• 대한수의학회지
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• 제38권1호
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• pp.101-106
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• 1998

The present study attempted to apply polymerase chain reaction (PCR) to develop a rapid differential diagnosis among Marek's disease, reticuloendotheliosis and avian leukosis. The primers chosen to detect Marek's disease virus (MDV) flank the 132bp tandem direct repeat of the MDV genome. The primers selected for reticuloendotheliosis virus (REV) and avian leukosis virus (ALV) are based on proviral long terminal repeats of spleen necrosis virus and Rous-associated virus-2 genomes, respectively. The specific PCR products of MDV, REV and ALV were observed with each primer and the reaction was not cross-reacted among the viruses. MDV-specific DNA was also amplified from the MDV-induced lymphoma (MDCC-MSB1) but not from the REV-induced tumor and ALV-induced lymphoma (LSCC-1104B1). In addition, proviral DNA of REV from REV-induced tumor and proviral DNA of ALV from ALV-induced lymphoma were also amplified by REV-specific and ALV-specific PCRs, respectively. Therefore these three PCR methods may be used to rapidly differentiate among MDV, REV and ALV-associated tumors in diagnosis.

• 한국가금학회지
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• 제34권4호
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• pp.301-318
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• 2007

Marek's disease (MD) is a highly contagious lymphoproliferative disease of poultry caused by the oncogenic herpesvirus designated Marek's disease virus (MDV). MD has a worldwide distribution and is thought to cause an annual loss over US$ one billion to the poultry industry. Originally described as a paralytic disease, today MD is mostly manifested as an acute disease with tumors in multiple visceral organs. MD is controlled essentially by the widespread use of live vaccines administered either in ovo into 18-day-old embryos or into chicks immediately after they hatch. In spite of the success of the vaccines in reducing the losses from the disease in the last 30 years, MDV strains have shown continuous evolution in virulence acquiring the ability to overcome the immune responses induced by the vaccines. During this period, different generations of MD vaccines have been introduced to protect birds from the increasingly virulent MDV strains. However, the virus will be countered each new vaccine strategy with ever more virulent strains. In spite of this concern, currently field problem from MD is likely to be controled by strategy of using bivalent vaccine. But, potential risk factors for outbreak of MD are still remained in this condition. The major factors can be thought that improper handling and incorrect administration of the vaccine, infection prior to establishment of immunity, suppression of immune system by environmental stress and outbreaks of more virulent MDV strain by using vaccine and genetic resistance of host.

• 한국수의병리학회지
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• 제5권2호
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• pp.49-56
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• 2001

Ocular lesions induced in 40 specific-pathogen-free Marek's disease (MD) resistant chicks by inoculation at 1 day of age with very virulent strain of Marek's disease virus (WV) were pathologically examined. Grossly,24/40 (60%) chicks had white gel-like materials in the vitreous body, whereas thickening and discoloration of iris (gray eye) were not observed. Microscopically, characteristic ocular MD lesions were observed in choroid (27/40), ciliary (30/40) and iris (23/40) in which small focal inflammatory to diffuse neoplastic Iymphoid cells were infiltrated. Five out of 40 MDV-inoculated birds revealed necrotizing Iymphomas in choroid. These lesions consisted of necrotic and degenerating Iymphoblasts accompanied by intranuclear inclusion body. There was retinal atrophy and necrosis with inclusion body detected in necrotic ganglion, inner or outer nuclear and infiltrated Iymphoblast cells. Conjunctiva showed lymphoid cell infiltration in 29/40 chicks inoculated with MDV, Vitreous body exhibited mild to severe exudation of eosinophilic proteinaceous material in 24/40 chicks. These lesions were associated with Iymphoid cell infutration, edema and fibrosis of choroid. Pecten (7/40) and optic nerve (13/40) were infiltrated usually mildly with Iymphoid cells. From these results, very virulent strain, Md/5 of MDV caused high incidence of ocular lesions in MD resistant chicks. In addition, Md/5 induced exudation of proteinaceous material into the vitreous body and fibrosis of choroid. Necrotizing ocular Iymphoma lesions in choroid is the first report in the MD literature.

