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At least 19 recordsLinked to original sources
PubMed1989

[Vaccinia and ectromelia recombinant viruses, causing an infection, characteristic for ectromelia, in mice].

Ten recombinants between the viruses of vaccinia and ectromelia were isolated that cause the ectromelia virus specific lesions in mice. The structure of recombinant viral genomes, the efficiency of viral propagation in mice, the nature of lesions induced by viruses have been studied. Eight of obtained recombinants have a DNA insertion originating from the right end of ectromelia viral genome, nine recombinants have an insertion originating from the left end, seven recombinants possess both insertions. The latter recombinants have more pronounced pathogenicity for mice. Both revealed regions are supposed to define the specific pathogenicity of ectromelia virus for mice.

Animals↗
PubMed1992

Restricted replication of ectromelia virus in cell culture correlates with mutations in virus-encoded host range gene.

Ectromelia virus (strain Moscow) was shown to replicate poorly or not at all in cell lines derived from the rabbit or hamster. The failure of ectromelia virus to replicate in cell lines derived from the hamster suggested that the virus lacked a functional CHO host range (hr) gene required for multiplication in these cells. A DNA fragment which hybridized to the CHO hr gene was cloned from the ectromelia virus genome and shown by sequence analysis to be deleted of 506 bp within the ectromelia virus CHO hr homologue. Two additional ectromelia viruses (Hampstead and Mill Hill strains) were also shown to lack an intact CHO hr gene. Insertion of the CHO gene from cowpox virus into the ectromelia virus genome extended the host range of ectromelia virus in tissue culture. These results demonstrate that an intact CHO hr gene is not required for maintenance of ectromelia virus in nature and provide a partial explanation for ectromelia virus' narrow host range, as opposed to the broad host range of cowpox virus, which has a functional CHO hr gene.

Animals↗
PubMed1983

Evaluation of an enzyme-linked immunosorbent assay for the detection of ectromelia (mousepox) antibody.

Ectromelia virus, an orthopoxvirus that can cause extensive morbidity and mortality (mousepox) in colonized mice, has been epizootically responsible for serious disruption of biomedical research since 1930. The lack of a sensitive and specific serological assay for infection with this virus became apparent during outbreaks of mousepox at the National Institutes of Health, Bethesda, Md., and other biomedical research institutions in 1979 and 1980. To fill this need, we evaluated an enzyme-linked immunosorbent assay. Sucrose gradient-purified ectromelia and vaccinia viruses were compared as antigens in tests on approximately 1,000 mouse sera from experimentally infected mice and conventional colonies of uninfected mice. A statistical analysis based on the frequency distribution of the absorbance values for 152 mouse sera (free of ectromelia antibody) gave 0.22 as a value to differentiate ectromelia-positive sera from ectromelia-negative sera. When enzyme-linked immunosorbent assay results were compared with those obtained by an indirect immunofluorescence assay, the former was found to be at least 10-fold more sensitive. With the procedures employed, including the use of purified vaccinia virions as antigen, the enzyme-linked immunosorbent assay proved to be highly sensitive and specific for detecting antibodies to ectromelia and vaccinia viruses. False-positive results were not encountered. False-negative results were observed in 3% of 108 separate tests of a known positive serum. Although data indicated that ectromelia antibody can be differentiated from vaccinia antibody with homologous and heterologous antigen, this procedure probably cannot be generally used because of unavailability of ectromelia antigens.

Animals↗
PubMed1993

In vitro and in vivo study of the ectromelia virus homolog of the vaccinia virus K1L host range gene.

Ectromelia virus encodes a protein which is homologous to the product of the vaccinia virus host range gene, K1L, except for eight conservative and two non-conservative substitutions and an additional threonine residue at the carboxyl terminus. Unlike the vaccinia virus gene, the ectromelia virus homolog failed to support optimal virus replication in RK-13 cells and appeared to be expressed 20-fold less efficiently. This lower level of expression was not due to the genetic background of the virus, K1L RNA transcription, sequence of the K1L RNA leader, or stability of K1L RNA or protein. Infections of RK-13 cells with ectromelia or vaccinia virus mutants lacking an intact K1L gene resulted in transient expression of early genes followed by a rapid and irreversible cessation of both virus and host protein synthesis. Infections of the disease-susceptible ANCR or -resistant C57BL/6 mice with the K1L-lacking ectromelia virus yielded a pathogenesis pattern indistinguishable from wild-type, suggesting that the ectromelia virus homolog of vaccinia virus K1L is not important for ectromelia virus in vivo replication and spread.

