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Query: UMLS:C0019693 (
HIV
)
170,526
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
CD8+ cell antiviral activity and cytomegalovirus (CMV) were investigated in vivo as possible cofactors influencing the outcome of
HIV
-1 infection. The role of CD8+ cell suppression of
HIV
replication was evaluated by depleting CD8+ cells in two infected chimpanzees by inoculation with monoclonal anti-CD8 antibodies. Two other infected animals were injected with chimpanzee CMV (CCMV)-infected human fibroblasts to determine if exposure to this virus would induce
HIV
replication. Treatment with anti-CD8 antibody resulted in recovery of virus from the CD4+ lymphocytes of one animal at 1, 4, and 6 months, and from a second animal at 1 month postinoculation. In contrast, virus had been recovered only once or not at all from these infected chimpanzees for 4 years prior to treatment. Similarly,
HIV
was recovered from the CD4+ cells of the two animals 2 to 3 months after inoculation of CCMV-infected fibroblasts but not after inoculation of control uninfected fibroblasts. These studies suggest that CD8+ cell-mediated suppression and the presence of other viruses (such as CMV) could act as cofactors in influencing the extent of
HIV
-1 replication in vivo and, possibly, progression to disease.
Clin Immunol Immunopathol 1992
Dec
PMID:HIV-1 expression in chimpanzees can be activated by CD8+ cell depletion or CMV infection. 133 78
The seroprevalence of antibodies to
HIV
-1, HTLV-I, and HCV was evaluated in three populations from northern rural Haiti: 1,727 patients attending the hospital for symptoms suggestive of
HIV disease
, 228 consecutive surgical patients, and 500 pregnant women were tested.
HIV
-1 seroprevalence was 6.1 and 4.0% in the last two groups, respectively, and 39.3% in the symptomatic population. Associated symptoms of wasting, cough, and diarrhea and a clinical diagnosis of AIDS were significantly predictive of
HIV
-1 seropositivity. Antibody to HTLV-I seroprevalence ranged from 2.2-5.3% in pregnant women, surgical patients, and
HIV
-seronegative symptomatic patients and was similar among the three groups when stratified by age. In contrast,
HIV
-1 seropositivity and HTLV-I seropositivity were significantly associated. The prevalence of confirmed antibody to HCV was low and not associated with either
HIV
-1 or HTLV-I seropositivity.
J Acquir Immune Defic Syndr (1988) 1992
Dec
PMID:Antibody to HIV-1, HTLV-I, and HCV in three populations of rural Haitians. 133 30
Previous studies have demonstrated a high prevalence of anal cytologic abnormalities as well as anal human papillomavirus (HPV) infection among homosexual men with group IV
HIV disease
. However, the natural history of these changes in this population has not yet been studied. To this end, 37 homosexual men with group IV
HIV disease
attending an outpatient
HIV
clinic were followed at approximately 9-month intervals for an average of 17 months, using anal cytology, anoscopy, anal biopsy, and anal HPV DNA hybridization. During the study, the proportion of the 37 subjects with anal cytologic abnormalities increased from 27 to 65%. The proportion of subjects with any grade of anal intraepithelial neoplasia rose from 8 to 32%, with high-grade anal intraepithelial neoplasia increasing from 0 to 16%. The proportion of subjects with anal HPV infection increased from 60 to 89%, and infection with multiple HPV types was noted in at least 48%. We conclude that a large proportion of homosexual men with group IV
HIV disease
develop anal cytologic abnormalities, including anal intraepithelial neoplasia, over a short period of time. Together with a rapidly increasing incidence of anal cancer among single, never-married men in the San Francisco Bay area, these results suggest that these men may be at significant risk of development of anal cancer.
J Acquir Immune Defic Syndr (1988) 1992
Dec
PMID:Natural history of anal cytologic abnormalities and papillomavirus infection among homosexual men with group IV HIV disease. 133 31
Two immature T cell lines (FT1 and FT4) were established after in vitro cloning of peripheral blood lymphocytes (PBLs) from an asymptomatic human immunodeficiency virus type 1 (HIV-1) seropositive, human T cell-lymphotropic virus type 1 seronegative homosexual subject. Although derived from a limiting dilution cell cloning assay, these cell lines were not recloned for this study. Their growth was independent of exogenous interleukin-2. Both cell lines were able to form colonies when cloned in agar, but failed to form solid tumours when injected into nude mice. FT lines belong to the very immature T cell lineage as they exhibit rearranged TCR genes but no expression of T cell membrane antigens, including CD2, CD3, CD4, CD6, CD7 and CD8. They also contain an
HIV
-1 genome that was detected only in an extra-chromosomal DNA form, even after several passages in vitro. The presence of unintegrated viral DNA was also detected by polymerase chain reaction analysis in the same sample of fresh uncultured PBLs. Furthermore, despite the absence of CD4 expression, both T cell lines were susceptible to CD4-independent
HIV
-1 superinfection (lack of superinfection inhibition in the presence of OKT4A monoclonal antibodies).
