Expression of the Full-Length Form of gp2 of Equine Herpesvirus 1 (EHV-1) Completely Restores Respiratory Virulence to the Attenuated EHV-1 Strain KyA in CBA Mice

Smith, Patrick M.; Kahan, Shannon M.; Rorex, Colin; Einem, Jens von; Osterrieder, Nikolaus; O’Callaghan, Dennis J.

doi:10.1128/jvi.79.8.5105-5115.2005

Cited by 29 publications

(28 citation statements)

References 39 publications

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“…Because upregulation of CCL3 in mice during EHV-1 infection had been observed previously (14,21), we decided to study the role of the chemokine during EHV-1 infection in more detail by using mice deficient in CCL3. CCL3…”

Section: Resultsmentioning

confidence: 99%

“…Intranasal infection of mice with EHV-1 results in an acute, productive infection of the lungs, followed by dissemination of the virus to visceral organs and the brain (6). Besides extensive perivascular and peribronchial cuffing, an interstitial inflammatory infiltrate in the lungs can be observed during EHV-1 infection, consisting mainly of neutrophils, lymphocytes, and macrophages (5,21,22). Such infiltration in the bronchoalveolar compartment also occurs in the natural host, the horse, as dynamic leukocyte migration has been observed upon EHV-1 infection (17).…”

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confidence: 99%

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CCL3 and Viral Chemokine-Binding Protein gG Modulate Pulmonary Inflammation and Virus Replication during Equine Herpesvirus 1 Infection

Walle

Sakamoto

Osterrieder

2008

J Virol

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CCL3 is a proinflammatory chemokine that mediates many of the cellular changes occurring in pulmonary disease. Here, CCL3؊/؊ mice were used to investigate the role of this chemokine during respiratory herpesvirus infection. Compared to wild-type mice, CCL3؊/؊ mice infected with the alphaherpesvirus equine herpesvirus 1 (EHV-1) displayed reduced body weight loss but had higher pulmonary viral loads. Lungs from infected CCL3 ؊/؊ mice suffered a milder interstitial pneumonia, and fewer immune cells were recovered from the pulmonary airways after infection. We could also demonstrate that herpesvirus-encoded chemokine-binding glycoprotein G (gG) was capable of inhibiting the chemotactic functions of CCL3. This CCL3-mediated chemotaxis, however, was restored in the presence of gG-specific antibodies, which puts into question the advertised use of gG deletion mutants as marker vaccines. In summary, we concluded that CCL3 is a major player in controlling herpesvirus replication in the target organ, the lung, and does so by evoking a strong inflammatory response. The immunomodulatory activity of CCL3 is balanced by the expression of viral gG, whose chemokine-binding activity is mitigated in secondary infections by the production of anti-gG antibodies.

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Section: Resultsmentioning

confidence: 99%

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confidence: 99%

CCL3 and Viral Chemokine-Binding Protein gG Modulate Pulmonary Inflammation and Virus Replication during Equine Herpesvirus 1 Infection

Walle

Sakamoto

Osterrieder

2008

J Virol

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“…Studies on culture-adapted forms of EHV-1 have shown that attenuation results from the expression of a truncated form of a single glycoprotein, gp2 (29). However, truncation of A8 was not observed in the attenuation of AlHV-1 (37).…”

Section: Vol 82 2008 Proteomic Analysis Of Alcelaphine Herpesvirus mentioning

confidence: 98%

Proteomic Analysis of Pathogenic and Attenuated Alcelaphine Herpesvirus 1

Dry

Haig

Inglis

et al. 2008

J Virol

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The gammaherpesvirus alcelaphine herpesvirus 1 (AlHV-1) causes malignant catarrhal fever in susceptible ungulates but infects its natural host, wildebeest, without obvious clinical signs. In tissue culture, AlHV-1 is initially predominantly cell associated and virulent but on extended culture becomes cell-free and attenuated. We wanted to determine what changes in protein composition had taken place during the transition from virulent to attenuated virus in culture. Purified virus preparations were fractionated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and proteins were analyzed by liquid chromatography-electrospray ionization-tandem mass spectrometry. Peptides were identified in serial gel slices by using MASCOT software to interrogate virus-specific and nonredundant sequence databases. Twenty-three AlHV-1-encoded proteins and six cellular proteins were identified in the attenuated and virulent viruses. Two polypeptides were detected in only the virulent virus preparations, while one other protein was found in only the attenuated virus. Two of these virus-specific proteins were identified by a single peptide, suggesting that these may be low-abundance virion proteins rather than markers of attenuation or pathogenesis. The results suggest that attenuation of AlHV-1 is not the result of gross changes in the composition of the virus particle but probably due to altered viral gene expression in the infected cell.

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“…CBA mice have been used as a model for the study of neuropathogenicity of EHV-1 KgI/gE/75 strain [7]. Smith et al [18] reported that CBA mice were more susceptible to EHV-1-mediated disease than BALB/c when using KyA, KyARgp2F and RacL11 strains. However, all of these studies used a limited number of EHV-1 strains.…”

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confidence: 99%

Diverse Pathogenicity of Equine Herpesvirus 1 (EHV-1) Isolates in CBA Mouse Model

Kasem

Tsujimura

et al. 2010

The Journal of Veterinary Medical Science

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ABSTRACT. The pathogenicity of equine herpesvirus 1 (EHV-1) isolates of Japan were evaluated by using the CBA mouse model. CBA mice were inoculated with eight Japanese EHV-1 strains (89c1, 90c16, 90c18, 97c11, 98c12, 00c19, 01c1 and HH-1) and one British strain (Ab4p). 89c1 caused slight body weight loss and nervous signs in mice at 8 days post infection (dpi). Severe weight loss and nervous signs were observed in mice inoculated with Ab4p at 6 dpi. The other strains did not cause apparent clinical signs. Infectious viruses were recovered from the lungs of all groups at 2 dpi. Histopathological analysis revealed interstitial pneumonia in the lungs of all mice inoculated with EHV-1. Encephalitis or meningoencephalitis was observed in the brains of mice inoculated with 89c1, 90c18, 97c11, 98c12, 01c1 and Ab4p. Japanese EHV-1 strains showed low pathogenicity in CBA mice, whereas the sequential affects of infection are similar to those of the highly pathogenic strain Ab4p. These results suggest that field isolates of EHV-1 have varying degrees of pathogenicity in CBA mice.

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Expression of the Full-Length Form of gp2 of Equine Herpesvirus 1 (EHV-1) Completely Restores Respiratory Virulence to the Attenuated EHV-1 Strain KyA in CBA Mice

Cited by 29 publications

References 39 publications

CCL3 and Viral Chemokine-Binding Protein gG Modulate Pulmonary Inflammation and Virus Replication during Equine Herpesvirus 1 Infection

CCL3 and Viral Chemokine-Binding Protein gG Modulate Pulmonary Inflammation and Virus Replication during Equine Herpesvirus 1 Infection

Proteomic Analysis of Pathogenic and Attenuated Alcelaphine Herpesvirus 1

Diverse Pathogenicity of Equine Herpesvirus 1 (EHV-1) Isolates in CBA Mouse Model

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