Elevation of cytokines associated with the thrombocytopenia of equine infectious anaemia.

Tornquist, Susan J.; Oaks, J. Lindsay; Crawford, Timothy B.

doi:10.1099/0022-1317-78-10-2541

Cited by 29 publications

(22 citation statements)

References 36 publications

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“…These observations extend previous findings from visna virus (9), simian immunodeficiency virus (4), and HIV-1 (7,28) indicating that the less-differentiated cells of the bone marrow can serve as a reservoir of latently infected cells. Recent studies detected increased levels of inflammatory cytokines in the bone marrow during EIAV infection in vivo (47) and in bone marrow derived macrophages in vitro (46), which are hypothesized to suppress platelet production (5). Thus, cytokine dysregulation could result in thrombocytopenia, a clinical finding consistently associated with recrudescence of disease.…”

Section: Discussionmentioning

confidence: 99%

Tissue Sites of Persistent Infection and Active Replication of Equine Infectious Anemia Virus during Acute Disease and Asymptomatic Infection in Experimentally Infected Equids

Harrold

Cook

et al. 2000

J Virol

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Equine infectious anemia virus (EIAV) infection of horses is characterized by recurring cycles of disease and viremia that typically progress to an inapparent infection in which clinicalEquine infectious anemia virus (EIAV) is unique among lentiviruses in that the clinical course of infection in equids results initially in a rapid and dynamic series of clearly demarcated cycles of disease and associated viremia that begin by 3 weeks postinfection and continue at irregular intervals separated by weeks or months (reviewed in reference 25). Disease cycles last 3 to 5 days and are characterized by fever, diarrhea, lethargy, edema, anemia, and thrombocytopenia. This stage of disease, defined as chronic equine infectious anemia (EIA), typically lasts about 8 to 12 months postinfection, with the frequency and severity of clinical episodes decreasing with time. In contrast to the progressive degenerative disease associated with most lentiviral infections, horses infected with EIAV typically make a transition during the first year postinfection from chronic EIA to an inapparent infection in which clinical symptoms are absent and viremia is usually undetectable for the remainder of the animal's life span of up to about 20 years. Thus, the EIAV systems provides a novel model in which to examine the dynamics of lentivirus replication during clearly defined cycles of disease and during long-term asymptomatic infections.Several lines of evidence indicate that the control of EIAV replication and disease in long-term inapparent carriers is mediated by virus-specific host immune responses that evolve during the first year postinfection to achieve an enduring effective suppression of virus replication. For example, experimental infection of foals with severe combined immunodeficiency results in a progressive infection leading to death, demonstrating the necessity of the host immune system in accomplishing the temporal control of virus replication associated with infection of immunocompetent horses (29). In addition, it has been shown that severe stress or treatment of long-term inapparent carriers with immunosuppressive drugs can cause recrudescence of viremia and disease, even after decades of clinical quiescence (16,48). Finally, it has been demonstrated that transfer of whole blood from long-term inapparent carriers to naive horses results in EIAV infection and disease in the recipient horses (12). Taken together, these observations demonstrate the lack of attenuation of the infect-* Corresponding author. Mailing address:

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Section: Discussionmentioning

confidence: 99%

Tissue Sites of Persistent Infection and Active Replication of Equine Infectious Anemia Virus during Acute Disease and Asymptomatic Infection in Experimentally Infected Equids

Harrold

Cook

et al. 2000

J Virol

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“…TNFα (Tumor Necrosis Factor alpha) and TGFβ (Transforming Growth Factor beta) are produced by macrophages and are known to have a suppressive effect on megakaryocyte genesis. Elevation of TNFα and TGFβ has been described in days preceding the onset of thrombocytopenia [175]; Costa et al [31] described a strong correlation between TNFα production, virulence of the infecting agent and clinical outcome in vaccinated and infected animals. TNFα and TGFβ may be released by macrophages upon EIAV infection and an increase in TNFα production has been shown to coincide with the onset of fever in African Swine Fever for example [151].…”

Section: Physiopathologymentioning

confidence: 99%

Equine Infectious Anemia Virus (EIAV): what has HIV?s country cousin got to tell us?

