Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Cowpox”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources
PubMed1986

Hemorrhage in lesions caused by cowpox virus is induced by a viral protein that is related to plasma protein inhibitors of serine proteases.

Several recombinant cowpox viruses were constructed and used to identify a viral gene that controls the production of hemorrhage in lesions caused by the Brighton Red strain of cowpox virus (CPV-BR). This gene is located in the KpnD fragment of CPV-BR DNA, between 31 and 32 kilobases from the end of the genome. This position corresponds well with that predicted from analyses of the DNA structures of spontaneously generated deletion mutants. The gene responsible for hemorrhage encodes a 38-kDa protein that is one of the most abundant early gene products. The 11-base-pair sequence GAAAATATATT present 84 base pairs upstream of its coding region is also present upstream of three other early genes of vaccinia virus; therefore, this sequence may be involved in the regulation of transcription. There is extensive similarity between the predicted amino acid sequence of the 38-kDa protein and the amino acid sequences of several plasma proteins that are inhibitors of various serine proteases involved in blood coagulation pathways. This suggests that the viral protein may possess a similar biological activity, which may enable it to effect hemorrhage by inhibiting one or more of the serine proteases involved in the host's normal processes of blood coagulation and wound containment.

Amino Acid Sequence↗
PubMed1980

Biochemical studies on early cell surface antigen induced by vaccinia and cowpox viruses.

The early cell surface antigen (ECSA) induced by vaccinia or cowpox virus infection was analysed by immunoprecipitation and SDS-polyacrylamide gel electrophoresis (SDS-PAGE), The components with a mol. wt. of about 40 000 (40 K) in vaccinia virus-infected cells and with a mol. wt. of about 43 000 (43 K) in cowpox virus-infected cells were specifically immunoprecipitated with anti-ECSA serum prepared by immunizing rabbits with rabbit kidney cells infected with a conditional lethal mutant. The 40 K and 43 K polypeptides were synthesized even in the presence of cytosine-I-beta-D-arabinofuranosyl-HCl (Ara C) and were detectable even in the cells pulse-labelled between I and 2 h p.i.

Animals↗
PubMed1984

The genome structure of cowpox virus white pock variants.

A previous report described restriction endonuclease analysis of white pock variants of red cowpox virus and their characterization as deletion mutants lacking certain sequences including the repetition from one specific terminus of the wild-type genome. Further analysis has confirmed the terminal deletion but demonstrated that this is compensated at the site of deletion by the presence of an inverted duplication of a variable amount of sequence from the opposite terminus, with the effect of restoring a terminal repetition and the covalent, terminal crosslink. Nine of 11 white pock variants showed a similar deletion of about 21 Mdal mapping contiguously from the right-hand terminus and extending into a 2.4 Mdal restriction fragment. Two white variants showed larger deletions of about 24 and 27 Mdal respectively. These deletions were compensated by a copy of sequences from the opposite terminus which ranged in size from 3 to 27 Mdal. No terminal deletions smaller than 21 Mdal were observed in cowpox white variants or in clones retaining the red phenotype. In contrast with other orthopoxviruses, no deletions involving the left-hand terminus were found. Some independent white isolates had similar sizes of sequence copied from the opposite terminus, but some sibling clones from a single, pock-purified white isolate with the same size of deletion had different sizes of duplicated sequence. Other siblings isolated from an independent, three times pock-purified white clone, itself derived from a single parental red pock, differed from each other in the size of both the deletion and the duplicated sequence. These observations suggest preference for deletion in a particular region, conjunction of the genome termini during DNA replication and a requirement for the preservation of symmetrical termini in orthopoxvirus genome function.

Base Sequence↗
PubMed2005

Effects of deletions of kelch-like genes on cowpox virus biological properties.

