Lymphocytes bearing the CD8 marker were shown to suppress replication of human immunodeficiency virus (HIV) in peripheral blood mononuclear cells. The effect was dose-dependent and most apparent with autologous lymphocytes; it did not appear to be mediated by a cytotoxic response. This suppression of HIV replication could be demonstrated by the addition of CD8+ cells at the initiation of virus production as well as after several weeks of virus replication by cultured cells. The observations suggest a potential approach to therapy in which autologous CD8 lymphocytes could be administered to individuals to inhibit HIV replication and perhaps progression of disease.
The three year actuarial progression rate to the acquired immune deficiency syndrome (AIDS) in a cohort of men in San Francisco who were seropositive for the human immunodeficiency virus (HIV) was 22%. An additional 26 (19%) developed AIDS related conditions. 12 Microglobulin concentration, packed cell volume, HIV p24 antigenaemia, and the proportion and number of T4 lymphocytes each independently predicted progression to AIDS. 12 Microglobulin was the most powerful predictor. The 111 subjects tested who were normal by all predictors (40%) had a three year progression rate of 7%, and the 68 subjects who were abnormal by two or more predictors (24%) had a progression rate of 57%. Two thirds of all men who progressed to AIDS were in the last group. The median T4 lymphocyte count in subjects who did not progress to AIDS
Six isolates of the human Immunodefldency virus (lIV) showed differences In their ability to productively infect glioma-derived cell lines and early-passage human brain cell cultures. Susceptibility to HIV infection correlated well with the expression of the astrocyte marker glial fibrillary acidic protein. The CD4 molecule was expressed on some, but not all, of the brain-derived cells; however, no correlation was observed between CD4 protein expression and susceptibility to virus infection. The results show that HIV can productively infect human brain cells, particularly those of gal origin, and suggest that these cell ypes in the brain can harbor the virus.The disease acquired immunodeficiency syndrome (AIDS) is characterized by helper-T-cell depletion, depressed immune function, opportunistic infections, and neoplasms, particularly Kaposi sarcoma and B-cell lymphomas (1). Neurological syndromes, including subacute encephalitis and vacuolar degeneration of the spinal cord, have also been described in AIDS patients (2-4). The human immunodeficiency virus (HIV) has been isolated from patients with AIDS and shown to be associated with the disease (5-8). The detection ofHIV DNA in the brain and the recovery of infectious virus from cerebrospinal fluid and brain tissues of patients with AIDS (9-11) have strongly suggested that HIV is also directly responsible for some ofthe neurological manifestations found in these individuals. To investigate the possible neurotropism of certain virus isolates and the cell type(s) in the brain susceptible to HIV infection, we attempted to infect brainderived cell cultures with various HIV isolates. The results show that the AIDS retrovirus can productively infect glioma-derived cell lines and normal brain cell cultures, particularly those that express the astrocyte-specific marker glial fibrillary acidic protein (GFAP). Furthermore, the results suggest that a receptor other than the CD4 molecule may govern viral tropism in the brain. MATERIALS AND METHODSCells and Cell Culture. The established cell lines ofprimary glial tumors either were derived at the Brain Tumor Research Center, University of California, San Francisco (SF210) or were a gift from J. Ponten, University of Uppsala, Sweden (U343MG, U343MGA, U251MG) ( Table 1). The glial cell origin of all four cell lines has been well-documented (12)(13)(14). These cells were maintained in Dulbecco's modified Eagle's medium (DMEM) supplemented with fetal bovine serum (20%Yo), glutamine (2 mM), penicillin (100 units/ml), and streptomycin (100 ug/ml).The early-passage cell cultures were established from samples minced and treated with an enzyme mixture (0.02% DNase/0.05% Pronase/0.02% collagenase) for 30 min at 370C and filtered through an 80-i&m mesh. The filtered fluids were then centrifuged, and the cell pellets were resuspended in DMEM with 20% fetal bovine serum plus glutamine and antibiotics. SF609, SF611, and SF612 were derived from human fetal brain specimens; SF407 was obtained from a cerebellar glioblastoma in a chi...
Scrapie is a slow infection of the nervous system which progresses in the absence of any apparent immune response. The recent development of a large-scale purification protocol for scrapie prions made it possible to obtain substantial quantities of electrophoretically purified prion protein (PrP 27-30) and we report here on the successful production of a rabbit antiserum to PrP 27-30. The antiserum reacted with PrP 27-30 and several lower molecular weight proteins as shown by Western blots; it did not react with protein preparations from uninfected brains. Discrete structures in the subependymal region of scrapie-infected hamster brains were stained immunocytochemically. These same structures also stained with Congo red dye and showed green birefringence with polarized light, a characteristic of purified prion rods. This staining pattern suggests that they are amyloid plaques.
Cytotoxic T lymphocyte (CTL) responses to the human papillomavirus (HPV) type 16 E6 and E7 proteins were measured in 20 women with known HPV and cervical disease status. CTL assays were performed after stimulation with E6 or E7 fusion proteins using autologous B lymphoblastoid cells infected with vaccinia viruses expressing E6 or E7. CTL responses to E6 and E7 were detected in 6 (75%) of 8 and 5 (56%) of 9 HPV-16-positive women without cervical intraepithelial neoplasia (CIN), respectively. Responses to E6 or E7 were each detected in only 2 (29%) of 7 HPV-16-positive women with CIN. Responses to both antigens were found in 63% of women without CIN and 14% of those with CIN. CTL responses to E6 or E7 are more commonly detectable in HPV-16-positive women without CIN than in HPV-16-positive women with CIN, suggesting that CTL response may play a role in disease protection.
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