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PubMed2004

Unusual presentations of cowpox infection in cats.

Cowpox virus infections are reported typically to cause focal ulcerated, crusted skin lesions, sometimes with mild systemic illness and concurrent oral lesions. Severe systemic illness usually only occurs in young or immunosuppressed individuals. This report describes four cases of cowpox infection in cats which illustrate variations to the usual presentation of the virus. The poxvirus infections were confirmed histopathologically, serologically and by PCR analysis.

Animals↗
PubMed2003

Aerosolized cidofovir is retained in the respiratory tract and protects mice against intranasal cowpox virus challenge.

We employed a murine model to test the concept of using an aerosolized, long-acting antiviral drug to protect humans against smallpox. We previously showed that a low dose of aerosolized cidofovir (HPMPC [Vistide]) was highly protective against subsequent aerosolized cowpox virus challenge and was more effective than a much larger dose of drug given by injection, suggesting that aerosolized cidofovir is retained in the lung. Because the nephrotoxicity of cidofovir is a major concern in therapy, delivering the drug directly to the respiratory tract might be an effective prophylactic strategy that maximizes the tissue concentration at the site of initial viral replication, while minimizing its accumulation in the kidneys. In the present study, we found that treating mice with aerosolized (14)C-labeled cidofovir ((14)C-cidofovir) resulted in the prolonged retention of radiolabeled drug in the lungs at levels greatly exceeding those in the kidneys. In contrast, subcutaneous injection produced much higher concentrations of (14)C-cidofovir in the kidneys than in the lungs over the 96-h time course of the study. As further evidence of the protective efficacy of aerosolized cidofovir, we found that aerosol treatment before or after infection was highly protective in mice challenged intranasally with cowpox virus. All or nearly all mice that were treated once by aerosol, from 2 days before to 2 days after challenge, survived intranasal infection, whereas all placebo-treated animals died.

Administration, Intranasal↗
PubMed2000

Treatment of cowpox virus respiratory infections in mice with ribavirin as a single agent or followed sequentially by cidofovir.

To better understand the potential of ribavirin in the treatment of orthopoxvirus infections (such as those acquired through bioterrorist activities), the efficacy of the drug was studied in a cowpox respiratory infection model in mice under varying disease severity. Mice did not survive a high intranasal cowpox virus challenge [3 x 10(6) plaque forming units (pfu)/animal] treated with subcutaneous ribavirin (100 mg/kg/day for 5 days), but lived 3.9 days longer than placebos. In contrast, 100% of animals receiving the same dose of drug survived a 3 x 10(5) pfu challenge compared with 0% survival of those that received placebo. Survival rates of 50 and 30% occurred with ribavirin doses of 50 and 25 mg/kg/day, respectively. At the 100 mg/kg/day dose, ribavirin reduced lung virus titres 40-fold on day 6 of the infection relative to titres in the placebo group. Weight loss resulting from illness and mean lung weights of mice treated with ribavirin were also significantly reduced. Mice were infected intranasally with the high 3 x 10(6) pfu virus challenge dose and treated with 100 mg/kg/day ribavirin for 5 days, followed by single injections of 75 mg/kg cidofovir on day 6, 7, 8 or 9. Cidofovir alone (without ribavirin) administered on day 6 had no beneficial effect on disease outcome. Ribavirin alone increased the mean time to death by 3.7 days. Ribavirin treatment for 5 days followed by cidofovir treatment on days 6 and 7 significantly increased the mean time to death beyond that achieved with ribavirin alone by 8.2 and 4.4 days, respectively, with 30 and 40% of mice surviving the infection. These results suggest that many individuals infected with an orthopoxvirus by aerosol route would benefit by a course of ribavirin therapy. Later, the fewer number of very sick individuals could be treated with intravenous cidofovir.

Animals↗
PubMed2002

Rat-to-human transmission of Cowpox infection.

We isolated Cowpox virus (CPXV) from the ulcerative eyelid lesions of a 14-year-old girl, who had cared for a clinically ill wild rat that later died. CPXV isolated from the rat (Rattus norvegicus) showed complete homology with the girl's virus. Our case is the first proven rat-to-human transmission of cowpox.

Adolescent↗
PubMed1992

Experimental infection of domestic cats by cowpox virus.

