The reaction of a mangabey monkey (<i>Cercocebus galeritus agilis</i>Milne-Edwards) to inoculation with yellow fever virus

Jp, Woodall

doi:10.1080/00034983.1968.11686593

Cited by 7 publications

(3 citation statements)

References 9 publications

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“…The ability of SMs to produce Ab responses even to viruses whose recognition by the innate immune system involves TLR7/9 may enable them to resist the range of potentially pathogenic virus infections they encounter in the wild. Indeed, experimental infection of SMs with pathogenic YFV has been reported to result in transient viremia that is cleared coincident with the production of YFVThe Journal of Immunologyneutralizing Abs (13). This feature, in concert with the discrete nature of the alteration in TLR7/9 signaling in SMs, as well as the apparent redundancy in innate immune activation inferred from studies of individuals with specific inherited polymorphisms (70), may explain why SMs are nevertheless able to control most infections.…”

Section: Discussionmentioning

confidence: 97%

“…SIV from chimpanzees has given rise to HIV-1 in humans, and SIV from a second primate reservoir host, the sooty mangabey (SM), is the zoonotic origin of SIVmac in rhesus macaques (RMs) and HIV-2 in humans (10). Similar to SIV, there is evidence that YFV also originates in Africa, infecting many of the same primate species, including SMs, which do not develop disease upon YFV infection and are important in the ecology of the sylvatic cycle of YFV transmission (12,13). In contrast, YFV infections of RMs (Asian primates that are not natural hosts for YFV) are severe and often lethal (14,15).…”

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confidence: 99%

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Distinctive TLR7 Signaling, Type I IFN Production, and Attenuated Innate and Adaptive Immune Responses to Yellow Fever Virus in a Primate Reservoir Host

Mandl

Akondy

Lawson

et al. 2011

The Journal of Immunology

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Why cross-species transmissions of zoonotic viral infections to humans are frequently associated with severe disease when viruses responsible for many zoonotic diseases appear to cause only benign infections in their reservoir hosts is unclear. Sooty mangabeys (SMs), a reservoir host for SIV, do not develop disease following SIV infection, unlike nonnatural HIV-infected human or SIV-infected rhesus macaque (RM) hosts. SIV infections of SMs are characterized by an absence of chronic immune activation, in association with significantly reduced IFN-α production by plasmacytoid dendritic cells (pDCs) following exposure to SIV or other defined TLR7 or TLR9 ligands. In this study, we demonstrate that SM pDCs produce significantly less IFN-α following ex vivo exposure to the live attenuated yellow fever virus 17D strain vaccine, a virus that we show is also recognized by TLR7, than do RM or human pDCs. Furthermore, in contrast to RMs, SMs mount limited activation of innate immune responses and adaptive T cell proliferative responses, along with only transient antiviral Ab responses, following infection with yellow fever vaccine 17D strain. However, SMs do raise significant and durable cellular and humoral immune responses comparable to those seen in RMs when infected with modified vaccinia Ankara, a virus whose immunogenicity does not require TLR7/9 recognition. Hence, differences in the pattern of TLR7 signaling and type I IFN production by pDCs between primate species play an important role in determining their ability to mount and maintain innate and adaptive immune responses to specific viruses, and they may also contribute to determining whether disease follows infection.

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Section: Discussionmentioning

confidence: 97%

mentioning

confidence: 99%

Distinctive TLR7 Signaling, Type I IFN Production, and Attenuated Innate and Adaptive Immune Responses to Yellow Fever Virus in a Primate Reservoir Host

Mandl

Akondy

Lawson

et al. 2011

The Journal of Immunology

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“…In contrast, recombination between unrelated groups of viruses is rare, but such situations can also arise, at least ecologically, if they coexist within a tolerant host, serving as a unique niche for them to stay together for long, interchange genomic sequences and undergo recombination to create viral strains with emergent properties. For example, both yellow fever virus (YFV; flavivirus) and SIV (retrovirus) might persist together in their natural hosts sooty mangabeys ( Woodall, 1968 ), which show tolerance to these viruses by significantly reducing the IFN-α level ( Mandl et al, 2011 ). Mosquito host A. aegypti is also known to tolerate both dengue (flavivirus) and chikungunya (alphavirus) virus (CHIKV) ( Kaur et al, 2018 ).…”

Section: Role Of Tolerance In Spillover and New Infectionsmentioning

confidence: 99%

Evolution of pathogen tolerance and emerging infections: A missing experimental paradigm

Seal

Dharmarajan

Khan

2021

eLife

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Researchers worldwide are repeatedly warning us against future zoonotic diseases resulting from humankind’s insurgence into natural ecosystems. The same zoonotic pathogens that cause severe infections in a human host frequently fail to produce any disease outcome in their natural hosts. What precise features of the immune system enable natural reservoirs to carry these pathogens so efficiently? To understand these effects, we highlight the importance of tracing the evolutionary basis of pathogen tolerance in reservoir hosts, while drawing implications from their diverse physiological and life-history traits, and ecological contexts of host-pathogen interactions. Long-term co-evolution might allow reservoir hosts to modulate immunity and evolve tolerance to zoonotic pathogens, increasing their circulation and infectious period. Such processes can also create a genetically diverse pathogen pool by allowing more mutations and genetic exchanges between circulating strains, thereby harboring rare alive-on-arrival variants with extended infectivity to new hosts (i.e., spillover). Finally, we end by underscoring the indispensability of a large multidisciplinary empirical framework to explore the proposed link between evolved tolerance, pathogen prevalence, and spillover in the wild.

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The enigma of yellow fever in East Africa

Ellis

Barrett

2008

Reviews in Medical Virology

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Despite a safe and effective vaccine, there are approximately 200,000 cases, including 30,000 deaths, due to yellow fever virus (YFV) each year, of which 90% are in Africa. The natural history of YFV has been well described, especially in West Africa, but in East Africa yellow fever (YF) remains characterised by unpredictable focal periodicity and a precarious potential for large epidemics. Recent outbreaks of YF in Kenya (1992-1993) and Sudan (2003 and 2005) are important because each of these outbreaks have involved the re-emergence of a YFV genotype (East Africa) that remained undetected for nearly 40 years and was previously unconfirmed in a clinically apparent outbreak. In addition, unlike West Africa and South America, YF has yet to emerge in urban areas of East Africa and be vectored by Aedes (Stegomyia) aegypti. This is a significant public health concern in a region where the majority of the population remains unvaccinated. This review describes historical findings, highlights a number of disease indicators, and provides clarification regarding the natural history, recent emergence and future risk of YF in East Africa.

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The reaction of a mangabey monkey (Cercocebus galeritus agilisMilne-Edwards) to inoculation with yellow fever virus

Cited by 7 publications

References 9 publications

Distinctive TLR7 Signaling, Type I IFN Production, and Attenuated Innate and Adaptive Immune Responses to Yellow Fever Virus in a Primate Reservoir Host

Distinctive TLR7 Signaling, Type I IFN Production, and Attenuated Innate and Adaptive Immune Responses to Yellow Fever Virus in a Primate Reservoir Host

Evolution of pathogen tolerance and emerging infections: A missing experimental paradigm

The enigma of yellow fever in East Africa

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