J Gen Virol 1992
Dec
PMID:Extrachromosomal human immunodeficiency virus type 1 DNA forms in fresh peripheral blood lymphocytes and in two interleukin-2-independent T cell lines derived from peripheral blood lymphocytes of an asymptomatic seropositive subject. 133 22
Tumor necrosis factor-alpha (TNF-alpha) induces the expression of human immunodeficiency virus type-1 (HIV-1) in vitro in chronically infected cells of T and monocytic origin. The tat protein from the
HIV
-1 virus has been shown to be essential for
HIV
replication and in the immunosuppression associated with the virus infection. Previous studies in our laboratory have shown that
HIV
-1 tat gene induces TNF-beta (lymphotoxin) in human B-lymphoblastoid cells (Sastry et al., 1990, J. Biol. Chem. 265, 20091-20093). In an attempt to characterize further the relationship between the host and
HIV
-1, we investigated the effect of the functional
HIV
-1 tat gene on the expression of TNF receptors in a human B lymphoblastoid cell line (Raji). We report here that Raji cells transfected with
HIV
-1 tat gene express fewer cell surface TNF receptors than control cells. At least a 5-fold decrease in the receptor number without any significant change in receptor affinity was observed. The decrease in TNF receptors in tat-transfected Raji cells (Raji-tat cells) was found not to be due to receptor occupancy by the autocrine production of TNF-beta. The decrease in the cell surface expression of TNF receptors in Raji-tat cells was also found to be not due to a decrease in the gene expression of the receptor. The kinetics, amount of TNF binding and its internalization were temperature dependent, and it was different in Raji-tat cells than in the control cells.(ABSTRACT TRUNCATED AT 250 WORDS)
Lymphokine Cytokine Res 1992
Dec
PMID:Down-modulation of cell surface expression of p80 form of the tumor necrosis factor receptor by human immunodeficiency virus-1 tat gene. 133 62
Metal-binding proteins are important components of retroviruses such as human immunodeficiency virus (HIV). Therefore, metals could be used as antiviral agents. However, most metals are toxic for humans with the exception of silver which is toxic only to prokaryotic cells and viruses. In addition,
HIV infection
causes a decrease in body cysteine. We formed a complex of silver and cysteine, named silver-cysteine. Healthy human lymphocytes were incubated with silver-nitrate or silver-cysteine. Negligible cell survival was seen at 50 microM silver-nitrate. However, in presence of 1 mM cysteine, the viability remained unaffected up to 1 mM of silver. Further, silver inhibition of isolated Na,K-ATPase was easily reversed by cysteine. Thus, non-toxic silver-cysteine could be used as an anti-viral and cysteine-replenishing agent.