Infection of young domestic cats by cowpox virus isolated from sick rodents (family Muridae) revealed their high susceptibility to the virus; a severe disease with 100% lethality developed after oral inoculation as well as upon skin scarification. The disease in dermally infected animals was accompanied by eruptions on the site of inoculation. High concentration of the virus was detected in lungs of animals infected by either of inoculation routes. The data testify the possible participation of domestic cats as intermediate hosts in the circulation of cowpox virus.

Animals↗
PubMed1997

The cowpox virus-encoded homolog of the vaccinia virus complement control protein is an inflammation modulatory protein.

Vaccinia virus complement control protein (VCP) is encoded by vaccinia virus, with its homolog encoded by other pathogenic poxviruses including variola virus. Since rodents are the primary reservoir hosts of cowpox virus (CPV) and since CPV encodes a highly conserved functional homolog of VCP, termed here the inflammation modulatory protein (IMP), the effects of injection of CPV into the footpads of mice was determined in order to study the precise in vivo effects of IMP. Macroscopic examination of the site of injection with a recombinant virus lacking IMP (CPV-IMP) showed greater tissue damage, with more hemorrhage and induration, than sites injected with the wild-type cowpox virus. In addition, the measurement of the specific swelling response carried out for several weeks revealed significantly greater swelling in mice injected with CPV-IMP. Thus, IMP modulates the complement-activated inflammatory response in vivo. Furthermore, the diminished destruction of host tissue observed in the presence of IMP indicates symbiosis in which the virus ensures the preservation of surrounding host tissue, possibly to support the growth of its progeny.

Amino Acid Sequence↗
PubMed2001

Cowpox virus and other members of the orthopoxvirus genus interfere with the regulation of NF-kappaB activation.

NF-kappaB comprises a family of transcription factors that regulate key immune processes. In this study, the effects of orthopoxvirus infection upon the activation of NF-kappaB were examined. During the early phase of infection, cowpox virus can inhibit the induction of NF-kappaB-regulated gene expression by interfering with the process of IkappaBalpha degradation. Although either okadaic acid or tumor necrosis factor (TNF) treatment of infected cells can induce IkappaBalpha phosphorylation, further processing of IkappaBalpha is inhibited. These results suggest that cowpox virus is capable of inhibiting the activation of NF-kappaB at a point where multiple signal transduction pathways converge. Other orthopoxviruses affect NF-kappaB activity, but in a type-specific manner. Raccoonpox virus and vaccinia virus (Copenhagen strain) negatively affect NF-kappaB induction by TNF. In contrast, the modified vaccinia virus Ankara strain induces NF-kappaB activation, even in the absence of other stimuli. These findings suggest that orthopoxviruses may affect a broad range of virus-host interactions through their effects upon NF-kappaB activation. Moreover, because of the central role for NF-kappaB in immune processes and disease, these type-specific effects may contribute significantly to the immunogenic and pathogenic properties of poxviruses.

Animals↗
PubMed1992

Viral inhibition of inflammation: cowpox virus encodes an inhibitor of the interleukin-1 beta converting enzyme.

Cowpox virus effectively inhibits inflammatory responses against viral infection in the chick embryo. This study demonstrates that one of the viral genes necessary for this inhibition, the crmA gene (a cytokine response modifier gene), encodes a serpin that is a specific inhibitor of the interleukin-1 beta converting enzyme. This serpin can prevent the proteolytic activation of interleukin-1 beta, thereby suppressing an interleukin-1 beta response to infection. However, the modification of this single cytokine response is not sufficient to inhibit inflammatory responses. This suggests that cowpox virus encodes several cytokine response modifiers that act together to inhibit the release of pro-inflammatory cytokines in response to infection. These viral countermeasures to host defenses against infection may contribute significantly to the pathology associated with poxvirus infections.

Amino Acid Sequence↗
PubMed1999

The genome of cowpox virus contains a gene related to those encoding the epidermal growth factor, transforming growth factor alpha and vaccinia growth factor.