2004

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-Equine Infectious Anemia Virus (EIAV) is a lentivirus, of the Retrovirus family, with an almost worldwide distribution, infecting equids. It causes a persistent infection characterized by recurring febrile episodes associating viremia, fever, thrombocytopenia, and wasting symptoms. The disease is experimentally reproducible by inoculation of Shetland ponies or horses with EIAV pathogenic strains. Among lentiviruses, EIAV is unique in that, despite a rapid virus replication and antigenic variation, most animals progress from a chronic stage characterized by recurring peaks of viremia and fever to an asymptomatic stage of infection. The inapparent carriers remain infective for life, as demonstrated by experimental transfer of blood to naive animals. The understanding of the correlates of this immune control is of great interest in defining vaccine strategies. Research on EIAV, this "country cousin" of HIV (Human Immunodeficiency Virus), over the last five decades has produced some interesting results on natural immunological control of lentivirus replication and disease and on the nature and role of virus variation in persistence and pathogenesis. These studies are of interest in the context of HIV and efforts to develop a vaccine. This review will focus on some of the most recent results. equine infectious anemia virus / lentivirus / equids / vaccine / viral evolution

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“…Tornquist et al [39] demonstrated that TGF-ß protein levels determined by immunohistochemical staining were significantly higher in prethrombocytopenia bone marrow in patients with lentivirus infection. Since TGF-ß 1 is a potent inhibitor of the proliferation and differentiation of megakaryocyte progenitor cells in vivo and in vitro [14,15,[27][28][29], can TGF-ß 1 levels be significantly elevated at the prethrombocytopenic stage?…”

Section: Discussionmentioning

confidence: 99%

Plasma Transforming Growth Factor β<sub>1</sub> Levels in Thrombocytopenic and Nonthrombocytopenic Neonates

Duman

İrken²,

Ören³

et al. 2003

Neonatology

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In this study, we determined the plasma TGF-β₁ levels in healthy and thrombocytopenic and nonthrombocytopenic neonates who had perinatal risk factors and examined the association between plasma TGF-β₁ levels and platelet counts in these newborns to investigate the role of TGF-β₁ in the pathogenesis of neonatal thrombocytopenia. Three groups were defined in this prospective study: group 1, thrombocytopenic neonates (n = 22) who had perinatal risk factors; group 2, nonthrombocytopenic neonates who had similar perinatal risk factors for thrombocytopenia (n = 20); group 3, healthy and nonthrombocytopenic neonates without any risk factors (n = 20). Plasma TGF-β₁ levels were measured with ELISA. Plasma TGF-β₁ levels of the thrombocytopenic neonates were significantly lower than those of healthy nonthrombocytopenic neonates but did not differ significantly from nonthrombocytopenic neonates who had similar perinatal risk factors for thrombocytopenia. There was a significant positive correlation between plasma TGF-β₁ levels and platelet counts. Further studies are needed to determine the cause of low plasma TGF-β₁ levels in thrombocytopenic neonates and to investigate the role of plasma TGF-β₁ levels in the pathogenesis of neonatal thrombocytopenia.

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Elevation of cytokines associated with the thrombocytopenia of equine infectious anaemia.

Cited by 29 publications

References 36 publications

Tissue Sites of Persistent Infection and Active Replication of Equine Infectious Anemia Virus during Acute Disease and Asymptomatic Infection in Experimentally Infected Equids

Tissue Sites of Persistent Infection and Active Replication of Equine Infectious Anemia Virus during Acute Disease and Asymptomatic Infection in Experimentally Infected Equids

Equine Infectious Anemia Virus (EIAV): what has HIV?s country cousin got to tell us?

Plasma Transforming Growth Factor β<sub>1</sub> Levels in Thrombocytopenic and Nonthrombocytopenic Neonates

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