Biochem Biophys Res Commun 1992
Dec
30
PMID:Cysteine protects Na,K-ATPase and isolated human lymphocytes from silver toxicity. 133 67
We have developed sets of degenerate oligonucleotides designed to detect pol gene sequences from any member of the lentivirus subfamily when used as primers in amplification techniques such as the polymerase chain reaction (PCR). This pan-lentivirus-specific primer set (PLSPS) consists of primers, LV1, LV2, and LV3, based on conserved regions common to lentiviruses only. Our protocol is based on primary amplification with LV1 and LV2 followed by secondary amplification with a nested primer set based on the YM/VDD motif found in all reverse transcriptases (or "DDMY," in the opposite direction), and LV3, a block of lentivirus homology nested just downstream of LV1. PLSPS-PCR analysis of DNA from cells infected with
HIV
-1,
HIV
-2, SIVmac239, BIV, visna, EIAV, CAEV, OPPV, or FIV resulted in the amplification of appropriately sized products. Sequence analysis of the LV1/2 products, cloned into pBluescript (pBS), indicated that at least 20% (most often, > 80%) contained the predicted lentivirus pol sequence. Greater than 95% of the LV3/DDMY products contained the expected lentiviral sequences. Using the PLSPS, lentivirus pol sequences could typically be detected at levels of one copy in 2 x 10(6) cells after secondary amplification. No specific lentiviral PCR products were detected in DNA from uninfected human or mouse monocytes, feline or bovine leukocytes, mouse, rat or human fibroblast cell lines, chicken embryo fibroblasts, Tahr lung cells, or cell lines infected with the following retroviruses which are not lentiviruses: Rous sarcoma virus, Moloney leukemia virus or Kirsten sarcoma virus, mouse mammary tumor virus, human T-cell lymphotropic virus I, and feline leukemia virus.(ABSTRACT TRUNCATED AT 250 WORDS)
AIDS Res Hum Retroviruses 1992
Dec
PMID:Identification and evaluation of new primer sets for the detection of lentivirus proviral DNA. 133 58
Tumor necrosis factor alpha (TNF alpha) levels were determined by enzyme-linked immunosorbent assay (ELISA) and by cell culture bioassay in supernatants of lipopolysaccharide-stimulated feline monocyte cultures and in cat serum samples. There was a good correlation between the results obtained by the two methods. From the fact that TNF alpha was neutralized quantitatively by antibodies to human TNF alpha in feline monocyte supernatants and in feline sera, it was concluded that feline TNF alpha immunologically cross-reacts with human TNF alpha and that the human TNF alpha ELISA can be used to quantitate feline TNF alpha. During the first 6 months after experimental feline immunodeficiency virus (FIV) infection no differences in serum TNF alpha values were observed between infected and non-infected cats. TNF alpha levels increased significantly after primary vaccination with a feline leukemia virus (FeLV) vaccine in FIV infected cats over those in the non-infected controls. During secondary immune response TNF alpha levels rose transiently for a period of a few days in both the FIV positive and the FIV negative cats. After FeLV challenge, TNF alpha levels increased in all animals challenged with virulent FeLV for a period of 3 weeks. This period corresponded to the time necessary to develop persistent FeLV viremia in the control cats. It was concluded from these experiments that in the asymptomatic phase of FIV infection no increased levels of TNF alpha are present, similar to the situation in asymptomatic
HIV
infected humans. Activation of monocytes/macrophages in FIV infected cats by stimuli such as vaccination or FeLV challenge readily leads to increased levels of TNF alpha.
Vet Immunol Immunopathol 1992
Dec
PMID:Tumor necrosis factor alpha levels in cats experimentally infected with feline immunodeficiency virus: effects of immunization and feline leukemia virus infection. 133 3
This study demonstrates the transmission of feline immunodeficiency virus (FIV) from infected queens to kittens in two separate litters. Queen 1 was infected by intravenous administration of FIV at 22 days prior to parturition. Two out of three kittens from the litter were found to be viremic at 10 weeks of age as detected by culture isolation and polymerase chain reaction detection of FIV DNA in peripheral blood mononuclear leukocytes. The third kitten remained aviremic through 40 weeks of age. Queen 2 was infected by subcutaneous administration of FIV 2 days prior to parturition. This litter also had two out of three kittens infected with FIV; however, viremia was not detected in one of the kittens until 21 weeks of age. Culture isolation was found to be superior to polymerase chain reaction for the early detection of FIV, and viremia was found to precede seroconversion by up to 4 weeks. Although all infected kittens have remained healthy, depressed CD4:CD8 lymphocyte ratios suggest that clinical disease may develop. This study suggests that FIV infection in cats may be a useful model system for the study of
HIV
transmission from mothers to infants.
Vet Immunol Immunopathol 1992
Dec
PMID:Transmission of feline immunodeficiency virus from infected queens to kittens. 133 4
GAP 31, DAP 32 and DAP 30 comprise a new class of plant proteins with potent anti-
HIV
activity and insignificant cytotoxicity. We report here the identification and characterization of a new DNA enzyme activity in these three proteins. They irreversibly relax and decatenate supercoiled DNA, as well as catalyze double-stranded breakage to form linear DNA. The relaxed molecules are topologically inactive and no longer serve as substrates for DNA gyrase to form supercoils, phenomena similar to those of cellular topoisomerases in the presence of topoisomerase poisons. The ability of these anti-
HIV
agents to interrupt essential topological interconversions of DNA may provide a novel mechanism for their antiviral and antitumor actions. The presence of this new DNA topological enzyme activity in these plant proteins also suggests that their anti-
HIV
activity may not be merely a consequence of ribosome inactivation previously recognized.
Biofactors 1992
Dec
PMID:Anti-HIV plant proteins catalyze topological changes of DNA into inactive forms. 133 69
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