• 한국가금학회지
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• 제35권3호
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• pp.225-240
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• 2008

Marek's disease virus(MDV) is a highly cell-associated, lymphotropic $\alpha$-herpesvirus that causes paralysis and neoplastic disease in chickens. The disease has been controlled by vaccination which was provided the first evidence for a malignant cancer being controlled by an antiviral vaccine. Marek's disease pathogenesis is complex, involving cytolytic and latent infection of lymphoid cells and oncogenic transformation of $CD4^+$ T cells in susceptible chickens. MDV targets a number of different cell types during its life cycle. Lymphocytes play an essential role, although within them virus production is restricted and only virion are produced. Innate and adaptive immune responses develop in response to infection, but infection of lymphocytes results in immunosuppressive effects. Hence in MDV-infected birds, MDV makes its host more vulnerable to tumour development as well as to other pathogens. All chickens are susceptible to MDV infection, and vaccination is essential to protect the susceptible host from developing clinical disease. Nevertheless, MDV infects and replicates in vaccinated chickens, with the challenge virus being shed from the feather-follicle epithelium. The outcome of infection with MDV depends on a complex interplay of factors involving the MDV pathotype and the host genotype. Host factors that influence the course of MD are predominantly the responses of the innate and adaptive immune systems, and these are modulated by: age at infection and maturity of the immune system; vaccination status; the sex of the host; and various physiological factors.

• 대한수의사회지
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• 제14권4호
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• pp.239-252
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• 1978

Two diotinot lymphomatous diseases occur in the field in domestic fowl: Lymphoid leukosis, which is caused by an oncornavirus and Marek's disease, which is caused by a herpesvirus. They are the most common neoplastic diseases of the chicken, and Marek's d

• 한국임상수의학회지
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• 제18권1호
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• pp.55-60
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• 2001

Immunohistochemical and Electron Microscopical Studies on the Initial Skin Lesions Induced Experimentally by Very Virulent Strain of Marek\`s Disease Virus in Chickens Marek\`s disease virus (MDV), which is an avian herpesvirus, causes malignant CD3+CD4+CD8-T cell lymphomas at many sites including visceral organs, muscles, peripheral nerves and skin. In the early skin lesions induced by MDV, corelationship between the translational activity of MDV early gene, pp38 and demonstration of MDV particles in the lymphoid cells are not well studied. Therefore, skin biopsies taken at weekly intervals for 2 weeks from the same specific-pathogen free chicknes inoculated with Md/5 MDV were examined immunohistochemically and electron microscopically. In the skin biopsies sampled at 1 week and 2 weeks post inoculation (PI), feather follicle epithelium (FFE) exhibited usually strong positive reaction for pp38, whereas only few lymphoblasts, which were infiltrated around FFE revealed positive reaction. Electron microscopically, small lymphocytes were detectable in the dermis and subcutaneous skin tissues sampled at 1 week PI. The number of small lymphocytes was increased and pleomorphic lymphoblasts, which were medium to large in size were scattered among the small lymphocytes at 2 weeks PI. Some of lymphoblasts revealed degenerative and necrotic changes. FFE contained a lot of MDV particles in the nucleus including mature and immature ones. Infrequently, immature virus particles were observed not only in the degenerative and necrotic lymphoblasts, but also rarely in the health lymphoblasts. From the present results, spontaneous MDV activation including translational activity of MDV pp38 gene and formation of MDV particles was occurred in the lymphoblasts of early MD skin lesions.

• 대한수의학회지
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• 제9권1호
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• pp.23-62
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• 1969

