The precise relationship between viral infection and malignancy remains an epidemiologic association and the subject of active investigation. Nonmalignant hematologic disorders have a similarly complex relationship with cancer-associated viruses and may offer insight into the pathogenesis of oncogenesis. This book explores the relationships between viral infections, immune impairments and the hematologic and malignant diseases, particularly against the backdrop of the HIV epidemic. By extending the scope to all of viral oncology the editors provide an invaluable resource on tumors related to other viruses other than HIV, particularly carcinomas of the cervix and anus with HPV and tumors of the liver with the various hepatitis viruses.

mouse tissue alloantigen detected by this procedure. An antigen of cross-reacting specificity was revealed in tissue extracts of many other animal species. We next wanted to learn more about the antigen responsible for induction of postoncolytic immunity. Extracts from virus-infected tumors were immunogenic, and both active and inactive fractions of such extracts were obtained. The growth of the virus in the tumor cells was studied with the electron microscope, in the hope that this might shed some light on the manner in which viral infection transforms a poorly immunogenic tumor into a highly immunogenic one. We consider none of the questions which our work has raised as definitely solved. In fact, we are still working on many of the aspects alluded to above. When we embarked on a study of postoncolytic immunity, we were supported in this endeavor by our lack of experience in the fields of transplantation and tumor immunology.

It has long been suspected, and recently confirmed, that there is an etiologic relationship between several viruses and naturally occurring neoplasias. Virus precursors in the form of nucleic acids or antigens have consistently been associated with certain neoplasias. However, the role of these virus-specified precursors in etiology remains obscure. Recent studies of virus-associated neo plasias have led to advances in molecular techniques, which have yielded increas ingly sensitive assays for detection of virus-specific nucleic acids, and which have enabled the disruption of virus particles without concomitant loss in antigenicity of the components. These procedures have, in turn, resulted in molecular probes that allow more definitive evaluation of the host response to its virus and to the tumor cell with which the virus or its precursors are associated. Evaluations of the immune response and status of the host have provided important informa tion about carcinogenesis and the tools for seroepidemiological studies of a variety of cancers. These seroepidemiological studies have demonstrated that several human cancers, e. g. , Burkitt's lymphoma and nasopharyngeal carcinoma, are probably virus-induced, and that antibodies that are diagnostic and prog nostic for these diseases are detectable. The conclusion that feline leukemia is a disease transmitted horizontally by a virus resulted primarily from immunologi cal experiments.

The discoveries of Burkitt, Epstein, and Henle have laid the foundation for continuing generation of information regarding the mechanisms of induction of diseases by Epstein-Barr virus. The discovery of the virus two decades ago resulted from clinical and basic science collaborative studies on Burkitt lymphoma. Subse quently, nasopharyngeal carcinoma and infectious mononucleosis have been linked etiologically with the virus. During the first decade of research following the discovery of the virus, the mechanisms for the induction of BL, NPC, and IM were sought. At that time one prevailing view was that individual oncogenic strains of EBV were responsible for the different disorders. Paralleling the development of immunology in the 1970's was the accrual of knowledge about immunological events occurring during IM. These studies suggest that immune defense mechanisms deter mine the outcome of this viral infection rather than different viral strains. During the early 1970's, Starzl and Penn and Gatti and Good had noted an increased frequency of malignancy in renal allograft recipients and children with primary immune deficiency disorders, respectively. These observations provoked investigators to restudy the role of immune surveillance against malignancy. At that time immune surveillance was thought to occur against tumor-specific antigens; thereby neoplasms were eliminated.

Natural resistance is now coming to be recognized as a potentially important phenomenon in host defense against infection and ma lignancy. Genetically controlled resistance mechanisms are usUally effective early in infection and before conventional immune responses are generated. Comparisons of experimental systems where natural resistance plays a prominent role demon strate the complexities of the host defense mechanisms involved, as evidenced in the present volume. Nevertheless, some com mon components of genetic resistance are discernible and largely comprise natural killer cells, macrophages, and interferon These and additional factors would seem to constitute a first line of de fense in host resistance against both viruses and tumors. It is evi dent that considerable variation in the relative importance of di stinct mechanisms may be found among various resistance sy stems and that, most likely, additional effector functions will be discovered. Resistance to tumors and most viruses is under polygenic control, has a complex mode of inheritance, and depends on appro priately complex effector mechanisms. Instances, however, whe re a single gene locus determines resistance or susceptibility to a virus, as in the case of resistance to flaviviruses or influenza viru ses, would seem to offer good prospects for elucidating the basic factors involved. Resistance to influenza virus would indeed seem to represent a comparatively simple situation: resistance is expressed at the host cell level, and interferon is its main media tor. The present volume provides insight into current concepts of such resistance mechanisms.

This unique book summarizes current knowledge on co-development of infectious diseases and cancer. It provides an overview of the complex and unique role of the immune system, inflammation, tumor-mediated immunosuppression and infection-induced immunomodulation in cancer and infection progression. Chapters are organized into themed parts, beginning with a look at the historical perspective of human tumor viruses, then aspects and examples of infection-related cancers and cancer-associated infections. The work discusses how cancer- and infection-associated immune responses interact in a bi-directorial fashion and how these interactions may evolve during both disease progression and in response to therapy. The phenomenon of independent development of cancer and infection in the same host, known as comorbid cancer-infection progression, is explored. Understanding the complex pathways involved in the progression of infection and cancer will allow the prevention of the development of certain types of cancer, as well as advancing prophylactic anti-cancer vaccines. Readers of this work will discover innovative approaches for multidisciplinary projects, focusing on the design of original therapeutic modalities for cancer therapy. The book will therefore be particularly valuable to scholars interested in cancer immunology and researchers and clinicians in the field of basic and applied immunobiology and microbiology.