 (DEN2) chimera (ChimeriVax-DEN2) in comparison to that of YF vaccine (YF-VAX). Forty-two healthy YF naïve adults randomly received a single dose of either ChimeriVax-DEN2 (high dose, 5 log plaque forming units [PFU] or low dose, 3 log PFU) or YF-VAX by the subcutaneous route (SC). To determine the effect of YF preimmunity on the ChimeriVax-DEN2 vaccine, 14 subjects previously vaccinated against YF received a high dose of ChimeriVax-DEN2 as an open-label vaccine. Most adverse events were similar to YF-VAX and of mild to moderate intensity, with no serious side-effects. One hundred percent and 92.3% of YF naïve subjects inoculated with 5.0 and 3.0 log10 PFU of ChimeriVax-DEN2, respectively, seroconverted to wt DEN2 (strain 16681); 92% of subjects inoculated with YF-VAX seroconverted to YF 17D virus but none of YF naïve subjects inoculated with ChimeriVax-DEN2 seroconverted to YF 17D virus. Low seroconversion rates to heterologous DEN serotypes 1, 3 and 4 were observed in YF naïve subjects inoculated with either ChimeriVax-DEN2 or YF-VAX. In contrast, 100% of YF immune subjects inoculated with ChimeriVax-DEN2 seroconverted to all 4 DEN serotypes. Surprisingly, levels of neutralizing antibodies to DEN 1, 2 and 3 viruses in YF immune subjects persisted after 1 year. These data demonstrated that (1) the safety and immunogenicity profile of the ChimeriVax-DEN2 vaccine is consistent with that of YF-VAX, and (2) preimmunity to YF virus does not interfere with ChimeriVax-DEN2 immunization, but induces a long lasting and cross neutralizing antibody response to all 4 DEN serotypes. The latter observation can have practical implications toward development of a dengue vaccine.

Adolescent↗
PubMed1965

International collaborative assay of the international reference preparation of anti-yellow-fever serum.

A yellow fever immune serum was established in 1962 by the WHO Expert Committee on Biological Standardization as the International Reference Preparation of Anti-Yellow-Fever Serum, intended to serve as an immune reference serum in the mouse protection test used in the control of yellow fever vaccines.Before its establishment as the International Reference Preparation, the proposed material was assayed in eleven laboratories in ten countries against a number of other immune and non-immune sera, and was found stable. Neutralization test results were consistent and the relative potency was sufficiently high. This paper not only reports on the collaborative assay, but also discusses errors in the testing method and problems connected with the distribution of mouse deaths during the observation period and with the preparation of dilutions.

Biological Assay↗
PubMed2004

Viscerotropic and neurotropic disease following vaccination with the 17D yellow fever vaccine, ARILVAX.

Yellow fever vaccine associated viscerotropic (YFV-AVD) and neurotropic (YFV-AND) diseases have been recently identified in various countries. Previously post-vaccination multiple organ system failure was recognised as a rare serious adverse event of yellow fever vaccination and 21 cases of post-vaccinal (YFV) encephalitis had been recorded. Incidence data is not available. On investigation of vaccine surveillance reports from Europe following distribution of more than 3 million doses of ARILVAX trade mark, four cases each of YFV-AVD and YFV-AND were found (each 1.3 cases per million doses distributed) for the period 1991 to 2003. The incidence for each is higher after 1996 (2.5 cases per million doses distributed). The incidence of these adverse events appears to be very low with ARILVAX trade mark. Similar incidence data is required from other countries for comparison.

Encephalomyelitis, Acute Disseminated↗
PubMed2002

Surface expression of an immunodominant malaria protein B cell epitope by yellow fever virus.

The yellow fever 17D virus (YF17D) has several characteristics that are desirable for the development of new, live attenuated vaccines. We approached its development as a vector for heterologous antigens by studying the expression of a humoral epitope at the surface of the E protein based on the results of modelling its three-dimensional structure. This model indicated that the most promising insertion site is between beta-strands f and g, a site that is exposed at the external surface of the virus. The large deletion of six residues from the fg loop of the E protein from yellow fever virus, compared to tick-born encephalitis virus, leaves space at the dimer interface for a large insertion without creating steric hindrance. We have tested this hypothesis by inserting a model humoral epitope from the circumsporozoite protein of Plasmodium falciparum consisting of triple NANP repeats. Recombinant virus (17D/8) expressing this insertion flanked by two glycine residues at each end, is specifically neutralized by a monoclonal antibody to the model epitope. Furthermore, mouse antibodies raised to the recombinant virus recognize the parasite protein in an ELISA assay. Serial passage analysis confirmed the genetic stability of the insertion made in the viral genome and the resulting 17D/8 virus is significantly more attenuated in mouse neurovirulence tests than the 17DD vaccine. The fg loop belongs to the dimerization domain of the E protein and lies at the interface between monomers. This domain undergoes a low pH transition, which is related to the fusion of the viral envelope to the endosome membrane. It is conceivable that a slower rate of fusion, resulting from the insertion close to the dimer interface, may delay the onset of virus production and thereby lead to a milder infection of the host. This would account for the more attenuated phenotype of the recombinant virus in the mouse model and lower extent of replication in cultured cells. The vectorial capacity of the yellow fever virus is being further explored for the expression and presentation of other epitopes, including those mediating T-cell responses.

