Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epstein-Barr virus and HTLV-1 are both lymphotropic viruses, capable of immortalizing lymphocytes in vitro (Fig. 1). Both viruses have been sequenced and subjected to intense molecular biologic scrutiny, and in both cases genes believed to be important in lymphocyte immortalization have been identified. These viral genes are not homologues of cellular oncogenes, nor is there any evidence to suggest insertional mutagenesis. Rather, these genes alter the expression of a variety of cellular genes and, in so doing, alter the growth characteristics of the host cell. Infection with either virus is most likely to be asymptomatic, associated with a benign self-limited lymphoproliferation, or both, but in a small fraction of instances these benign lymphoproliferations give rise to a lymphoma or leukemia. In the case of the Epstein-Barr virus, a variety of cofactors have been identified that are important to the evolution of malignancy. These cofactors include immunosuppression in transplant recipients, cogenital immunodeficiency in the X-linked lymphoproliferative syndrome, human immunodeficiency virus infection in AIDS patients, and malaria in patients with endemic Burkitt's lymphoma. In the case of HTLV-1, cofactors have not been identified. Nonetheless, the importance of cofactors is suggested by the small fraction of the population infected by the virus who actually develop lymphoproliferative disease, and the long latency period between infection and the development of frank lymphoproliferative disease. In organ transplant recipients with lymphomas associated with Epstein-Barr virus infection, the EBV immortalizing/transforming genes are expressed in the malignant tissue. But in Burkitt's lymphoma and in adult T-cell leukemia/lymphoma, the EBV and HTLV-1 immortalizing/transforming genes are not detectably expressed. In Burkitt's lymphoma, it is suggested that the dysregulated myc gene renders the growth effects of Epstein-Barr virus latency genes superfluous. No comparable proto-oncogene translocation or activation has yet been identified in HTLV-1 lymphoma/leukemia.
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PMID:Human lymphotropic viruses associated with lymphoid malignancy: Epstein-Barr and HTLV-1. 217 3

The Epstein-Barr virus (EBV), a B lymphotropic virus, is involved in a growing number of immunopathological disorders benign or malignant. The X-linked lymphoproliferative syndrome and its multifaceted clinical expression in a unique situation described in this issue by Purtilo. Among recent findings, the association between EBV and idiopathic interstitial pneumopathy (also named cryptogenic fibrosing alveolitis), is to be noted (6). From a molecular biology view-point, in vitro immortalization of B lymphocytes by EBV is under a pluri-genic (EBNA 2, EBNA 1, LYDMA) control. The role of EBV in oncogenesis appears different in Burkitt's Lymphoma (BL) and in nasopharyngeal carcinoma (NPC). In development of African BL, EBV appears to initiate the multistage carcinogenic event, through an early and massive infection. Other events include specific depression of T-cell immunity by hyperendemic malaria and c-myc onc-gene activation through chromosome translocation. In the genesis of NPC, the role of EBV still remain to be clarified although the strong and consistent association between EBV and the undifferentiated carcinoma of the nasopharyngeal (NPC) around the world favours an etiological relationship. The simple detection of IgA antibodies to VCA and EA allows early detection of the NPC, thus permitting a 95% cure rate at 5 years post-radiotherapy. Such an early diagnostic is of paramount public health importance. Furthermore, IgA/VCA and IgA/EA antibodies characterize precancerous conditions, giving the theoretical possibility of preventive interventions.
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PMID:The Epstein-Barr virus (EBV): a Rosetta Stone for understanding the role of viruses in immunopathological disorders and in human carcinogenesis. 299 May 89