Animals↗
PubMed1985

Ectromelia virus-induced changes in primary cultures of mouse hepatocytes.

Mouse hepatocytes were isolated by collagenase perfusion, maintained in non-proliferating monolayer culture and shown to retain liver cell function as judged by gluconeogenesis for 15 to 18 h. Such cells could be infected with and support the replication of a virulent strain of ectromelia virus. Virus antigen and characteristic cytoplasmic 'B'-type poxvirus inclusion bodies were demonstrated by immunofluorescence in virtually all cells. By electron microscopy it was shown that 'B'-type inclusions were the site of virus replication, and that the biogenesis of ectromelia virus and ultrastructural changes in hepatocytes were similar to those observed in infected mouse livers. Early cell rounding effects, a normal characteristic of poxvirus infections in tissue culture cells, were not seen in ectromelia-infected hepatocytes, although late degenerative changes did occur. Pulse-labelling of hepatocyte cultures with [35S]methionine showed that ectromelia virus inhibited the rise in protein synthesis seen in controls and imposed a gradual decline in host protein synthesis to an extent and at a rate significantly different from that in mouse L929 cells. Gluconeogenesis was inhibited by ectromelia virus infection of hepatocytes.

Animals↗
PubMed2003

The genomic sequence of ectromelia virus, the causative agent of mousepox.

Ectromelia virus is the causative agent of mousepox, an acute exanthematous disease of mouse colonies in Europe, Japan, China, and the U.S. The Moscow, Hampstead, and NIH79 strains are the most thoroughly studied with the Moscow strain being the most infectious and virulent for the mouse. In the late 1940s mousepox was proposed as a model for the study of the pathogenesis of smallpox and generalized vaccinia in humans. Studies in the last five decades from a succession of investigators have resulted in a detailed description of the virologic and pathologic disease course in genetically susceptible and resistant inbred and out-bred mice. We report the DNA sequence of the left-hand end, the predicted right-hand terminal repeat, and central regions of the genome of the Moscow strain of ectromelia virus (approximately 177,500 bp), which together with the previously sequenced right-hand end, yields a genome of 209,771 bp. We identified 175 potential genes specifying proteins of between 53 and 1924 amino acids, and 29 regions containing sequences related to genes predicted in other poxviruses, but unlikely to encode for functional proteins in ectromelia virus. The translated protein sequences were compared with the protein database for structure/function relationships, and these analyses were used to investigate poxvirus evolution and to attempt to explain at the cellular and molecular level the well-characterized features of the ectromelia virus natural life cycle.

Animals↗
PubMed1976

The cell-mediated immune response to ectromelia virus infection. Secondary response in vitro: specificity, nature of effector and responder cells and requirements for induction of antigenic changes in stimulator cells.

An in vitro culture method was used to study secondary cell-mediated responses to ectromelia virus infection in mice. Infected, syngeneic spleen cells or peritoneal cells were efficient "stimulator" cells when cultured with "responder" cells obtained from mice infected with ectromelia 4-6 weeks previously. The kinetics of generation of cytotoxic cells in cultures were determined; a peak occurred on days 4-5. A separation procedure performed on the cytotoxic cells showed that activity was associated mainly with the Ig-negative subpopulation (T cell-rich) and that H-2 compatibility between cytotoxic cells and target cells was required. The secondary response was virus-specific, at the level of both induction and target cell lysis, at least so far as ectromelia and lymphocytic choriomeningitis (LCM) viruses are concerned. Seperation of responder cells prior to culture showed that a potent secondary response was generated with the Ig-negative (T cell-rich) subpopulation and only a weak response was observed when the responder cells were Ig-positive (rich in B cells). Infected stimulator cells did not appear to secrete significant amounts of soluble antigen into the medium over 4 days of culture. Thus, antigenic patterns effective in memory T cell stimulation may be largely associated with the surfaces of infected cells.Pretreatment of ectromelia virus with UV- or gamma-irradiation did not impair its ability to induce antigenic changes in stimulator cells. Stimulator cells treated with UV-or gamma-irradiated virus for 1 h and then immediately with pactamycin to inhibit further viral protein synthesis and replication were efficient stimulators, thus indicating that antigenic changes are induced very rapidly on the surface of stimulator cells after uptake of virus. These treatments are being used to further characterize the cellular requirements in the stimulator population.

