547
TAETABOLISNIJ El\]DOCRI1'JOLOGY AND IIvIMTJr~JOLOG":(
in the viral CV.Uo~lir.,o,a For these reasons AIDS-associated retrovirus fits best into this subfamily of retroviruseso P T A 4 figures, 1 41 references
Lymphadenopathy-Agsociated Viru§: From Molecular Biology to Pathogenicity L. MONTAGNIER, Viral Oncology Unit, Institut Pasteur, Paris, France
Anno Interno Med., 103: 689-693
1985
A recent report indicates that 3 characteristic morphological aspects of lymphadenopathy-associated virus can be seen in sections of infected lymphocytes or certain lymphoid cell lines, including budding of particles from the cell surface, presence of immature free particles and mature virions showing a small eccentric core, sometimes bar-shapedo Comparison of these ultrastructural characteristics with those of animal or other human retroviruses shows close resemblance with those of the equine infectious anemia virus, whose classification has some similarities with lentiviruses. This finding, including the cross reactivity of the core of proteins of lymphadenopathy-associated virus with those of the equine infectious anemia virus, and a similarity in genome structure and biological properties allows lymphadenopathy-associated virus to be placed in the retroviral subfamily of lentiviruseso Molecular studies indicate a high degree of genetic variation of this retrovirus, especially in the protein responsible for its tropism and presumably its genicity. This potential for genetic variation perhaps is the greatest danger in the future of the lymphadenopathy-associated virus epidemic. It will be difficult to produce efficient vaccines protective against all strains, and a further change of the virus in its tropism and ways of transmission cannot be excluded. Primary infection with lymphadenopathy-associated virus generally results in an immune response and, less frequently, in clinical signs. Persistent lymphadenopathy most likely is owing to a cytotoxic response (TS cells) against infected T4 cells, which are a minority in the lymph nodes of infected patientso P r A 2 figures, 2 tables, 13 references
Antigens of Hu.man T-Lymphot:rnpic Virus Type HI/ Lymphadenopathy-Associated Virus Mo ESSEX, J. ALLAN, po L. KITCHEN AND To H. LEE, of Cancer Harvard School of Public Health, Boston, Massachusetts Ann. Interno
103: 700-703
1985
The major recognized antigens of human T-lymphotropic virus type III/lymphadenopathy-associated virus (HTL V-III/ LAV) that induce antibodies in exposed humans are encoded the gag and enu genes. The gag gene, which encodes a polyprotein of approximately 55 kilodaltons (kd.) that yields p24 as the major virus core protein, is present in large amounts in virus-infected cellso The env gene, which encodes a polyprotein of about 90 kdo in its nonglycosylated form and migrates as a glycoprotein of about 160 kd., is found in infected cellso This is the most immunogenic protein in humans. Although glycoprotein 160 is not present in virus particles it gives rise to an amino terminus glycoprotein 120 that serves as the virus peplomer attachment protein and glycoprotein 41, the carboxyterminus transmembrane proteino Since glycoprotein 120 represents the external virus protein it would be the most appro-
for vaccine ~,, •. ,." '"' It found that about half of the healthy African green monkeys appeared to have been exposed to simian T-lymphotropic virus type III (STLV-III), which is morphologically and biologically similar to HTL V-III/LA V A characterization of the STL V-III glycoprotein 120 and immune response of the host may provide additional information for vaccine aesve1opmEmt Several immunodiagnostic tests used most frequently to test patients and blood donors for exposure to HTL V-III/LAV are enzymelinked immunosorbent assay, the immunoblotting or Western blotting test, radioimmunoprecipitation with sodium dodecylsulfate polyacrylamide gel electrophoresis analysis, cytoplasmic irnmunofluorescence and membrane immunofluorescence. F. T.A 1 figure, 1 table, 32 references
Immunologic Reconstitution in the Acquired Immunodeficiency Syndrome
H. C. LANE AND Ao S. FAUCI, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland Anno Interno Medo, 103: 714-718
1985
The acquired immunodeficiency syndrome is caused the retrovirus human T-lymphotrophic virus type III (HTL V-III). In this syndrome induction of a selective depletion of the helper /inducer T-lymphocytes results in a nr,ntrmn cellular immunodeficiency. This progressive immunodeficiency renders the patient susceptible to opportunistic infections and neoplasia. While effective therapies are available for many of these infections and effective antitumor therapy exists for Kaposi's sarcoma no treatments currently are available for the underlying immunodeficiencyo The 3 approaches currently used to treat AIDS patients are whole scale immune replacement, immunological enhancement and antiviral agents. Whole scale immune replacement has been attempted with lymphocyte transfer, thymic implantation and bone marrow transplantationo Clinical trials emphasizing immunological enhancement with biological response modifiers, such as gamma interferon, interleukin-2, transfer factor, inosine pranobex and a few other drugs, have been initiated. Fou.r antiretroviral agents bavirin and trials using trisodium ,_ ...._,,_h••·'."l-r,,.,..,,..~.., and monoclonal antibodies directed of the HTLV.-III virus throughout the course of the illness, immune replacement and enhancement probably will be ineffective unless effective strategies are developed against the viruso The value of all antiviral agents being tested is unproved to date. R Co N 2 figures, 1 table, 23 references
Immunopathogenesis of the Acquired Immunodeficiency Syndrome
D. L.
BOWEN, H. C. LANE AND k S. FAUCI, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland
Anno Intern. Med., 103: 704-709 (Nov.) 1985 The acquired immunodeficiency syndrome (AIDS) has been