Enhanced Integumental and Ocular Amelanosis Following the Termination of Cyclosporine Administration

Pardue, S. L.; Fite, Katherine V.; Bengston, Lynn; Lamont, Susan J.; Boyle, Milton L; Smyth, J. Robert

doi:10.1111/1523-1747.ep12470453

Cited by 36 publications

(15 citation statements)

References 20 publications

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“…cyclosporine and dexamethasone were administered to three ducks (1001, 1005, and 1006) and water was administered as placebo to two ducks (1003 and 1007) for 4 weeks. The cyclosporine dose was similar to doses used in published experiments with chickens (7,28,29,34,39) and the dexamethasone dose was based on a report on its use in ducks (10). Liver tissue and serum were collected from all ducks pretreatment and after 2 and 4 weeks of treatment and examined for residual DHBV DNA.…”

Section: Resultsmentioning

confidence: 99%

Covalently Closed Circular DNA Is the Predominant Form of Duck Hepatitis B Virus DNA That Persists following Transient Infection

Mire

Miller

Foster

et al. 2005

J Virol

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Residual hepatitis B virus (HBV) DNA can be detected in serum and liver after apparent recovery from transient infection. However, it is not known if this residual HBV DNA represents ongoing viral replication and antigen expression. In the current study, ducks inoculated with duck hepatitis B virus (DHBV) were monitored for residual DHBV DNA following recovery from transient infection until 9 months postinoculation (p.i.). Resolution of DHBV infection occurred in 13 out of 15 ducks by 1-month p.i., defined as clearance of DHBV surface antigen-positive hepatocytes from the liver and development of anti-DHBV surface antibodies. At 9 months p.i., residual DHBV DNA was detected using nested PCR in 10/11 liver, 7/11 spleen, 2/11 kidney, 1/11 heart, and 1/11 adrenal samples. Residual DHBV DNA was not detected in serum or peripheral blood mononuclear cells. Within the liver, levels of residual DHBV DNA were 0.0024 to 0.016 copies per cell, 40 to 80% of which were identified as covalently closed circular viral DNA by quantitative PCR assay. This result, which was confirmed by Southern blot hybridization, is consistent with suppressed viral replication or inactive infection. Samples of liver and spleen cells from recovered animals did not transmit DHBV infection when inoculated into 1-to 2-day-old ducklings, and immunosuppressive treatment of ducks with cyclosporine and dexamethasone for 4 weeks did not alter levels of residual DHBV DNA in the liver. These findings further characterize a second form of hepadnavirus persistence in a suppressed or inactive state, quite distinct from the classical chronic carrier state.Hepatitis B virus (HBV) infections in adult humans are typically characterized by recovery and the development of anti-surface antibodies (anti-HBs) and immunity to reinfection. Despite the apparent clearance of HBV infection, a number of studies of patient sera have demonstrated persistence of viral DNA for months or years after resolution of transient HBV infection (2,19,24,41). Cytotoxic T-lymphocyte responses also persist, and reactivation of infection can occur following immunosuppression or after liver transplantation (5,6,16,17,38).Yotsuyanagi et al. found traces of residual HBV DNA in sera collected from 10 out of 11 patients up to 19 months after the diagnosis of transient HBV infection (41). Michalak et al. reported residual HBV DNA in the serum and peripheral blood mononuclear cells (PBMC) collected from four out of five patients up to 70 months after the resolution of HBV infection (24). Ultracentrifugation and PCR were used to determine that the viral DNA-positive fraction in serum sedimented at the same rate as HBV virions, suggesting that the residual HBV DNA was present within viral particles (24). In another study, evidence for HBV closed circular viral DNA (cccDNA) in the liver almost 4 years after resolution of HBV infection was obtained using PCR techniques (20). However, this result is not totally unambiguous inasmuch as HBV DNA may integrate into host DNA during infection and integrated ...

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Section: Resultsmentioning

confidence: 99%

Covalently Closed Circular DNA Is the Predominant Form of Duck Hepatitis B Virus DNA That Persists following Transient Infection

Mire

Miller

Foster

et al. 2005

J Virol

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“…New-onset vitiligo has followed bone marrow transplants or lymphocyte infusions for the treatment of leukemias and lymphomas. [133][134][135][136] Finally, the severity of hypopigmentation in the vitiligo animal model, the Smyth chicken, is lessened by suppressing T cell activity with cyclosporine A, 137 and B cell activity through neonatal bursectomy. 138 Humoral immunity.…”

Section: Autoimmune Hypothesismentioning

confidence: 99%

Vitiligo: A comprehensive overview

Alikhan

Felsten

Daly

et al. 2011

Journal of the American Academy of Dermatology

561

206

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“…183 Cyclophosphamide, when given in pulse therapy with dexamethasone for the treatment of pemphigus vulgaris, induced repigmentation in a patient with vitiligo universalis that had previously been recalcitrant to systemic steroids. 184 Chicken models suggested a role for cyclosporine in treating vitiligo 185 ; however, only one of six human subjects showed even minimal to moderate improvement when treated with 6 mg/kg/day. 186 COST Key points d Vitiligo is a lifelong disease that can become expensive to treat both for the patient and the health care system d Treatment should start with less aggressive, cost effective modalities, reserving more invasive and expensive options for those who fail first-line therapy…”

Section: Systemic Immunosuppressantsmentioning

confidence: 99%