Cowpox virus (CPV) is a member of the Orthopoxvirus genus and has the genetic capacity to encode a multitude of genes that interfere with the host inflammatory and immune response or modulate the physiological state of infected and non-infected cells. Among these CPV factors are receptors homologous to interferon and tumor necrosis factor receptors and also a viral cellular serine-proteinase analog. Here we describe the detection of a CPV gene that encodes a protein homologous to epidermal growth factor, transforming growth factor alpha and poxvirus growth factors, such as the vaccinia growth factor (VGF). The VGF and other poxvirus growth factors are produced early in the infection and are secreted into the medium where they bind to the EGF receptors, generating mytotic responses. The cowpox growth factor (CGF) gene was detected in three copies on the virus genome by PCR, and by northern and southern blot hybridization using VGF nucleotide sequences as primers and probes. The CPV gene has a strong nucleotide and predicted amino acid similarity with VGF, and is also produced early in the infection.

Amino Acid Sequence↗
PubMed1995

Granzyme B is inhibited by the cowpox virus serpin cytokine response modifier A.

The ability of cytolytic cells to cause apoptosis in target cells is in part due to the action of the serine proteinase granzyme B. We demonstrate that granzyme B is inhibited, with an association rate constant of 2.9 x 10(5) M-1 s-1, by the cowpox viral serpin cytokine response modifier A (CrmA). Previously we have shown CrmA to be an inhibitor of the cysteine proteinase interleukin-1 beta-converting enzyme (ICE). Thus the mechanism of CrmA involves the unusual ability to efficiently inhibit proteinases from two distinct catalytic classes, in this case serine and cysteine proteinases. Granzyme B and ICE are both used to combat viral infection, and we propose that cowpox virus uses CrmA to evade the contribution of these two proteinases. Thus, through CrmA, the virus may influence two of the pathways normally used to kill virus-infected cells: acting on endogenous proteinases such as ICE and on exogenous proteinases delivered by cytotoxic lymphocytes to infected cells.

Binding, Competitive↗
PubMed2000

Cidofovir protects mice against lethal aerosol or intranasal cowpox virus challenge.

The efficacy of cidofovir for treatment of cowpox virus infection in BALB/c mice was investigated in an effort to evaluate new therapies for virulent orthopoxvirus infections of the respiratory tract in a small animal model. Exposure to 2(-5)x10(6) pfu of cowpox virus by aerosol or intranasally (inl) was lethal in 3- to 7-week-old animals. One inoculation of 100 mg/kg cidofovir on day 0, 2, or 4, with respect to aerosol infection, resulted in 90%-100% survival. Treatment on day 0 reduced peak pulmonary virus titers 10- to 100-fold, reduced the severity of viral pneumonitis, and prevented pulmonary hemorrhage. The same dose on day -6 to 2 protected 80%-100% of inl infected mice, whereas 1 inoculation on day -16 to -8 or day 3 to 6 was partially protective. Cidofovir delayed but did not prevent the death of inl infected mice with severe combined immunodeficiency. Treatment at the time of tail scarification with vaccinia virus did not block vaccination efficacy.

Administration, Intranasal↗
PubMed1995

Delay of vaccinia virus-induced apoptosis in nonpermissive Chinese hamster ovary cells by the cowpox virus CHOhr and adenovirus E1B 19K genes.

The infection of vaccinia virus in Chinese hamster ovary (CHO) cells produces a rapid shutdown in protein synthesis, and the infection is abortive (R.R. Drillien, D. Spehner, and A. Kirn, Virology 111:488-499, 1978; D.E. Hruby, D.L. Lynn, R. Condit, and J.R. Kates, J. Gen. Virol. 47:485-488, 1980). Cowpox virus, which can productively infect CHO cells, had previously been shown to contain a host range gene, CHOhr, which confers on vaccinia virus the ability to replicate in CHO cells (D. Spehner, S. Gillard, R. Drillien, and A. Kirn, J. Virol. 62:1297-1304, 1988). We found that CHO cells underwent apoptosis when infected with vaccinia virus. The expression of the CHOhr gene in vaccinia virus allowed for the expression of late virus genes. CHOhr also delayed or prevented vaccinia virus-induced apoptosis in CHO cells such that there was sufficient time for replication of the virus before the cell died. The E1B 19K gene from adenovirus also delayed vaccinia virus-induced apoptosis; however, there was no detectable expression of late virus genes. Furthermore, E1B 19K also delayed cell death in CHO cells which had been productively infected with vaccinia virus. This study identifies a new antiapoptotic gene from cowpox virus, CHOhr, for which the protein contains an ankyrin-like repeat and shows no significant homology to other proteins. This work also indicates that an antiapoptotic gene from one virus family can delay cell death in an infection of a virus from a different family.