Animals↗
PubMed1983

Induction of resistance to ectromelia virus infection by corynebacterium parvum in murine peritoneal macrophages.

An in vitro model has been developed to study the replication of ectromelia virus in murine macrophages (M phi). Infection of mineral oil-elicited peritoneal M phi cultures with either the virulent (Moscow) or attenuated (Hampstead) strain of ectromelia virus led to productive infections. The kinetics of virus synthesis was similar to those seen following infection of murine fibroblasts. In contrast, peritoneal M phi s activated by intraperitoneal injection of Corynebacterium parvum vaccine were found to be totally refractory to infection by the attenuated strain and significantly more resistant to the virulent strain of ectromelia virus. Administration of C. parvum doses as small as 7 micrograms were sufficient to induce antiviral activity. M phi resistance became maximal at 5-9 days after C. parvum administration; however, M phi resistance was unstable during in vitro culture. Decay of antiviral activity was detected within the first 24 hr of culture and complete virus susceptibility returned after 5 days in culture. Peritoneal exudate cells (PEC) from C. parvum-immunized mice could induce resistance in susceptible M phi cultures during overnight cocultivation. In addition, cell-free culture supernatants from C. parvum-immune PEC could also induce resistance in susceptible M phi cultures, suggesting that a soluble factor, induced by C. parvum immunization and possessing interferon activity, may account for the intrinsic resistance to ectromelia virus by activated M phi s.

Animals↗
PubMed1984

Abortive ectromelia virus infection in peritoneal macrophages activated by Corynebacterium parvum.

We have previously demonstrated that peritoneal macrophages (M phi S) from C3H mice were resistant to in vitro infection by ectromelia virus, following activation by intraperitoneal injection of the immunomodulator Corynebacterium parvum. In contrast, resident and mineral oil-elicited M phi S were fully susceptible to virus infection. This report analyzes the infectious cycle of ectromelia virus in C parvum-activated and mineral oil-elicited M phi S and demonstrates that an abortive infection occurred in the activated M phi S that blocked the infectious cycle prior to the release of DNA from the infecting virions. The kinetics of adsorption of radiolabeled virus were similar in both susceptible and resistant M phi cultures; however, viral-induced incorporation of uridine and thymidine occurred only in the mineral oil-elicited and not the C parvum-activated M phi S. In addition, the late protein hemagglutinin was only detected in infected cultures of susceptible mineral oil-elicited M phi S. An electron micrographic analysis of the infectious cycle indicated that the adsorption of virus to the plasma membrane, uptake into lysosomes, and the primary undercoating and release of viral cores into the M phi cytoplasm were identical in both M phi types. In contrast, secondary uncoating (release of genomic DNA from the viral cores into the cytoplasm) was never detected in infected C parvum M phi S. These data are consistent with our previous findings and with the hypothesis that activation of M phi S by C parvum induces an interferon-mediated resistance to ectromelia virus infection.

Animals↗
PubMed1988

Mousepox in inbred mice innately resistant or susceptible to lethal infection with ectromelia virus. IV. Studies with the Moscow strain.