계백혈병(鷄白血病) 및 "계백혈병군(鷄白血病群)"속에 오래도록 포함(包含)되어 오든 Marek 병(病)은 오늘날 양계산업(養鷄産業)에 있어 가장 문제시(問題視)되는 질병(疾病)의 위치(位置)를 점(占)하고 있다. 신속(迅速)하고 대규모적(大規模的)인 양계산업(養鷄産業)의 발전(發展)과 더불어 이들 질병(疾病)에 의한 경제적손실(經濟的損失)은 막대(莫大)한 것이며 더구나 과거(過去) 수년(數年)에 걸쳐 구미(歐美)에서 급성형(急性型) Marek 병(病)이 출현(出現), 외연하므로서 Marek 병(病)은 가장 흥미(興味)있는 질병(疾病)의 하나로 등장(登場)하게끔 되었다. 지난 몇년동안에 이들 질병(疾病)에 관(關)하여 새롭고 의미(意義)있는 연구업적(硏究業績)이 이룩되었으며 그 중에서도 가장 중요(重要)한 진전(進展)은 지금(只今)까지 "계백혈병군(鷄白血病群)"이라는 한 묶음의 통칭(通稱)속에 포함(包含)되어오든 이들 신생물종양질환(新生物腫瘍疾患)이 두가지의 명백(明白)한 질병징후(疾病徵候)로 나누어진 사실(事實)일 것이다. 소견상(所見上) 유사(類似)한 종양(腫瘍)을 야기(惹起)하는 이들 질병(疾病)의 분리(分離)를 위한 첫째 근거(根據)는 물론(勿論) 그들의 병인(病因)의 차이(差異)에 의한 것이며, 이것은 또한 질병분류(疾病分類)에 있어 가장 중요(重要)한 관점(觀點)이 되는 것이다. 그러나 이와같은 분리(分離)를 위한 증명(證明)은 불과(不過) 일년여전(一年餘前) 각각(各各) 다른 Marek 병(病) 병인분리주(病因分離株)로, 영국(英國) 및 미국(美國)의 두 연구단(硏究團)이 독립적(獨立的)으로 동시(同時)에 조직배양(組織培養)에 의 하여 Marek 병(病) 병인(病因)의 가장 유력(有力)한 후보(候補)로서 한 herpes virus 를 발견(發見), 시현(示顯)하므로서 이루어졌다. 실상(實上) 1954 년(年) 이래(以來), 그 병인(病因)이 확실(確實)히 구명(究明)되지는 못하였지만 야외(野外)에서의 전염력(傳染力), 실험적전달시험등(實驗的傳達試驗等)에 의하여, 이 질병(疾病) myxovirus 에 의한 계백혈병(鷄白血病)과는 다른 징후(徵候)일것이라는 것이 여러 학자(學者)들에 의하여 주장(主張)되어 왔다. 조직배양(組織培養)에 의한 Marek 병(病) 병인(病因)의 확인(確認)이 비록 예비적실험단계(豫備的實驗段階)에 있기는 하나 본병(本病) 연구(硏究)의 한 큼직한 돌파구(突破口)를 이룩하였다고 불 수 있으며 따라서 Marek 병(病)과 herpes virus 와의 상호관계(相互關係)(병인(病因)으로서의)의 더 진전(進展)된 연구(硏究)가 시급(時急)히 요청(要請)되고 있는 것이다. 본실험(本實險)은 Marek 병(病) 병인(病因)을 검색분석(檢索分析)하기 위한 조직배양법(組織培養法)을 더욱 진전(進展)시키므로서 GF 정형(定型) Marek 병(病)(Keny et al., 1964)과 CR-64 급성형(急性型) Marek 병(病)(Staples, 1964)의 병인(病因)을 구명(究明)하여 그 분리병인주(分離病因株)의 특성(特性)을 분석(分析), 또한 숙주(宿主)-세포간(細胞間)의 상호관계(相互關係)를 밝히고 더 나아가 Marek 병(病)의 각각(各各) 다른 분리주간(分離株間) 병인(病因)의 차이여부(差異如否), 또는 후보병인(候補病因)으로서의 herpes virus의 타당성(妥當性)을 검토(檢討)코져 시행(施行)되었으며, 다음과 같은 실험결과(實驗結果)를 얻었다. GF 정형(定型) 및 CR-64 급성형(急性型) Marek 병(病) 감염계신세포(感染鷄腎細胞)의 일차적(一次的) 단층(單層)(막(膜))배양세포(培養細胞)에 있에서 병인(病因)에 virus 의 증식(增殖)은 뚜렷이 변형(變形)된 종양세포화(腫瘍細胞化)(원형화(圓形化)병소(病巢)의 형성(形成)으로 나타났으며 이 종양(腫瘍))(암(癌))세포화병소(細胞化病巢) 형성(形成)의 특성(特性)은 감염(感染)된 배양세포(培養細胞)(탈락(脫落)시킨)를 비감염신세포단층배양(非感染腎細胞單層培養)에 가(加)하므로서(접종(接種)) 규칙적(規則的)으로 전달(傳達)(계대(繼代))되었다. 