Infectious retrovirus(es) associated with the human (LAV, HTLV-III, ARV) and simian (SAIDS-1) acquired immune deficiency syndrome were compared by electron microscopy, immunofluorescence and immunoblotting techniques and by restriction endonuclease mapping of the viral genomes. The extracellular virus particles had similar type D morphology, but intracytoplasmic type A nucleoids were found only in SAIDS virus infected cells. Although the antigens of the three prototype AIDS viruses were similar, no cross-reactivity with the SAIDS virus was detected. Molecular hybridization and restriction enzyme analysis also revealed that the SAIDS and AIDS viruses were genetically unrelated. However, only minor differences, consistent with strain polymorphism, were found between the three AIDS virus isolates. Thus, the retroviruses associated with AIDS in macaques and humans are unique to each species.

Acquired Immunodeficiency Syndrome↗

PubMedDate not supplied

An immunopathologic evaluation of lymph nodes from monkey and man with acquired immune deficiency syndrome and related conditions.

Morphology and immunostaining of lymph nodes taken from rhesus monkeys and man are compared. The monkeys were inoculated with biologic materials known to transmit simian acquired immune deficiency syndrome (SAIDS) and the human biopsies were obtained from homosexual men with persistent generalized lymphadenopathy syndrome or acquired immune deficiency syndrome (AIDS). The lymph nodes from monkey and man share common immunohistochemical features, ranging from exhuberant follicular hyperplasia to lymphocyte depletion stage. The follicular hyperplasia differed from reactive controls by the larger follicular size and disorganization within the follicular centers as well as an increase in the number of cells with the T suppressor/cytotoxic phenotype. The lymphocyte depletion stage showed a loss of reactive follicles and small T lymphocytes with a predominance of mature monocytes/macrophages. Most monkeys and humans with the lymphocyte depletion morphology fulfilled the case definitions for AIDS and SAIDS while those with follicular hyperplasia usually had 'prodromal' findings. The simian agent is associated with alterations in lymph node morphology and immunostaining which parallel the changes seen in spontaneous human cases supporting a similar pathogenesis for AIDS and SAIDS.

Acquired Immunodeficiency Syndrome↗

PubMedDate not supplied

Isolation of a feline leukaemia provirus containing the oncogene myc from a feline lymphosarcoma.

The molecular mechanism by which feline leukaemia virus (FeLV) induces lymphoid malignancy in domestic cats is largely unknown. Using the insertional activation model of c-myc by avian leukosis virus in the induction of bursal lymphoma in chickens, we have now characterized the c-myc locus in feline tissues and investigated the possibility that FeLV may also insert within feline c-myc. We used the 1.5 kilobase (kb) PstI fragment of MC29 v-myc in Southern blot analysis to characterize the structure of the c-myc locus in the DNA of 31 naturally occurring feline lymphomas. Analysis of a cloned c-myc gene from one lymphoma demonstrated that sequences homologous to v-myc occupy 2.6 kb of feline DNA in which a putative intron of 0.5 kb separates sequences homologous to the 5' and 3' exons represented in avian v-myc. We also observed in the DNA of this lymphoma tumour-specific fragments homologous to v-myc. Characterization of these molecularly cloned myc-hybridizing fragments revealed the presence of at least two identical FeLV proviruses 5.5 kb in length, each containing long terminal repeats enclosing a spliced version of the feline myc gene.

Animals↗

PubMedDate not supplied

Retroviral spongiform polioencephalomyelopathy.

Aging wild mice (Mus musculus domesticus) from several different trapping areas in southern California are uniquely prone to a naturally occurring hind-leg paralytic disease and/or lymphoma. Both conditions are caused by an indigenous ecotropic murine leukemia virus (MuLV). These mice have a lifelong persistent viremia with total immunologic tolerance to the virus. The characteristic pathologic features are centered on the anterior-lateral horns of the lumbosacral spinal cord and consist primarily of a noninflammatory spongiform change, with reactive gliosis and neuronal dropout. The main cause of neuronal death apparently is abortive intracytoplasmic replication of virus particles. Genetic control of the naturally occurring disease in wild mice is achieved by segregation of a dominant ecotropic virus restriction gene, Akvr-1R/Fv-4R. The neurologic and/or neoplastic diseases are readily reproduced by experimental inoculation of newborn susceptible laboratory mice with purified, cloned ecotropic virus derived from the affected wild mice. The biologic and pathologic features of the experimental paralysis closely resemble those of the natural disease. This nononcogenic retroviral disease is useful in understanding the molecular basis of direct, virus-induced, neuronal and glial cell degeneration and their sequelae.

Animals↗