Immunization Against Feline Coronaviruses

Scott, F. W.

doi:10.1007/978-1-4684-1280-2_72

Cited by 14 publications

(14 citation statements)

References 22 publications

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“…Cats exposed to UCD1 and succumbing to disease after inoculation with UCD8 had a significantly shortened survival time as compared to cats that succumbed to disease but were only exposed to UCD8 (mean of 4.6 days versus 8.6 days, P = 0.004, Student's t-test). This is consistent with several previous reports demonstrating antibody-dependent enhancement of disease progression in seropositive cats subsequently exposed to FIPV (Pedersen and Boyle, 1980;Scott, 1987;Scott et al, 1995;Vennema et al, 1990;Weiss and Scott, 1981a,b).…”

Section: Fipv Infection and Clinical Coursesupporting

confidence: 93%

In vivo cytokine response to experimental feline infectious peritonitis virus infection

Dean

Olivry

Stanton

et al. 2003

Veterinary Microbiology

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Feline infectious peritonitis virus (FIPV) is a coronavirus that causes sporadic fatal disease in cats characterized by vasculitis, granulomatous inflammation and effusive pleuritis/peritonitis. Histologic changes in lymphoid tissues include lymphoid hyperplasia, lymphoid depletion, histiocytosis, and granuloma formation. Although viremia occurs, histologic lesions are not found uniformly throughout lymphoid tissues. We used experimental infection of cats with a highly pathogenic FIPV isolate, UCD8, to study histologic lesions, virus replication, and cytokine expression in multiple lymphoid tissues during the effusive phase of disease. Viral RNA was found in 76% of central tissues (mediastinal lymph node, spleen, mesenteric lymph node) examined, as compared to 27% of peripheral tissues (popliteal lymph node, cervical lymph node, femoral bone marrow). All tissues positive for virus replication also demonstrated lymphoid depletion. Generally, affected tissues had lower levels of IL-4 and IL-12-p40 mRNA and higher levels of IL-10 mRNA. Although no differences in IFN-gamma or TNF-alpha mRNA were measured, TNF-alpha protein expression was greater in affected tissues and demonstrated a shift in the source of TNF-alpha from macrophages to lymphocytes. Together, these results colocalize FIPV replication, lymphocyte depletion in tissues, and alterations in cytokine transcription and translation. A possible role for TNF-alpha in the previously described FIPV-induced lymphocyte apoptosis is also suggested.

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Section: Fipv Infection and Clinical Coursesupporting

confidence: 93%

In vivo cytokine response to experimental feline infectious peritonitis virus infection

Dean

Olivry

Stanton

et al. 2003

Veterinary Microbiology

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“…An exception is IBV for which at least five serotypes are described (Kusters et al, 1987). Although FIPV and FECV strains at present comprise a single serotype, strains vary greatly in infectivity and virulence and constitute multiple biotypes (Pedersen, 1987a,b;Scott, 1987;Mostl, 1990).…”

Section: Animal Hosts Antigenic Relationships and Diseasesmentioning

confidence: 99%

“…A broad spectrum exists in the virulence of FIPV strains, with the ability of strains to infect and replicate in macrophages and spread systemically correlated with virulence (Stoddart et al, 1989). Serum antibodies accentuate the pathogenesis of FIP via the generation of immune complexes which are deposited in affected organs and via mediation of antibodydependent enhancement (ADE) of FIPV infection of macrophages (Scott, 1987;Olsen et al, 1992).…”

Section: Animal Hosts Antigenic Relationships and Diseasesmentioning

confidence: 99%

Coronavirus immunogens

Saif

1993

Veterinary Microbiology

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Coronaviruses (CV) infect a variety of livestock, poultry and companion animals. They belong to at least five antigenic groups. CV cause localized infections of the respiratory and/or intestinal tracts, with the exception of feline infectious peritonitis virus (FIPV) and hemagglutinating encephalomyelitis (HEV) which cause systemic infections. The enteropathogenic CV infect the villous enterocytes resulting in villous atrophy leading to malabsorptive diarrhea. Several CV (bovine CV-BCV, porcine respiratory CV-PRCV, infectious bronchitis virus-IBV) cause respiratory disease. Current evidence indicates that protection against enteric and respiratory CV infections is mediated by passive or active immunity at the primary site of CV replication. Maternal vaccination approaches to induce passive immunity include the use of inactivated and modified live viral vaccines. Modified live viruses and a Ts mutant CV (FIPV) are also used as oral or intranasal vaccines to induce active mucosal immunity. The success of these vaccines in the field is often compromised by a number of potential problems. Coronaviruses are spherical, enveloped viruses, ranging from 80-160 nm in diameter and containing a positive-stranded RNA genome. They possess prominent surface spikes and some species display a fringe of smaller surface projections believed to be the hemagglutinin (HE). Coronaviruses possess 3 to 4 structural proteins: the spike (S) glycoprotein (150-200 kDa), the integral membrane glycoprotein (M; 20-30 kDa) and the nucleocapsid phosphoprotein (N; 43-50 kDa). A subset of CV (BCV, HEV, turkey CV) possess a third glycoprotein on the virion surface, the HE (60-65 kDa). These proteins can be quantitated using pooled monoclonal antibodies (mAb) to distinct epitopes of each protein in ELISA. Most research has focused on the S protein as a candidate antigen for CV vaccines since it induces virus neutralizing (VN) antibodies. However the HE protein stimulates the production of VN and HE inhibiting antibodies and the M protein induces antibodies that neutralize virus in the presence of complement. Attempts to correlate in vitro VN antibody activity with in vivo protection have shown that the passive transfer of VN mAb to the S or HE protein conferred passive protection against CV challenge in some studies, but not others. Additional research has implicated a possible role for other CV proteins in immunity. Studies of mAb to the M protein of transmissible gastroenteritis (TGEV) have provided evidence for a direct role of the M protein in the induction of alpha IFN by porcine blood leukocytes. The potential significance of this phenomenon to immunity to TGEV is unclear.(ABSTRACT TRUNCATED AT 400 WORDS)

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“…Diagnosis is by isolation of the virus from fetuses or neonates submitted for necropsy, by documenting seroconversion in the dam, or clinically by the characteristic ataxia observed in the neonates. Vaccination of queens against FPLV prior to breeding is recommended [108,109].…”

Section: Feline Panleukopenia Virusmentioning

confidence: 99%

Canine and feline pregnancy loss due to viral and non-infectious causes: A review

2008

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Among the causes for pregnancy loss, viruses and non-infectious factors are among the most important. In both dogs and cats, research and clinical evidence provide proof that there is an increasing incidence of pregnancy loss associated with infectious diseases like herpesvirus, as well as the presence of toxicants or chemicals in the animal's diet and environment. Endocrine causes must be taken into consideration when dealing with pregnancy loss. This review will cover the most recent knowledge regarding viral and non-infectious of pregnancy losses in the dog and cat.

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Immunization Against Feline Coronaviruses

Cited by 14 publications

References 22 publications

In vivo cytokine response to experimental feline infectious peritonitis virus infection

In vivo cytokine response to experimental feline infectious peritonitis virus infection

Coronavirus immunogens

Canine and feline pregnancy loss due to viral and non-infectious causes: A review

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