또한 계태아간(鷄胎兒肝) 및 신경교배양세포(神經膠培養細胞)에도 종양세포화특성(腫瘍細胞化特性)이 계대(繼代)될수 있었으나 정상계태아섬유세포배양(正常鷄胎兒纖維細胞培養)에 감염(感染)된 신배양세포(腎培養細胞)를 접종(接種)하였을 때는 아무런 세포변성(細胞變成)(CPE)을 확인(確認)할수 없었다. 또한 양형(兩型)의 Marek 병(病) 감염계(感染鷄)로부터의 전혈(全血) 및 buffy coat(말초백혈구일혈수(末梢白血球一血數)) 부유액(浮游液)을 정상(正常) 계신배양세포(鷄腎培養細胞)에 접종(接種)하므로서도 똑같은 세포변성(細胞變性)을 나타내었으나 다만 이 경우에는 그 병소수(病巢數)는 직접(直接) Mirek 병리환계(病罹患鷄)로부터 취(取)한 신세포배양(鷄腎細胞培養)에 비(比)하여 훨씬 적은 수(數)로 나타났다. 실상(實上) 조직배양상(組織培養像)에 관(關)한 한(限) Marek 병(病)의 GF 정형분리병인주(定型分離病因株)와 CR-64 급성형분리병인주간(急性型分離病因株間)에는 아무런 差異點을 발견(發見)할 수 없었다. 이와같은 특성(特性)을 갖는 감염병인(感染病因)은 극도(極度)의 세포결합성(細胞結合性)을 지니고 있었으며 본실험조건하(本實驗條件下)에서는 종속(從屬)되어있는 세포(細胞)들로부터 감염상태(感染狀態)의 병인(病因)을 분리(分離)하는 것은(유리병인(遊離病因)) 불가능(不可能)하였으며, 따라서 계대(繼代)(전달(傳達))접종물(接種物)은 항시(恒時) 세포함유물(細胞含有物)이 였다. 배양세포(培養細胞)에 있어서의 변성(變性)은, 비종양황기(非腫瘍荒起) virus 에 의한 점진적(漸進的)으로 이루어지는 세포변성(細胞變性)인 plaque 인 것 보다 오히려 종양황기(腫瘍荒起) virus 에 의한 특이적세포변형병소(特異的細胞變形病巢)(focus)로 보여졌으며 그 양상(樣相)은 여러가지 관점(觀點)에서 계태아섬유농배양세포상에서의 Rous sarcoma virus 의 그것에 유이(類似)하였다. 본(本) 병인(病因)의 병소분석(病巢分析)은 접종(接種)된 감염세포농도(感染細胞濃度)와 계수(計數)된 원형화병소간(圓形化病巢間)에 고도(高度)의 직선상관관계(直線相關關係)를 표시(表示)하였다. 양(兩) 분리병인주감염신배양세포(分離病因株感染腎培養細胞)의 이화학적(理化學的) 처리(處理)에 의한 특성분석(特性分析), 핵내봉입체(核內封入體)의 형성(形成)과 감별염색법(鑑別染色法) 및 세포화학적처리(細胞化學的處理)에 의한 virus 의 핵산형판별등(核酸型判別等)은 이들 원형화병소형성능력(圓形化病巢形成能力)을 지닌 분리병인주(分離病因株)의 성상(性狀)이 B 군(群) herpes virus의 그것과 극(極)히 유사(類似)함을 나타내었으며, 그 외(外)에 여러가지 분석방법(分析方法)에 의하여 이 병인(病因)들이 계백혈병(鷄白血病)/육종군(肉腫群) virus 들 및 PPLO들과는 전연(全然) 상관관계(相關關係)가 없음이 밝혀졌다. 감염신배양세포(感染腎培養細胞)의 음성염색법(陰性染色法)에 의한 전자현미경관찰(電子顯微鏡觀察)은 herpes virus 양(樣)특성(特性)을 갖춘 vius 입자(粒子)들을 밝혀 내었으며 또한 감염신배양세포(感染腎培養細胞)의 무(無) 백혈병(白血病)/Marek 병(病) 감수성계추(感受性鷄雛)로의 접종결과(接種結果)는 Marek 병(病)의 특이적병변(特異的病變)을 계추(鷄雛)에 발현(發現)시켰으며, 살처분후(殺處分後) 핵(該) 계추(鷄雛)들로부터의 신조직배양(腎組織培養)에 있어서도 명확(明確)한 세포변형(細胞變形)에 의한 병소형성(病巢形成)(암세포화(癌細胞化))특성(特性)을 훌륭히 재현(再現)시켜 주었다. 이와같은 실험결과(實驗結果)로서 배양세포(培養細胞)를 괴사(壞死)시키지 않고 변형(變形)(transfermation) 시키는 능력(能力)을 지닌 이들 분리주(分離株)는 Marek 병(病) 병인(病因) 그것이며, 다분(多分)히 B 군(群) herpes virus 에 속(屬)하는 한 멤버일(一)임이 단정(斷定)되었으며, 또한 이들 virus 군(群)의 어떤 것들은 고도(高度)의 종양양기특성(oncogenicity) 을 지니고 있을 것으로 추정(推定)되었다.

