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Current Inhibitors of Dengue Virus
Published in Venkatesan Jayaprakash, Daniele Castagnolo, Yusuf Özkay, Medicinal Chemistry of Neglected and Tropical Diseases, 2019
J. Jonathan Harburn, G. Stuart Cockerill
Both the R form of 6-1 and 6-2 were active against DENV2 and 3 but not DENV1 or 4. Of other viruses evaluated, only moderate activity was observed for yellow fever virus for 6-2 (6.4 μM). R form 6-1 showed a 2 log suppression in viral titre up to 10 hours post infection and resistance studies located the V63 residue as the key point of mutation in the NS4B (polymerase) gene. Interestingly, this V63 mutation is conserved in DENV2 and 3 but not retained in DENV1 and 4. Direct interaction with this gene was demonstrated through the preparation of a 3H labelled 6-2, gel filtration of the labelled compound in combination with an NTD NS4b construct was observed. No co-elution with a V63I mutant construct was observed. Further publications on the expansion of this series into DENV1 and 4 inhibition are awaited.
Yellow Fever
Published in James H. S. Gear, CRC Handbook of Viral and Rickettsial Hemorrhagic Fevers, 2019
Wilbur G. Downs, Robert E. Shope
This recognition5 of the transmission of yellow fever virus by a mosquito, specifically Aedes aegypti, a mosquito of pantropical distribution, even capable of making incursions into contiguous Palaearctic and Nearctic regions, and a mosquito commonly associated with man and human habitation, stimulated investigations into other diseases with possible arthropod vectors as factors in cycles of transmission. These studies continue up to the present time. Deriving from such studies is the present position of a number of viruses under a main heading of “enveloped RNA viruses”. These enveloped viruses are broken down into a series of groupings including the “alphaviruses”, “flaviviruses”, including yellow fever, “bunyaviruses”, and others.9 The International Catalogue of Arboviruses10 contains a frequently revised updating of the several groups. This involves updating the more than 400 arthropod-borne viruses. Many of the enveloped RNA viruses are indeed arthropod-transmitted, but there are important members which are not, including measles, influenza, the agent causing AIDS (be it LAV or HTLV-III), and others.
Bites and stings
Published in Biju Vasudevan, Rajesh Verma, Dermatological Emergencies, 2019
Yellow fever: This is caused by the yellow fever virus that is transmitted by the Aedes aegypti mosquito. In severe cases it causes high fever, jaundice, epigastric pain with vomiting, prostration, dehydration, deteriorating kidney function, epistaxis, hematemesis, and CNS manifestations such as confusion; coma, seizure, and death may occur within 7–10 days of onset.
Mayaro virus detection in patients from rural and urban areas in Trinidad and Tobago during the Chikungunya and Zika virus outbreaks
Published in Pathogens and Global Health, 2021
Gabriel Gonzalez-Escobar, Candice Churaman, Carlos Rampersad, Risha Singh, SueMin Nathaniel
In the Americas, urban-dwelling Aedes aegypti mosquitoes are the primary vectors for the more common arboviruses including CHIKV, Yellow Fever virus, DENV, and MAYV [24]. The anthropophilic nature of the Aedes aegypti mosquitoes as well as the movement of these mosquitoes and their host to urban environments and their ability to effectively carry the MAYV offers a great opportunity for the expansion of the virus into more developed areas. Such movement increases the probability of a new epidemic [25]. In vitro studies conducted by Pereira et al. [26], have demonstrated the vector competence of A. aegypti and A. albopictus in the transmission of MAYV. The spillover in transmission from rural forested habitats into urbanized areas could be possible due to the evolution of mosquito species within the Aedes and the Culex mosquitoes having the ability to bear the virus [13,27].
Vogt–Koyanagi–Harada-like Disease following Yellow Fever Vaccination
Published in Ocular Immunology and Inflammation, 2021
Wesley R. Campos, Sarah P. F. Cenachi, Matheus Schmidt Soares, Priscila Freitas Gonçalves, Daniel V. Vasconcelos-Santos
Magnetic resonance imaging of the head and chest X-ray were unremarkable. Tuberculin skin test, as well as serological tests for hepatitis B and C, herpes simplex virus, human T-lymphotropic virus, HIV, and syphilis (venereal diseases research laboratory and fluorescent treponemal antibody absorption tests), was negative. Positive results were only for anti-cytomegalovirus and anti-varicella zoster virus IgG antibodies, and not IgM, in the serum. Results of other investigations were unremarkable, including full blood count, C-reactive protein, erythrocyte sedimentation rate, serum rheumatoid factor, angiotensin-converting enzyme, antinuclear antibodies, and antineutrophilic cytoplasmic antibodies (p- and c-antineutrophilic cytoplasmic antibodies). Lumbar puncture was performed and disclosed mild cerebrospinal fluid (CSF) pleocytosis (cells/mm3, with predominance of neutrophilic granulocytes −60%) and increased protein level (55 mg%). RNA of yellow fever virus was not found in serum or CSF by reverse-transcriptase polymerase chain reaction, and no pathogens were detected in cerebrospinal fluid culture.
Rapid travel to a Zika vaccine: are we heading towards success or more questions?
Published in Expert Opinion on Biological Therapy, 2018
Carl Britto, Christina Dold, Arturo Reyes-Sandoval, Christine S. Rollier
The development of effective vaccines against flaviviruses is possible: vaccines against yellow fever virus, Japanese encephalitis, tick-borne encephalitis and dengue viruses are licensed. However, vaccine development for ZIKV poses unique problems. The small number of symptomatic infections and the incidence of the severe endpoints cause difficulties in designing efficacy trials, as these will require a rather large sample size in both, the experimental and control arms to demonstrate protective efficacy. Acquiring these prohibitively large numbers may prove to be challenging given the recent trend of decreasing symptomatic cases, particularly in the current context of declining incidence of ZIKV infection. The declining rates of ZIKV infection in South and Central America is also a rate limiting step for developing new diagnostic tools as reported in the proceedings of a recently held meeting discussing ZIKV diagnostics [85]. The absence of a correlate of protection, as well as difficulties in choosing meaningful endpoints in gauging vaccine impact, both contribute to the difficulties in ZIKV vaccine development. Moreover, the animal challenge models used to establish preclinical efficacy (interferon-gamma deficient mice, non-human primates where ZIKV infection is asymptomatic) might not be relevant, specifically with regard to the potential safety issues surrounding ADE and neurovirulence.