Amino Acid Sequence↗
PubMed1999

Complete nucleotide sequence and phylogeny of an American strain of yellow fever virus, TRINID79A.

Yellow fever was presumably imported to the Americas from West-Africa from the 16th to the 19th century. American and African genotypes of the virus are distinguishable, indicating separate evolution in different vector/host cycles. The complete nucleotide sequence of the yellow fever virus strain TRINID79A, isolated in Trinidad in 1979, has been established. It exhibits extensive homology with those of current West-African strains and attenuated strain FNV. However, a unique deletion of the 3' non-coding region (NCR) of the viral RNA has been identified. It indicates that RYF1 and RYF2 repeated sequences of the 3' NCR are not necessary to the replication of the virus.

3' Untranslated Regions↗
PubMed1995

Nucleotide sequence variation of the envelope protein gene identifies two distinct genotypes of yellow fever virus.

The evolution of yellow fever virus over 67 years was investigated by comparing the nucleotide sequences of the envelope (E) protein genes of 20 viruses isolated in Africa, the Caribbean, and South America. Uniformly weighted parsimony algorithm analysis defined two major evolutionary yellow fever virus lineages designated E genotypes I and II. E genotype I contained viruses isolated from East and Central Africa. E genotype II viruses were divided into two sublineages: IIA viruses from West Africa and IIB viruses from America, except for a 1979 virus isolated from Trinidad (TRINID79A). Unique signature patterns were identified at 111 nucleotide and 12 amino acid positions within the yellow fever virus E gene by signature pattern analysis. Yellow fever viruses from East and Central Africa contained unique signatures at 60 nucleotide and five amino acid positions, those from West Africa contained unique signatures at 25 nucleotide and two amino acid positions, and viruses from America contained such signatures at 30 nucleotide and five amino acid positions in the E gene. The dissemination of yellow fever viruses from Africa to the Americas is supported by the close genetic relatedness of genotype IIA and IIB viruses and genetic evidence of a possible second introduction of yellow fever virus from West Africa, as illustrated by the TRINID79A virus isolate. The E protein genes of American IIB yellow fever viruses had higher frequencies of amino acid substitutions than did genes of yellow fever viruses of genotypes I and IIA on the basis of comparisons with a consensus amino acid sequence for the yellow fever E gene. The great variation in the E proteins of American yellow fever virus probably results from positive selection imposed by virus interaction with different species of mosquitoes or nonhuman primates in the Americas.

Aedes↗
PubMed1993

[Current situation of yellow fever in Latin America].

Yellow fever endemicity is currently stabilized in South America: an average of 115 cases has officially been notified each year since 25 years (between 12 and 304 annual cases). These figures are underevaluated but no epidemic has been observed since 1983. Only sporadic or limited grouped cases have been reported. All declared cases correspond to people who have been infected within sylvatic areas, mainly adult forestmen. Within the last years, the majority of cases have occurred in Peru and Bolivia; the other cases have been observed in Brazil, in Columbia, in Ecuador and in French Guiana (imported strains from Surinam). This apparently low virus circulation may be due to massive campaigns of vaccination and to mosquito vector control. But this situation could suddenly reverse as observed in the past with yellow fever and the spring of the urban Aedes aegypti vector. Genetic and immunochemical heterogeneity has been demonstrated between South American and African yellow fever strains, which may reveal evolutionary divergence due to different ecological environment between the two continents. Yellow fever definitely remains a topical disease which requires a constant surveillance.

Aedes↗
PubMed2005

Phenotypic and molecular characterization of a non-lethal, hamster-viscerotropic strain of yellow fever virus.

Viscerotropic yellow fever virus (YFV) infection occurs primarily in humans and non-human primates. Lack of an appropriate small animal model of viscerotropic YFV infection has been a major deterrent to molecular studies of viscerotropism. A hamster model of viscerotropic YFV infection has recently been described; however, these studies have focused on hamster-viscerotropic strains of YFV (including Asibi hamster P7 virus) that caused outward clinical signs of infection and mortality. In order to map more closely the molecular determinants of viscerotropism in the hamster model, a second sequential series of seven liver-to-liver passages of Asibi virus was undertaken through hamsters to generate Asibi P7b virus. Asibi hamster P7b virus did not cause clinically detectable signs of YFV infection; however, high quantities of circulating virus were isolated from the serum, and microscopic evaluation of the liver and spleen demonstrated histopathological lesions consistent with YFV infection. The genomic sequence of Asibi P7b virus was determined and compared to wild-type Asibi virus and the lethal, hamster-viscerotropic Asibi P7 virus and found to differ by only two amino acids in the envelope protein, E-98 and E-331.

