Natural human infections with Vaccinia virus during bovine vaccinia outbreaks

Silva‐Fernandes, André Tavares da; Travassos, Carlos Eurico Pires Ferreira; Ferreira, Jaqueline Maria Siqueira; Abrahão, Jônatas Santos; Rocha, Eliseu Soares de Oliveira; Viana-Ferreira, Flávia; Santos, João Rodrigues dos; Bonjardim, Cláudio Antônio; Ferreira, Paulo César Peregrino; Kroon, Erna Geessien

doi:10.1016/j.jcv.2009.01.007

Cited by 83 publications

(121 citation statements)

References 28 publications

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“…First, remaining within the orthopoxviruses, reports of other zoonoses such as cowpox and buffalopox have also risen in the aftermath of smallpox eradication [59][60][61]. The data are less systematic, so quantitative comparisons are challenging, but these patterns are broadly consistent with competitive release arising from the decline of cross-immunity from smallpox and its vaccine.…”

Section: Application To Other Pathogensmentioning

confidence: 99%

Vacated niches, competitive release and the community ecology of pathogen eradication

Lloyd‐Smith

2013

Phil. Trans. R. Soc. B

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A recurring theme in the epidemiological literature on disease eradication is that each pathogen occupies an ecological niche, and eradication of one pathogen leaves a vacant niche that favours the emergence of new pathogens to replace it. However, eminent figures have rejected this view unequivocally, stating that there is no basis to fear pathogen replacement and even that pathogen niches do not exist. After exploring the roots of this controversy, I propose resolutions to disputed issues by drawing on broader ecological theory, and advance a new consensus based on robust mechanistic principles. I argue that pathogen eradication (and cessation of vaccination) leads to a ‘vacated niche’, which could be re-invaded by the original pathogen if introduced. Consequences for other pathogens will vary, with the crucial mechanisms being competitive release, whereby the decline of one species allows its competitors to perform better, and evolutionary adaptation. Hence, eradication can cause a quantitative rise in the incidence of another infection, but whether this leads to emergence as an endemic pathogen depends on additional factors. I focus on the case study of human monkeypox and its rise following smallpox eradication, but also survey how these ideas apply to other pathogens and discuss implications for eradication policy.

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Section: Application To Other Pathogensmentioning

confidence: 99%

Vacated niches, competitive release and the community ecology of pathogen eradication

Lloyd‐Smith

2013

Phil. Trans. R. Soc. B

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“…However, VACV infection is fairly common in Brazil, and several outbreaks of cattle and human infections have been reported in the last decades. 5,8,25 The current report contributes to the recognition and diagnosis of vesicular diseases in cattle in Brazil. …”

mentioning

confidence: 92%

An outbreak of pseudocowpox in fattening calves in southern Brazil

et al. 2012

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Pseudocowpox virus is a parapoxvirus frequently associated with papulovesicular and scabby lesions on the teats and udders of milking cows and is often transmitted to human beings. An unusual outbreak of skin disease in fattening calves in southern Brazil is described. Fourteen of 17 male cattle (82%), aged 6–48 months, feeding on grass pastures were affected. Animals developed papules, vesicles, and scabby proliferative lesions on the muzzle in a clinical course of approximately 10–15 days. The scabby lesions often presented with exudation and bleeding. Histological examination of mucocutaneous tissue in detached scabs revealed acanthosis with thickening of the corneal layer and premature keratinization (parakeratotic hyperkeratosis). The dermis had multifocal lymphoplasmacytic infiltrates. Electron microscopic examination of scab specimens revealed typical parapoxvirus particles: oval shaped (260 nm × 160 nm), enveloped, and covered with a helical layer. Polymerase chain reaction using a set of pan-parapoxvirus primers for the B2L gene amplified a 590-bp product out of DNA extracted from scabs. Nucleotide sequencing of the amplicons revealed a nucleotide homology of 97% with Pseudocowpox virus and lower homology with other parapoxviruses: Bovine papular stomatitis virus (84%) and Orf virus (94%). A phylogenetic tree based on the B2L sequence was constructed, showing that the virus clustered with Pseudocowpox virus isolates.

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“…They reported that these two VACV-based vaccination platforms induced highly functional CD8 ϩ T cells that displayed significant levels of degranulation and the coexpression of several cytokines and the chemokine MIP1␤. However, since the last reported case of smallpox occurred several decades ago, and VACV is not a natural human pathogen (although humans can be incidental hosts [49]), it could not be determined whether the functional profile of T cells induced by VACV is similar to that of smallpoxspecific T cells in the context of a truly natural infection. Therefore, in the present study, we used the mouse model of smallpox to compare the functional capacities of CD8 ϩ and CD4 ϩ T cells that arise following natural infection (ECTV) and nonnatural infection (VACV) of mousepox-resistant C57BL/6 mice.…”

mentioning

confidence: 99%

Comparable Polyfunctionality of Ectromelia Virus- and Vaccinia Virus-Specific Murine T Cells despite Markedly DifferentIn VivoReplication and Pathogenicity

Hersperger

Siciliano

Eisenlohr

2012

J Virol

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Vaccinia virus (VACV) stimulates long-term immunity against highly pathogenic orthopoxvirus infection of humans (smallpox) and mice (mousepox [ectromelia virus {ECTV}]) despite the lack of a natural host-pathogen relationship with either of these species. Previous research revealed that VACV is able to induce polyfunctional CD8 ؉ T-cell responses after immunization of humans. However, the degree to which the functional profile of T cells induced by VACV is similar to that generated during natural poxvirus infection remains unknown. In this study, we monitored virus-specific T-cell responses following the dermal infection of C57BL/6 mice with ECTV or VACV. Using polychromatic flow cytometry, we measured levels of degranulation, cytokine expression (gamma interferon [IFN-␥], tumor necrosis factor alpha [TNF-␣], and interleukin-2 [IL-2]), and the cytolytic mediator granzyme B. We observed that the functional capacities of T cells induced by VACV and ECTV were of a similar quality in spite of the markedly different replication abilities and pathogenic outcomes of these viruses. In general, a significant fraction (>50%) of all T-cell responses were positive for at least three functions both during acute infection and into the memory phase. In vivo killing assays revealed that CD8 ؉ T cells specific for both viruses were equally cytolytic (ϳ80% target cell lysis after 4 h), consistent with the similar levels of granzyme B and degranulation detected among these cells. Collectively, these data provide a mechanism to explain the ability of VACV to induce protective T-cell responses against pathogenic poxviruses in their natural hosts and provide further support for the use of VACV as a vaccine platform able to induce polyfunctional T cells.

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Natural human infections with Vaccinia virus during bovine vaccinia outbreaks

Cited by 83 publications

References 28 publications

Vacated niches, competitive release and the community ecology of pathogen eradication

Vacated niches, competitive release and the community ecology of pathogen eradication

An outbreak of pseudocowpox in fattening calves in southern Brazil

Comparable Polyfunctionality of Ectromelia Virus- and Vaccinia Virus-Specific Murine T Cells despite Markedly DifferentIn VivoReplication and Pathogenicity

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