Cowpox virus (CPXV) strain GRI-90 contains six genes encoding kelch-like proteins. All six proteins contain both, the N-terminal BTB domain and the C-terminal kelch domain. We constructed mutant variants of a CPXV strain with targeted deletions of one to four genes of the kelch family, namely D11L, C18L, G3L, and A57R. As kelch genes are located in terminal variable regions of the CPXV genome, we studied the relationship of these genes with integral biological characteristics such as virulence, host range, reproduction in vitro and in ovo (in chicken embryos). It was demonstrated that the following effects occurred in a gene dose dependent manner with an increase of the number of genes deleted: (1) range of sensitive cells altered--deletion mutants lacking three genes displayed a considerably decreased ability to reproduce in MDCK cells; mutants lacking four genes lost this ability completely; (2) analysis of pocks formed by mutants with deletion of three and four kelch-like genes on chorioallantoic membranes of chicken embryos demonstrated that pock size and virus yield were significantly decreased; (3) light microscopic analysis of the pocks revealed impaired proliferation and reduced vascularisation in the pock region. More alterations were detected by electron microscopic analysis: the reproduction of mutants results in a reduction of the number of mature virions formed, and in many cells this process was arrested at the stage of assembly of immature virions; and (4) the evaluation of LD(50) and body weight loss in BALB/c mice infected intranasally with CPXVs revealed a reduction of the virulence of the deletion mutants, which became statistically significant when four kelch-like genes were excised.

Animals↗
PubMed2004

Cutaneous infections of mice with vaccinia or cowpox viruses and efficacy of cidofovir.

Orthopoxviruses, including smallpox, monkeypox and molluscipox, pose risks to human health through bioterrorist acts or natural transmission. There is no approved therapy for orthopoxvirus infections; however, cidofovir (CDV) has been approved as an investigational new drug for emergency treatment of adverse effects following smallpox vaccination. For evaluation of new therapies directed against orthopoxvirus infections, we have utilized immunocompetent, hairless mice (SKH-1) inoculated by a cutaneous route with cowpox virus (CV) or vaccinia virus (VV). Mice subsequently developed skin lesions and virus was recovered from the site of inoculation and quantified. Skin biopsies were evaluated microscopically, revealing brick-like eosinophilic, intracytoplasmic inclusion bodies characteristic of orthopoxvirus infection. SKH-1 mice fully recovered from either CV or VV infection. Immunodeficient Athymic or Rhino mice inoculated with CV or VV had more lesions and severe disease than SKH-1 mice. CV-infected SKH-1 mice were treated either with systemic or topical CDV. Although some protection was achieved with systemic treatment, 5% topical CDV was most effective at reducing virus titers in skin, lung, kidney, and spleen. These models may provide a means for evaluating efficacy of new therapies directed against orthopoxvirus diseases and further confirm the topical activity of CDV against cutaneous infections.

Administration, Cutaneous↗
PubMed2000

Intranasal treatment of cowpox virus respiratory infections in mice with cidofovir.

Orthopoxvirus infections in mice have been effectively treated with cidofovir, a clinically approved drug given by intravenous infusion to treat cytomegalovirus infections. In a bioterrorist scenario it would be technically difficult to give this drug to a large number of exposed individuals. New treatment approaches are being sought, which include giving cidofovir by alternative routes or designing oral prodrugs of cidofovir. In this report, intranasal cidofovir was investigated as a treatment of pulmonary cowpox virus infections in BALB/c mice. Ninety to 100% of animals given a single intranasal drug treatment (10, 20 or 40 mg/kg) 24 h after virus challenge survived the infection, whereas all placebo-treated mice died. Doses of 2.5 and 5 mg/kg resulted in 60 and 80% survival, respectively. Single treatments of 20 and 40 mg/kg could be given up to 3 days after virus inoculation and still be 80-90% protective. A single 40 mg/kg treatment of infected mice given 1 or 2 days after infection also resulted in statistically significant decreases in virus titer in lungs and nose/sinus compared to the placebo group. Drug efficacy was found to be contingent upon treatment volume. A 10 mg/kg intranasal dose given 24 h after virus challenge was 100 and 50% effective in volumes of 40 and 20 microl, respectively. The same dose in 5 and 10 microl volumes caused no decrease in mortality. The results of these studies establish the utility of cidofovir treatment of poxvirus infections in mice by intranasal route. The data suggest the possibility that aerosol delivery of cidofovir to human lungs may be a viable alternative to intravenous dosing.

