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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
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초록· 키워드
오류제보하기
Like the other herpesviruses, the virion of MDV consists of an envelope, which surrounds an amorphous tegument. Within the tegument, and icosahedral capsid encloses a linear double-stranded DNA core. Although the genome structure of MDV indicates that it is an α-herpesvirus like herpes simplex and varicella-zoster viruses, biological properties indicate MDV is more akin to the γ-herpesvirus group, which includes Epstein-Barr and Kaposi's sarcoma herpesviruses. These herpesviruses replicate lytically in lymphocytes, epithelial and fibroblastic cells, and persist in lymphoblastoid cells. MDV has a complex life cycle and uses two means of replication, productive and non-productive, to exist and propagate. The method of reproduction changes according to a defined pattern depending on changes in virus-cell interactions at different stages of the disease, and in different tissues. Productive (lytic) interactions involve active invasion and take-over of the host cell, resulting in the production of infectious progeny virions. However, some herpesviruses, including MDV, can also establish a non-productive (abortive) infection in certain cell types, resulting in production of cell-associated progeny virus. Non-productive interactions represent persistent infection, in which the viral genome is present but gene expression is limited, there is no structural or regulatory gene translation, no replication, no release of progeny virions and no cell death. Reactivation of the virus is rare, and usually the infectious virus can be re-isolated only after cultivation in vitro. MDV establishes latency in lymphoid cells, some of which are subsequently transformed. In this review article, recent knowledges of the pathogenesis mechanisms followed by MDV infection to sensitive cells and chickens are discussed precisely.
목차
ABSTRACT
서론
MDV의 생활 주기
MDV 감염에 의한 병원성 발현에 영향을 미치는 요인
MDV의 자연 감염 형성 과정
초기 세포 용해성 감염
잠복 감염
잠복기 이후 재활성화에 의한 세포 용해성 감염
우포상피세포의 세포 용해성 감염
형질 전환
결론
인용문헌
참고문헌 (74)
참고문헌 신청
1. [학술지(정기간행물)] - Addinger HK / 1973 / Pathogenesis of Marek's disease: early distribution of virus and viral antigens in infected chickens / J Natl Cancer Inst 50 : 1287 ~ 1298
2. [학술지(정기간행물)] - Afonso CL / 2001 / The genome of herpesvirus of turkey / J Virol 75 : 971 ~ 978
3. [학술지(정기간행물)] - Baaten BJ / 2004 / Study of host-pathogen interactions to identify sustainable vaccine strategies to Marek's disease / Vet Immunol Immunopathol 100 : 165 ~ 177
4. [학술지(정기간행물)] - Baigent SJ / 1998 / Differential susceptibility to Marek's disease is associated with differences in number, but not phenotype or location, of pp38+ lymphocytes / J Gen Virol 79 : 2795 ~ 2802
5. [학술지(정기간행물)] - Baigent SJ / 1999 / Development and composition of lymphoid lesions in the spleens of Marek's disease virus-infected chickens: association with virus spread and the pathogenesis of Marek's disease / Avian Pathol 28 : 287 ~ 300
2. [학술지(정기간행물)] - Afonso CL / 2001 / The genome of herpesvirus of turkey / J Virol 75 : 971 ~ 978
3. [학술지(정기간행물)] - Baaten BJ / 2004 / Study of host-pathogen interactions to identify sustainable vaccine strategies to Marek's disease / Vet Immunol Immunopathol 100 : 165 ~ 177
4. [학술지(정기간행물)] - Baigent SJ / 1998 / Differential susceptibility to Marek's disease is associated with differences in number, but not phenotype or location, of pp38+ lymphocytes / J Gen Virol 79 : 2795 ~ 2802
5. [학술지(정기간행물)] - Baigent SJ / 1999 / Development and composition of lymphoid lesions in the spleens of Marek's disease virus-infected chickens: association with virus spread and the pathogenesis of Marek's disease / Avian Pathol 28 : 287 ~ 300
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UCI(KEPA) : I410-ECN-0101-2010-527-001428016