Human orf and milkers' nodule: A clinicopathologic study

Groves, Richard; Wilson‐Jones, E.; Macdonald, D.M.

doi:10.1016/0190-9622(91)70257-3

Cited by 112 publications

(79 citation statements)

References 11 publications

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“…Disruption of the viral VEGF gene and the loss of VEGF activity had no detectable effect on the growth of orf virus in cultured cells; however, infection of its natural host was significantly affected. Analysis of vascularization associated with the viral lesions allowed us to confirm previous reports that the dermis underlying an orf virus lesion is intensely vascularized (18). As early as 6 days p.i., the density of endothelial cells was, on average, fivefold greater than that seen in the dermis of a mock-infected lesion.…”

Section: Discussionsupporting

confidence: 71%

“…More recently, Groves described "massive capillary proliferation and dilation [that] gave the impression of an angiomatous lesion" (18). Construction of a recombinant orf virus in which the viral VEGF was inactivated allowed us to examine for the first time the role played by the viral VEGF in the vascular response seen in orf virus lesions.…”

Section: Discussionmentioning

confidence: 99%

“…The pathological features of human and ovine orf virus lesions are the same, and in both hosts infection is confined to the epidermis, with no evidence of systemic spread. The lesions are remarkable for extensive vascular proliferation and dilation as well as marked proliferation of the epidermis, with finger-like projections of the epidermis deep into the dermis (18). The expression of an orf virusencoded member of the VEGF family of molecules may provide an explanation for some of these observations.…”

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confidence: 93%

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Viral Vascular Endothelial Growth Factor Plays a Critical Role in Orf Virus Infection

Savory¹,

Stacker

Fleming³

et al. 2000

J Virol

125

116

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Infection by the parapoxvirus orf virus causes proliferative skin lesions in which extensive capillary proliferation and dilation are prominent histological features. This infective phenotype may be linked to a unique virus-encoded factor, a distinctive new member of the vascular endothelial growth factor (VEGF) family of molecules. We constructed a recombinant orf virus in which the VEGF-like gene was disrupted and show that inactivation of this gene resulted in the loss of three VEGF activities expressed by the parent virus: mitogenesis of vascular endothelial cells, induction of vascular permeability, and activation of VEGF receptor 2. We used the recombinant orf virus to assess the contribution of the viral VEGF to the vascular response seen during orf virus infection of skin. Our results demonstrate that the viral VEGF, while recognizing a unique profile of the known VEGF receptors (receptor 2 and neuropilin 1), is able to stimulate a striking proliferation of blood vessels in the dermis underlying the site of infection. Furthermore, the data demonstrate that the viral VEGF participates in promoting a distinctive pattern of epidermal proliferation. Loss of a functional viral VEGF resulted in lesions with markedly reduced clinical indications of infection. However, viral replication in the early stages of infection was not impaired, and only at later times did it appear that replication of the recombinant virus might be reduced.

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Section: Discussionsupporting

confidence: 71%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 93%

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Viral Vascular Endothelial Growth Factor Plays a Critical Role in Orf Virus Infection

Savory¹,

Stacker

Fleming³

et al. 2000

J Virol

125

116

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“…Orf virus and Pseudocowpox virus are distinct species within the genus Parapoxvirus, and infect sheep and goats and cattle, respectively, but both readily infect humans (28,29). The resulting lesions in the skin demonstrate extensive vascular dilation, dermal edema, and proliferation of endothelial cells (28,30). We have shown that the disruption of the VEGF-like gene in Orf virus strain NZ2 markedly reduces these characteristics of infection (31).…”

mentioning

confidence: 96%

Viral Vascular Endothelial Growth Factors Vary Extensively in Amino Acid Sequence, Receptor-binding Specificities, and the Ability to Induce Vascular Permeability yet Are Uniformly Active Mitogens

Wise

Ueda

Dryden

et al. 2003

Journal of Biological Chemistry

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Infections of humans and ungulates by parapoxviruses result in skin lesions characterized by extensive vascular changes that have been linked to viral-encoded homologues of vascular endothelial growth factor (VEGF). VEGF acts via a family of receptors (VEGFRs) to mediate endothelial cell proliferation, vascular permeability, and angiogenesis. The VEGF genes from independent parapoxvirus isolates show an extraordinary degree of inter-strain sequence variation. We conducted functional comparisons of five representatives of the divergent viral VEGFs. These revealed that despite the sequence divergence, all were equally active mitogens, stimulating proliferation of human endothelial cells in vitro and vascularization of sheep skin in vivo with potencies equivalent to VEGF. This was achieved even though the viral VEGFs bound VEGFR-2 less avidly than did VEGF. Surprisingly the viral VEGFs varied in their ability to cross-link VEGFR-2, induce vascular permeability and bind neuropilin-1. Correlations between these three activities were detected. In addition it was possible to correlate these functional variations with certain sequence and structural motifs specific to the viral VEGFs. In contrast to the conserved ability to bind human VEGFR-2, the viral growth factors did not bind either VEGFR-1 or VEGFR-3. We propose that the extensive sequence divergence seen in the viral VEGFs was generated primarily by selection against VEGFR-1 binding.

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“…It is endemic among cattle, causing lesions in the udder, trunk, legs and oral cavity as a bovine papular stomatitis (2,3,5) Human infection is accidental, occurring when men come into contact with infected animals or handle meat contaminated by the virus. Human-to-human transmission has not been described yet.…”

Section: Milker's Nodulesmentioning

confidence: 99%

Diseases caused by poxvirus - orf and milker's nodules: a review

Barraviera¹

2005

J. Venom. Anim. Toxins incl. Trop. Dis

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Sheep and cattle parapoxviruses cause in human beings diseases of very similar aspect, named orf and milker's nodules, respectively. These infections are generically called farmyard pox. In the present article, we show the epidemiological, clinical, and histopathological aspects, as well as the treatment of these two viral diseases that are very similar, being differentiated only by their epidemiological aspects.

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Human orf and milkers' nodule: A clinicopathologic study

Cited by 112 publications

References 11 publications

Viral Vascular Endothelial Growth Factor Plays a Critical Role in Orf Virus Infection

Viral Vascular Endothelial Growth Factor Plays a Critical Role in Orf Virus Infection

Viral Vascular Endothelial Growth Factors Vary Extensively in Amino Acid Sequence, Receptor-binding Specificities, and the Ability to Induce Vascular Permeability yet Are Uniformly Active Mitogens

Diseases caused by poxvirus - orf and milker's nodules: a review

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