Administration, Intranasal↗
PubMed2001

Cowpox virus in a 12-year-old boy: rapid identification by an orthopoxvirus-specific polymerase chain reaction.

Although smallpox was eradicated 20 years ago, other members of the genus Orthopoxvirus (OPV), such as cowpox virus (CPXV) or monkeypox virus, are still a threat to humans. Because human CPXV infection is rare, it is seldom suspected on clinical grounds only. We report a boy who presented with two necrotic ulcers with surrounding erythema. Infection with OPV was suspected, as antibiotic treatment had not produced improvement and smears were negative for anthrax. An OPV was isolated and an OPV-specific polymerase chain reaction combined with a subsequent restriction enzyme fragment length polymorphism assay confirmed infection by CPXV. Although the patient's cat had had no skin lesions, OPV-specific antibodies were found at a titre of 1 : 8 in a plaque reduction assay, suggesting that the cat had transmitted the virus to the boy.

Child↗
PubMed2004

Disease dynamics in cyclic populations of field voles (Microtus agrestis): cowpox virus and vole tuberculosis (Mycobacterium microti).

The possible role of pathogens in rodent population cycles has been largely neglected since Elton's 'epidemic hypothesis' of 1931. To revisit this question, 12 adjacent, cyclic but out-of-phase populations of field voles (Microtus agrestis) in North East England were studied and the initial results are presented here. The prevalences of antibodies to cowpox virus and of clinical signs of Mycobacterium microti infection (vole tuberculosis) showed delayed (not direct) density dependence (with a lag of three to six months). This did not result from changes in population structure, even though there were such changes associated with the different phases of the cycle. The prevalences rose as vole numbers rose, and peaked as numbers declined. The apparent lag in the numerical response of infection prevalence to changes in host abundance is consistent with the hypothesis that diseases, singly or in combination, play a hitherto underestimated role in the dynamics of cyclic populations.

Animals↗
PubMed2003

Efficacy of multiple- or single-dose cidofovir against vaccinia and cowpox virus infections in mice.

Orthopoxviruses, including variola and monkeypox, pose risks to human health through natural transmission or potential bioterrorist activities. Since vaccination has not recently been utilized for control of these infections, there is renewed effort in the development of antiviral agents not only for postexposure smallpox therapy but also for treatment of adverse reactions following vaccination. The objectives of this study were to expand on the results of others that cidofovir (CDV) is effective in mice inoculated with cowpox virus (CV) or vaccinia virus (VV) and to document the efficacy of single and interval dosing beginning prior to or after infection, particularly including evaluations using suboptimal doses of CDV. We utilized BALB/c or SCID mice inoculated with CV or VV as models for systemic poxvirus infections. BALB/c mice were inoculated intranasally with CV or VV and treated with CDV prior to or after virus inoculation. CDV, at concentrations as low as 0.7 to 6.7 mg/kg of body weight/day for 5 days, conferred significant protection when treatment was initiated as late as 72 to 96 h postinfection. A single-dose pretreatment or posttreatment with CDV at 3 to 100 mg/kg was effective when given as early as 5 days prior to infection or as late as 3 days after infection with either VV or CV. Interval treatments given every third day beginning 72 h postinfection using 6.7 or 2 mg of CDV/kg also proved effective against CV infections. When SCID mice were inoculated intraperitoneally with CV or VV and treated for 7 to 30 days with CDV, all the mice eventually died during or after cessation of treatment; however, significant delays in time to death and reduction of virus replication in organs occurred in most treated groups, and no resistance to CDV was detected.