• 한국가금학회지
• /
• 제35권1호
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• pp.39-55
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• 2008

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 ${\alpha}-herpesvirus$ like herpes simplex and varicella-zoster viruses, biological properties indicate MDV is more akin to the ${\gamma}-herpesvirus$ 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.

• Asian-Australasian Journal of Animal Sciences
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• 제9권6호
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• pp.679-684
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• 1996

This study evaluates the susceptibility of scaleless mutant chickens to very virulent Marek's disease virus (vvMDV) inoculation. One day old chickens were inoculated subcutaneously with Taiwanese isolates of LTB-1 and LTS-1 strains, and standard strain of Md/5. Compared with the non-inoculated group the vvMDV-inoculated chickens showed decreased body weights and atrophy of lymphoid organs before 35 days old. These results indicate that scaleless chickens show the same susceptibility as the wild type chickens to vvMDV infection. Furthermore, the protective effect of herpesvirus of turkey (HVT) vaccination at 1 day old against vvMDV challenge was evaluated. Scaleless mutant chickens of treated groups showed 20-30% early death, and 85.7-100% and 12.5-14.2% had lymphomatous lesions in visceral organs and peripheral nerves, respectively. No significant lesions were observed in non-challenged chickens of the control group. The HVT vaccination did not provide an effective protection against vvMDV infection. It is concluded that scaleless mutant chickens are susceptible to vvMDV infection.

• 대한수의학회지
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• 제41권3호
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• pp.373-380
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• 2001

Marek's disease virus (MDV) can cause skin lesions including inflammatory to tumorous. The phenotypical changes of lymphocytes infiltrating in the skin lesions induced by MDV were not clear. Therefore, the skin biopsies taken at weekly intervals for 8 weeks from the same specific-pathogen free chickens inoculated with Md/5 MDV were examined to analysis the phenotypical changes of lymphocytes. Histologically skin lesions progressed from initial inflammatory to late tumorous. Sequentially CD4+ T lymphocytes increased gradually in number from initial skin lesions and were major composition cells in the tumor lesions. Regardless of inflammatory or tumor lesions, CD8+ T cells and ${\gamma}{\delta}$ T cells infiltrated particularly in the dermis and subcutaneous on which MDV was actively replicated in the feather follicle epithelium(FFE). In addition, IgG bearing B lymphocytes in considerable number infiltrated in the dermis and subcutaneous tissues. From these results, the development of MDV-induced skin lesions was inflammatory following tumorous. In addition, each CD8+, ${\gamma}{\delta}$ and CD4+ T cells and B cell might act to protect MDV replication in the FFE or tumor cells which turned on lytic cycle.