The pathogenesis and transmission of infection with the Moscow strain of ectromelia virus were studied in inbred mice. BALB/cAnNcr had high morbidity and mortality and C57BL/6Ncr (B6) mice had high morbidity and low mortality. Virus was detected in B6 mice for 2 weeks after subcutaneous (s.c.) inoculation and infected mice developed lesions compatible with acute mousepox. B6 inoculated by footpad transmitted infection to cagemates for up to five weeks and soiled cages that had housed infected mice were infectious for three weeks. S.c.-inoculated B6 mice also transmitted by contact for 2 weeks. Transmission was attributed to oronasal excretion of virus. Airborne transmission of infection between adjacent cages occurred at a low rate. Ectromelia virus-free progeny were derived from previously infected dams. These studies indicate that the highly virulent and infectious Moscow strain of ectromelia virus caused self-limiting infection in inbred mice and that direct contact is the most efficient means of transmission. These findings support the concept that mousepox can be contained by husbandry practices that minimize or eliminate the spread of infection by direct contact or fomites.

Animals↗
PubMed2000

Analysis of host response modifier ORFs of ectromelia virus, the causative agent of mousepox.

From the right-hand end of the ectromelia virus (strain Moscow) genome, 32318 bps have been sequenced, and characterized to include a total of 18 open reading frames (ORFs) and six regions which apparently no longer code for functional proteins. At least six of the ORFs appear to be involved in blocking the inflammatory/immune host response to infection, and therefore probably contribute significantly to the virulence of this virus in its natural host, the mouse. One of these genes encoded an isolog of the poxvirus chemokine binding protein, and was shown to be the most abundant protein secreted from ectromelia virus infected cells. Two regions were found to have significant similarity to poxvirus genes encoding tumor necrosis factor (TNF) binding proteins. Both are distinct from cytokine response modifier (crm)B and crmC but only one is predicted to encode a functional TNF binding protein. A novel similarity between the C-terminal domain of poxvirus TNF binding proteins and several other poxvirus proteins is also presented. The results are discussed in the context of ectromelia virus pathogenesis of mice.

Amino Acid Sequence↗
PubMed1976

Regulation of the T-cell response to ectromelia virus infection. I. Feedback suppression by effector T cells.

Spleen cells and serum from mice immunized with ectromelia virus suppressed the immune response to infectious virus when transferred intravenously into recipient mice given an immunizing virus dose. The suppression was reflected in decreased cytotoxic T-cell activity directed against H-2 compatible virus-infected target cells in the spleens of recipients. Suppression was observed when immune cells or serum were transferred 1-2 h or 1 day after immunization of recipients, but not 2 days after, and was maximal when 6-day immune spleen cells were used as suppressor cells. H-2 compatibility between donor and recipient mice was necessary for suppression to be expressed. Use of recombinant mice showed that I-region compatibility was neither sufficient nor necessary, and that D-region compatibility was sufficient. Specificity of suppression was suggested by the finding that cells and serum from mice immunized with Listeria monocytogenes, a bacterium, had no suppressive activity on the antiviral response. Anti-theta treatment eliminated the ability of immune cells to suppress, and the suppressive effect was not markedly dose-dependent with respect to both cell dose and virus dose under the conditions employed. Virus levels in the spleens of recipients were significantly reduced after injection of immune cells. Adult thymectomy had no effect on the primary immune response to ectromelia virus infection, thus indicating no role for T1 cells in the suppressive mechanism. The results obtained therefore suggested that suppression in this system was due to effector T cells which triggered clearance of virus (and thus, of virus-induced antigens) necessary for the induction of precursors of effector T cells, and that this simple feed-back mechanism normally plays an important role in the regulation of the primary immune response to ectromelia infection at the level of precursor induction. The existence of other postinduction regulatory mechanisms, however, is unknown and under investigation.

Animals↗
PubMed1991

Chromosomal locations and gonadal dependence of genes that mediate resistance to ectromelia (mousepox) virus-induced mortality.

Four genetic loci were tested for linkage with loci that control genetic resistance to lethal ectromelia virus infection in mice. Three of the loci were selected because of concordance with genotypes assigned to recombinant inbred (RI) strains of mice derived from resistant C57BL/6 and susceptible DBA/2 (BXD) mice on the basis of their responses to challenge infection. Thirty-six of 167 male (C57BL/6 x DBA/2)F1 x DBA/2 backcross (BC) mice died (22%), of which 27 (75%) were homozygous for DBA/2 alleles at Hc and H-2D. Twenty-eight percent of sham-castrated and 6% of sham-ovariectomized BC mice were susceptible to lethal mousepox, whereas 50% of gonadectomized mice were susceptible. There was no linkage evident between Hc or H-2D and loci that controlled resistance to lethal ectromelia virus infection in 44 castrated BC mice. Mortality among female mice of BXD RI strains with susceptible or intermediate male phenotypes was strongly correlated (r = 0.834) with male mortality. Gonadectomized C57BL/6 mice were as resistant as intact mice to lethal ectromelia virus infection. These results indicate that two gonad-dependent genes on chromosomes 2 and 17 and one gonad-independent gene control resistance to mousepox virus infection, that males and females share gonad-dependent genes, and that the gonad-independent gene is fully protective.