Animals↗
PubMed2004

Oral treatment of cowpox and vaccinia virus infections in mice with ether lipid esters of cidofovir.

Four newly synthesized ether lipid esters of cidofovir (CDV), hexadecyloxypropyl-CDV (HDP-CDV), octadecyloxyethyl-CDV (ODE-CDV), oleyloxypropyl-CDV (OLP-CDV), and oleyloxyethyl-CDV (OLE-CDV), were found to have enhanced activities against vaccinia virus (VV) and cowpox virus (CV) in vitro compared to those of CDV. The compounds were administered orally and were evaluated for their efficacies against lethal CV or VV infections in mice. HDP-CDV, ODE-CDV, and OLE-CDV were effective at preventing mortality from CV infection when treatments were initiated 24 h after viral inoculation, but only HDP-CDV and ODE-CDV maintained efficacy when treatments were initiated as late as 72 h postinfection. Oral pretreatment with HDP-CDV and ODE-CDV were also effective when they were given 5, 3, or 1 day prior to inoculation with CV, even when each compound was administered as a single dose. Both HDP-CDV and ODE-CDV were also effective against VV infections when they were administered orally 24 or 48 h after infection. In animals treated with HDP-CDV or ODE-CDV, the titers of both CV and VV in the liver, spleen, and kidney were reduced 3 to 7 log(10). In contrast, virus replication in the lungs was not significantly reduced. These data indicate that HDP-CDV or ODE-CDV given orally is as effective as CDV given parenterally for the treatment of experimental CV and VV infections and suggest that these compounds may be useful for the treatment of orthopoxvirus infections in humans.

Administration, Oral↗
PubMed1996

Characteristic but unfamiliar--the cowpox infection, transmitted by a domestic cat.

An 11-year-old girl had been suffering from 2 recently developed reddish ulcerated nodules on the right side of her neck and, concomitantly, from a very hard swelling as well as from painless lymphadenopathy. Subsequently, thick black eschars appeared on the surface of the ulcers. Using the negative staining technique, an orthopox virus infection could be identified by electron microscopy. The patient's characteristic history as well as her close contact with a cat frequently hunting nice indicated the diagnosis of a cowpox infection, which was unequivocally confirmed by identification of both the viral culture and specific antibodies in the serum of the patient.

Animals↗
PubMed2006

Cowpox virus transmission from rats to monkeys, the Netherlands.

We report an outbreak of cowpox virus among monkeys at a sanctuary for exotic animals. Serologic analysis and polymerase chain reaction were performed on blood and swab samples from different rodent species trapped at the sanctuary during the outbreak. Sequence comparison and serologic results showed that brown rats (Rattus norvegicus) transmitted the virus to monkeys.

Animals↗
PubMedDate not supplied

[The study of orthopoxvirus genes for Kelch-like proteins. II. Construction of cowpox virus variants with targeted gene deletions].

Integrative plasmids p delta C, p delta D, and p delta G were designed to contain a selective marker beyond the region of homology to virus DNA and to allow construction of recombinant cowpox viruses (CPV) that lack C18L, D11L, or G3L coding for kelch-like proteins. CPV mutants lacking one (C18L, D11L, or G3L), two (D11L/G3L or C18L/D11L), or three (D11L/G3L/C18L, that is, all) kelch-like protein genes of the left variable region of the virus genome were obtained. Impaired reproduction was observed for the triple mutant. Pocks produced by the triple mutant and the original virus differed in size and morphology. In addition, the two CPV variants differed in destructive changes caused in the chorioallantoic membrane of chicken embryos.

Animals↗
PubMedDate not supplied

[An experimental infection caused by the EP-2 strain of cowpox virus in mice of different ages].

