Orf is one of the most widespread viral diseases worldwide, affecting mostly small ruminants and, sometimes, other species, including wild animals. Of late, there have been an increasing number of reports of new species being affected by the disease, implying a dynamic host-pathogen interaction. The causative agent, orf virus, has been extensively investigated over recent years, owing to its zoonotic importance and ability to cross-infect other species sporadically. The evasive mechanisms that the virus has developed to adapt and grow in the presence of an active immune response helps to explain the ability of the virus to repeatedly reinfect the same host. The apparent diversity in the antigenic/immune targets of different orf virus strains involved in such repeat infections may also be contributing factors. Exposure of animals to stress or immunosupression as a result of therapy or primary viral infection can accentuate the severity of disease. Genes homologous to host cytokines or their antagonists, and which contribute to viral virulence, have been found in the viral genome. A combination of electron microscopy, histology and PCR is the most accurate laboratory approach for confirmation of the disease, although clinical signs are often typical. However, some infections may be confounded by similar clinical manifestations caused by other infections. This review presents, in brief, a recent understanding of the virus at the host-pathogen level, molecular biology of the virus, disease epidemiology, clinical manifestations in man and animals, diagnostic procedures, and the economic and environmental impact of the disease.

The surface treatment of polystyrene, which is required to make polystyrene suitable for cell adhesion and spreading, was investigated. Examination of surfaces treated with sulfuric acid or various oxidizing agents using (a) x-ray photoelectron and attenuated total reflection spectroscopy and (b) measurement of surface carboxyl-, hydroxyl-, and sulfurcontaining groups by various radiochemical methods showed that sulfuric acid produces an insignificant number of sulfonic acid groups on polystyrene. This technique together with various oxidation techniques that render surfaces suitable for cell culture generated high surface densities of hydroxyl groups. The importance of surface hydroxyl groups for the adhesion of baby hamster kidney cells or leukocytes was demonstrated by the inhibition of adhesion when these groups were blocked: blocking of carboxyl groups did not inhibit adhesion and may raise the adhesion of a surface. These results applied to cell adhesion in the presence and absence of serum. The relative unimportance of fibronectin for the adhesion and spreading of baby hamster kidney cells to hydroxyl-rich surfaces was concluded when cells spread on such surfaces after protein synthesis was inhibited with cycloheximide, fibronectin was removed by trypsinization, and trypsin activity was stopped with leupeptin.

No abstract

The parapoxvirus orf virus encodes a novel soluble protein inhibitor of ovine granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-2 (IL-2). The GM-CSF- and IL-2-inhibitory factor (GIF) gene was expressed as an intermediate-late viral gene in orf virus-infected cells. GIF formed homodimers and tetramers in solution, and it bound ovine GM-CSF with a Kd of 369 pM and ovine IL-2 with a Kd of 1.04 nM. GIF did not bind human GM-CSF or IL-2 in spite of the fact that orf virus is a human pathogen. GIF was detected in afferent lymph plasma draining the skin site of orf virus reinfection and was associated with reduced levels of lymph GM-CSF. GIF expression by orf virus indicates that GM-CSF and IL-2 are important in host antiviral immunity.

Infectious disease introduced by non-native species is increasingly cited as a facilitator of native population declines, but direct evidence may be lacking due to inadequate population and disease prevalence data surrounding an outbreak. Previous indirect evidence and theoretical models support squirrelpox virus (SQPV) as being potentially involved in the decline of red squirrels (Sciurus vulgaris) following the introduction of the non-native gray squirrel (Sciurus carolinensis) to the United Kingdom. The red squirrel is a major UK conservation concern and understanding its continuing decline is important for any attempt to mitigate the decline. The red squirrel–gray squirrel system is also exemplary of the interplay between infectious disease (apparent competition) and direct competition in driving the replacement of a native by an invasive species. Time series data from Merseyside are presented on squirrel abundance and squirrelpox disease (SQPx) incidence, to determine the effect of the pathogen and the non-native species on the native red squirrel populations. Analysis indicates that SQPx in red squirrels has a significant negative impact on squirrel densities and their population growth rate (PGR). There is little evidence for a direct gray squirrel impact; only gray squirrel presence (but not density) proved to influence red squirrel density, but not red squirrel PGR. The dynamics of red SQPx cases are largely determined by previous red SQPx cases, although previous infection of local gray squirrels also feature, and thus, SQPV-infected gray squirrels are identified as potentially initiating outbreaks of SQPx in red squirrels. Retrospective serology indicates that approximately 8% of red squirrels exposed to SQPV may survive infection during an epidemic. This study further highlights the UK red squirrel – gray squirrel system as a classic example of a native species population decline strongly facilitated by infectious disease introduced by a non-native species. It is therefore paramount that disease prevention and control measures are integral in attempts to conserve red squirrels in the United Kingdom.