Alleles↗
PubMed1987

Observations on the replication of ectromelia virus in mouse-derived cell lines: implications for epidemiology of mousepox.

Ectromelia virus was shown to replicate in vitro in all lymphoma cell lines and in a small proportion of hybridoma lines tested. It was demonstrated that certain hybridoma cell lines, which were passed in ectromelia virus-infected mice, yielded ectromelia virus infectivity on explantation into tissue culture. This finding further substantiated the belief that ascitic fluid and hybridoma cell lines exposed to virus during mouse-passage could be important in the epidemiology of mousepox.

Animals↗
PubMed1975

Cell-medicated cytotoxicity against ectromelia virus-infected target cells. III. Role of the H-2 gene complex.

The role of the H-2 gene complex in expression of cytotoxicity exerted by specific ectromelia-immune thymus-derived (T) cells against ectromelia-infected target cells was examined. A repertoire of inbred mouse strains (some congenic) including the H-2 haplotypes k, d, b, s, q, the recombinant H-2a(k/d) and F1 hybrids (k/b and d/b) were immunized with virus and their spleen cells tested 6 days later, at the peak of the primary response, against H-2k,H-2d and H-2b target cells. Significant specific cytotoxicity occurred only when the immune cell donors and the target cells shared all or part of the same H-2 gene complex. For example, H-2a (k/d) immune cells killed both H-2k and H-2d target cells. There was no detectable effect of the non-H-2 genetic background, H-2 public specificities, or the M-locus. Target cells infected with ectromelia virus exhibited quantitative or qualitative changes (or both) in expression of normal H-2 antigens as indicated by reduced susceptibility to killing by T cells activated against H-2 antigens in mixed lymphocyte culture. These data are consistent with the hypothesis that T cells in this system are responding to virus-induced, specific changes in antigens on infected cells which are controlled by genes in the H-2 complex; these genes seem likely to be those coding for H-2 private specificities, or genes closely linked to them.

Animals↗
PubMed1994

Fine mechanisms of ectromelia virus thymidine kinase-negative mutants avirulence.

Three independently selected spontaneous thymidine kinase-negative mutants (TK-phenotype) and a recombinant with Escherichia coli beta-galactosidase gene (LacZ+ phenotype) inserted in the viral thymidine kinase gene (tk) were derived from a plaque-cloned isolate of K-1 ectromelia virus strain (TK+ phenotype). Dramatically decreased virulence of TK- variants was observed for all routes of mouse inoculation. The kinetics of TK+ and TK- variants in various target organs indicated a significant decrease of production and dissemination of TK- mutants and recombinant in the organs of mice. In the spleen and liver of intranasally or intracerebrally infected mice TK- virus was not detected during the entire period of observation. Analysis of organs homogenates of mice intranasally infected by a mixture of recombinant with TK-LacZ+ phenotype and parental isolate with TK+LacZ- phenotype on the monolayers of TK- cells indicated that only white plaques (LacZ-) with the TK+ phenotype appeared from liver and spleen homogenates. Thus, the mouse acts as a live filter much more efficiently than any other selective systems. Ultrastructural studies showed that viral damage in animals infected by TK- variants was far less than that observed in mice, infected with wild type of ectromelia virus and pathological lessions were slight and reversible. Replication of ectromelia virus TK- variants was blocked at the viroplasma stage in cells with a high level of differentiation in contrast to TK+ variants. Most likely, such restriction of target cells assortment is the general reason of reduced virulence in the case of tk-gene inactivation.

Animals↗