The specificity of lethal infection was studied in noninbred white mice (age--15 to 20 and 25 to 30 days) infected intraperitoneally with the EP-2 strain of cowpox virus (CPV) in doses 10(5), 10(6) and 10(7) PFU. The virus caused the lethal infection in the 15-20-day mice; while the 25-30-day mice remained healthy and survived. Virologic, immunologic-and-histochemical and electron-microscopy examinations of the 15-20-day mice revealed a replication of the EP-2 strain in tissues bordering on the virus introduction area; there was no generalization of infection. The virus replicated first in the mesothelium cells, and after that, in fibroblasts as well as in the endothelial, fatty, adventicial, cross-striated and muscle cells and in myosatellites.

Adipose Tissue↗
PubMedDate not supplied

[Intranasal infection in mice inoculated with cowpox virus strain EP-2 isolated from the elephant].

The specific features of reproduction of EP-2 strain of cowpox virus (CPV) were studied in intranasally infected BALC/C mice by light and electron microscopy. Virus replication was found in the ciliated, intercalary, basal, and goblet cells (the nasal respiratory area), basal and supporting cells (the nasal olfactory area), ciliated, intercalary, goblet cells (the tracheal and bronchial epithelium), and collagen-producing, Schwann's, endothelial, smooth muscle, and adventitial cells. It has been shown that the CPV strain EP-2 locally replicates in the nasal cavity, trachea, and large bronchi and that there is no generalized infection.

Animals↗
PubMedDate not supplied

[The biotype and genetic characteristics of an isolate of the cowpox virus causing infection in a child].

A virus, identified as cowpox virus by its biological properties and the results of the analysis of its DNA, was isolated from a sick 4-year-old child with a clinical picture of pox, though having had no contacts with known natural carriers of the causative agent of this infection. At the same time the isolated virus was found to differ from the reference strain, as well as from other isolates of vaccinia virus by some biological markers (and in particular by the structure of cytoplasmic inclusions of type A) and by the restriction profile of DNA. The Hind III maps indicating the location of restriction sites made it possible to localize the genome differences established in this study. The specific feature of this case was the previous close contact of the child with a mole which was probably the source of infection.

Animals↗
PubMed1993

The effects of serpin gene mutations on the distinctive pathobiology of cowpox and rabbitpox virus following intranasal inoculation of Balb/c mice.

Intranasal infection of Balb/c mice with 106 plaque forming units (PFU) of wild-type cowpox virus (CPV) and rabbitpox virus (RPV) induced strikingly different pulmonary pathology despite nearly identical clinical signs of illness and LD50. Intranasal infection with CPV induced severe peribronchial, peribronchiolar, and perivascular hemorrhage with a mixed inflammatory cell infiltrate, bronchial and bronchiolar epithelial cell hyperplasia with intracytoplasmic acidophilic inclusion bodies, and alveolar hemorrhage and edema. In contrast, infection with RPV induced a mixed peribronchial and peribronchiolar inflammatory cell infiltrate, multifocal areas of bronchiolar epithelial cell coagulation necrosis, alveolar edema, and a conspicuous absence of pulmonary hemorrhage. Viremia was not detected following CPV infection and only 1 of 11 mice had brain-associated virus at death. Mice infected with RPV exhibited a viremia 2-3 days after infection and all mice had virus associated with the brain at death. Mice infected with viruses containing certain serine protease inhibitor (SPI) gene mutations (CPV delta SPI-1, CPV delta SPI-3, and RPV SPI-1-) exhibited no difference in clinical disease manifestation when compared with those infected with wild-type viruses. However, inactivation of the SPI-2 genes in either CPV or RPV resulted in disease attenuation and alteration of pulmonary pathology. Mice infected with the CPV delta SPI-2 mutant showed decreased pulmonary hemorrhage, reduced inflammation, and an absence of alveolar edema, while mice infected with the RPV delta SPI-2 mutant had a marked increase in intrapulmonary inflammatory cells and only a transient viremia.

Animals↗