Adenoviridae↗
PubMed1997

[A case of cowpox].

A 37-year-old woman was admitted to the dermatology department at a regional hospital with a severe ulceration at the medial angle of the right eye. Virus culture yielded orthopoxvirus-like particles, later identified as cowpox virus. The clinical picture and virological diagnosis of cowpox are discussed. Emphasis is placed on the need for awareness among health personnel that such infections may well be encountered in an increasingly unvaccinated population. Guidelines for clinicians and for virology laboratories are given. Cats as a zoonoic source is discussed.

Adult↗
PubMed1986

Isolation of cowpox virus A-type inclusions and characterization of their major protein component.

A-type inclusions (ATI)2 are large well-defined structures that appear in the cytoplasm during the late stages of the multiplication cycles of many poxviruses. The ATIs produced by the CPRC1 strain of cowpox virus in strain 143 human osteosarcoma cells have been isolated and characterized. These inclusions which can be recovered in large amounts (about 20 mg per 10(9) cells), appear to consist entirely of a single protein species that has a molecular weight of 160,000. It is a late protein, stable in infected cells, and during the late stages of the multiplication cycle it is one of the most abundantly synthesized proteins. Very similar ATIs composed of a serologically closely related protein of the same size are formed in cells infected with raccoonpox virus. In cells infected with vaccinia virus strain WR much smaller inclusions are formed; further, in such cells large amounts of a late protein with a molecular weight of 94,000 are produced that is also closely related to the cowpox virus ATI protein.

Cell Fractionation↗
PubMed1982

An outbreak of cowpox in captive cheetahs: virological and epidemiological studies.

This paper describes virological and epidemiological features of an infection which killed two of three affected cheetahs at Whipsnade Park in 1977. Two animals had profuse skin lesions and the third had an acute haemorrhagic pneumonia. The outbreak was shown to be caused by cowpox virus. Cowpox virus is believed to circulate in small wild animals, but the source of infection was not traced despite virological and serological tests on 93 captive and 102 wild animals. Sub-clinical infections did not occur in susceptible contact cheetahs. Immune globulin did not influence the outcome and smallpox vaccine does not take in cheetahs. Management of any future outbreak will rely on prompt diagnosis and segregation of infected animals.

Acinonyx↗
PubMed1982

Arginine deprivation and the generation of white variants in cowpox virus-infected cell cultures.

The white pock variant of cowpox virus shows limited growth in chick embryo fibroblasts maintained in arginine-deprived culture medium. Since these conditions inhibit the growth of parental virus, there is a marked increase in the frequency of the white variant in the virus population recovered after passage in the absence of arginine. The variants generated in this system have been characterized by restriction endonuclease analysis of virus DNA in the total DNA recovered from infected cell cultures. Such analysis shows that the white variants arise as deletion mutants of the parental virus, but there was considerable heterogeneity in the restriction patterns of different isolates examined shortly after their generation. Further passage selected white cowpox virus populations with a stable genome configuration comparable with the DNA of pock-purified white variants.

Animals↗
PubMed2002

Amplification of 'variola virus-specific' sequences in German cowpox virus isolates.

In 1995 a polymerase chain reaction (PCR) protocol describing the specific detection of variola virus, the causative agent of smallpox, was published by Knight and others. Virulent variola major strains could be differentiated from less virulent variola minor strains because of the distinct amplicon sizes. Here, we applied this PCR protocol to DNA from various orthopoxvirus isolates. There was no amplification with the orthopoxvirus species vaccinia, monkeypox, mousepox, or camelpox viruses. However, amplification was observed in six out of 15 cowpox virus strains investigated. The size of the amplicons corresponded exactly with the size described for variola minor strains and the nucleotide sequence identity accounted for 97%. Findings are discussed with respect to the evolution of orthopoxvirus species assuming that variola virus most probably stems from a rodent-transmitted cowpox virus-like progenitor.

Animals↗