Amino Acid Substitution↗
PubMed1972

A clinicopathological study of human yellow fever.

During an epidemic of yellow fever in the Jos Plateau area of Nigeria, 9 adult males with clinically diagnosed yellow fever were studied by haematological, biochemical, virological, serological, and liver biopsy methods. The ages of the patients ranged from 20 to 55 years and the duration of illness was 3-62 days. No virus was isolated from any patient but all patients should biochemical evidence of severe hepatocellular damage. Leucopenia was a feature of the late acute stage of the disease. Five sera had antibodies to yellow fever at titres greater than 1: 32, 3 of them being monospecific for yellow fever. The classical histological features of yellow fever were present only in the acute or late acute stages, when complement-fixation tests may be negative. With convalescence and the production of complement-fixing antibodies in high titres, the histological features resembled those of a persisting nonspecific hepatitis. In an endemic area, the histological features of yellow fever will depend on the stage of the disease and a picture of nonspecific hepatitis would not exclude yellow fever in the absence of confirmation from serological tests.

Adult↗
PubMed2002

Rapid detection and quantification of RNA of Ebola and Marburg viruses, Lassa virus, Crimean-Congo hemorrhagic fever virus, Rift Valley fever virus, dengue virus, and yellow fever virus by real-time reverse transcription-PCR.

Viral hemorrhagic fevers (VHFs) are acute infections with high case fatality rates. Important VHF agents are Ebola and Marburg viruses (MBGV/EBOV), Lassa virus (LASV), Crimean-Congo hemorrhagic fever virus (CCHFV), Rift Valley fever virus (RVFV), dengue virus (DENV), and yellow fever virus (YFV). VHFs are clinically difficult to diagnose and to distinguish; a rapid and reliable laboratory diagnosis is required in suspected cases. We have established six one-step, real-time reverse transcription-PCR assays for these pathogens based on the Superscript reverse transcriptase-Platinum Taq polymerase enzyme mixture. Novel primers and/or 5'-nuclease detection probes were designed for RVFV, DENV, YFV, and CCHFV by using the latest DNA database entries. PCR products were detected in real time on a LightCycler instrument by using 5'-nuclease technology (RVFV, DENV, and YFV) or SybrGreen dye intercalation (MBGV/EBOV, LASV, and CCHFV). The inhibitory effect of SybrGreen on reverse transcription was overcome by initial immobilization of the dye in the reaction capillaries. Universal cycling conditions for SybrGreen and 5'-nuclease probe detection were established. Thus, up to three assays could be performed in parallel, facilitating rapid testing for several pathogens. All assays were thoroughly optimized and validated in terms of analytical sensitivity by using in vitro-transcribed RNA. The >or=95% detection limits as determined by probit regression analysis ranged from 1,545 to 2,835 viral genome equivalents/ml of serum (8.6 to 16 RNA copies per assay). The suitability of the assays was exemplified by detection and quantification of viral RNA in serum samples of VHF patients.

Animals↗
PubMed2001

Fever and multisystem organ failure associated with 17D-204 yellow fever vaccination: a report of four cases.

BACKGROUND: In 1998, the US Centers for Disease Control and Prevention was notified of three patients who developed severe illnesses days after yellow fever vaccination. A similar case occurred in 1996. All four patients were more than 63 years old. METHODS: Vaccine strains of yellow fever virus, isolated from the plasma of two patients and the cerebrospinal fluid of one, were characterised by genomic sequencing. Clinical samples were subjected to neutralisation assays, and an immunohistochemical analysis was done on one sample of liver obtained at biopsy. FINDINGS: The clinical presentations were characterised by fever, myalgia, headache, and confusion, followed by severe multisystemic illnesses. Three patients died. Vaccine-related variants of yellow fever virus were found in plasma and cerebrospinal fluid of one vaccinee. The convalescent serum samples of two vaccinees showed antibody responses of at least 1:10240. Immunohistochemical assay of liver tissue showed yellow fever antigen in the Kuppfer cells of the liver sample. INTERPRETATION: The clinical features, their temporal association with vaccination, recovery of vaccine-related virus, antibody responses, and immunohistochemical assay collectively suggest a possible causal relation between the illnesses and yellow fever vaccination. Yellow fever remains an important cause of illness and death in South America and Africa; hence, vaccination should be maintained until the frequency of these events is quantified.

Adverse Drug Reaction Reporting Systems↗