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嗜淋巴细胞病毒、爱泼斯坦-巴尔病毒(EBV)、人类嗜T淋巴细胞病毒I型(HTLV-I)/成人T细胞白血病病毒(ATLV)以及HTLV-III/人类免疫缺陷病毒(HIV)作为恶性淋巴瘤和免疫缺陷的病原体。

Lymphotropic viruses, Epstein-Barr virus (EBV) and human T-cell lymphotropic virus-I (HTLV-I)/adult T-cell leukemia virus (ATLV), and HTLV-III/human immune deficiency virus (HIV) as etiological agents of malignant lymphoma and immune deficiency.

作者信息

Purtilo D T

出版信息

AIDS Res. 1986 Dec;2 Suppl 1:S1-6.

PMID:2881552
Abstract

The ubiquitous, DNA herpesvirus, EBV, has B cell tropism and the geographically restricted RNA retrovirus, ATLV/HTLV-I has T cell tropism. Clinical descriptions by Burkitt and Takatsuki led to discovery of these viruses which infect silently early in life; however, ATLV is also transmitted to a spouse or by blood transfusion. In normal seropositive persons both viruses infect only 1 in about 10,000 B or T cells, respectively. EBV is associated with Burkitt's lymphoma, nasopharyngeal carcinoma, and infectious mononucleosis. ATLV is associated with adult T cell leukemia/lymphoma and smoldering T cell lymphoma. EBV infects polyclonally and is controlled by multiple cellular and humoral control mechanisms. Escape from immune surveillance as in immune deficient African children with malaria, males with x-linked lymphoproliferative syndrome, organ transplant recipients, and AIDS patients permits conversion from polyclonal to oligoclonal and finally, monoclonal malignancy. T cell immune defects permit proliferation of cells which undergo molecular and/or cytogenetic alterations. In contrast to EBV, which is integrated and nonintegrated in B cells, ATLV is monoclonally integrated. Viral transforming proteins and immune suppressive substances are produced. Immune deficiency in silent carriers of ATLV and in those with smoldering ATL suggest that immune surveillance deters emergence of ATL. Prevention of primary infection by vaccination against these lymphotropic viruses, and use of immunotherapy and antiviral drugs may potentially retard conversion of infected B or T cells to monoclonal malignancy.

摘要

普遍存在的DNA疱疹病毒EBV具有B细胞嗜性,而地理分布受限的RNA逆转录病毒ATLV/HTLV-I具有T细胞嗜性。Burkitt和Takatsuki对疾病的临床描述促成了这些病毒的发现,它们在生命早期就开始隐匿感染;然而,ATLV也可通过配偶传播或输血传播。在正常血清学阳性个体中,这两种病毒分别仅感染约一万分之一的B细胞或T细胞。EBV与伯基特淋巴瘤、鼻咽癌和传染性单核细胞增多症相关。ATLV与成人T细胞白血病/淋巴瘤和潜伏性T细胞淋巴瘤相关。EBV以多克隆方式感染,并受多种细胞和体液控制机制的调控。在免疫缺陷的非洲疟疾儿童、患有X连锁淋巴细胞增生综合征的男性、器官移植受者和艾滋病患者中,由于逃避免疫监视,使得感染从多克隆转变为寡克隆,最终发展为单克隆恶性肿瘤。T细胞免疫缺陷会促使发生分子和/或细胞遗传学改变的细胞增殖。与在B细胞中既有整合型又有非整合型的EBV不同,ATLV是单克隆整合的。病毒会产生转化蛋白和免疫抑制物质。ATLV潜伏携带者和潜伏性成人T细胞白血病患者的免疫缺陷表明,免疫监视可阻止成人T细胞白血病的发生。通过接种针对这些嗜淋巴细胞病毒的疫苗预防初次感染,以及使用免疫疗法和抗病毒药物,可能会延缓受感染的B细胞或T细胞转变为单克隆恶性肿瘤。

相似文献

1
Lymphotropic viruses, Epstein-Barr virus (EBV) and human T-cell lymphotropic virus-I (HTLV-I)/adult T-cell leukemia virus (ATLV), and HTLV-III/human immune deficiency virus (HIV) as etiological agents of malignant lymphoma and immune deficiency.嗜淋巴细胞病毒、爱泼斯坦-巴尔病毒(EBV)、人类嗜T淋巴细胞病毒I型(HTLV-I)/成人T细胞白血病病毒(ATLV)以及HTLV-III/人类免疫缺陷病毒(HIV)作为恶性淋巴瘤和免疫缺陷的病原体。
AIDS Res. 1986 Dec;2 Suppl 1:S1-6.
2
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IARC Sci Publ. 1984(63):749-70.
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N Engl J Med. 1986 Apr 3;314(14):874-9. doi: 10.1056/NEJM198604033141403.
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Epstein-Barr virus permissively infects human syncytiotrophoblasts in vitro and induces replication of human T cell leukemia-lymphoma virus type I in dually infected cells.爱泼斯坦-巴尔病毒在体外可有效感染人合体滋养层细胞,并在双重感染的细胞中诱导I型人类T细胞白血病-淋巴瘤病毒复制。
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