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Query: UMLS:C0019693 (
HIV
)
170,526
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Incidence of
HIV
and of several other sexually transmitted diseases (STDs) was determined in 171 female prostitutes from 3 sites in San Juan, Puerto Rico. The sites were selected by high incidence of
penicillinase
-producing N. gonorrhoeae in clients of prostitutes. These women came from about a dozen different countries, mostly Latin American. 14% reported they always used condoms. Specimens were taken of blood, endocervix, cervix, rectum and oropharynx, and tested for
HIV
, gonorrhea, syphilis, herpes, chlamydia, hepatitis B and cytomegalovirus. 18% harbored gonorrhea, of which 13% were
penicillinase
positive. Syphilis occurred in 8%. Chlamydia was the most prevalent infection, in 47% of subjects. Serological evidence of hepatitis B was apparent in 53%, and of cytomegalovirus in 99%.
HIV
status was tested after unlinking identifying information from 80 serum samples, and 16% were confirmed
HIV
positive. Women from the site frequented by more street walkers than bar girls had a higher incidence of hepatitis B, and were known to be more frequent users of IV drugs. These data confirm observations made elsewhere that
HIV infection
may coexist with other STDs.
...
PMID:Interactions of HIV and STDs in a group of female prostitutes. 1234 95
As an early event in the viral life cycle, the entry of enveloped viruses into target cells has received considerable attention. Viral fusion to cellular targets has been studied principally with fusion assays in which cells engineered to express the viral envelope are cultured with the target cells. These assays yield valuable information but do not fully recapitulate all of the variables governing the fusion of actual virions to their cellular targets. The virion membrane and the plasma membrane, for example, differ strikingly in their lipid and protein compositions. Two virion-based fusion assays have been described. One is based on the redistribution of a self-quenching fluorophore, whereas the second depends on photosensitized activation of a hydrophobic probe by a fluorescent lipid loaded into the target membrane. These assays are complex and have not been adapted to study fusion in complex cell populations. We have developed a simple, rapid assay allowing the detection of
HIV
-1 virion fusion to biologically relevant target cells, including primary CD4(+) T lymphocytes. It is based on the incorporation of
beta-lactamase
-Vpr chimeric proteins (BlaM-Vpr) into
HIV
-1 virions and their subsequent delivery into the cytoplasm of target cells as a result of virion fusion. This transfer is then detected by enzymatic cleavage of the CCF2 dye, a fluorescent substrate of
beta-lactamase
(BlaM), loaded in the target cells. BlaM cleaves the beta-lactam ring in CCF2, changing its fluorescence emission spectrum from green (520 nm) to blue (447 nm) and thereby allowing fusion to be detected by fluorescence microscopy, flow cytometry, or UV photometry.
...
PMID:A sensitive and specific enzyme-based assay detecting HIV-1 virion fusion in primary T lymphocytes. 1235 96
Although nonhuman primates are genetically close to humans, their T cells do not support productive replication of
HIV
-1. In contrast,
HIV
-1 replicates in activated human CD4(+) T cells, monocytes, and metabolically active human cells of a variety of cell types become permissive for
HIV
-1 replication when transduced to express CD4 and CCR5 or CXCR4. The molecular basis of this species restriction to
HIV
-1 replication was investigated by using African green monkey and rhesus macaque cell lines that were stably transduced to express human CD4 and CCR5. The cells supported replication of cognate viruses [simian immunodeficiency virus from African green monkeys (SIV-AGM) and macaques (SIVmac239)] but did not support replication of an R5-tropic cytopathic
HIV
-1. A
beta-lactamase
-based
HIV
-1 entry assay was used to show that the virus efficiently entered the nonhuman primate cells. Provirus formation was reduced 50-fold compared with similarly infected human cells. Real-time PCR quantitation demonstrated that reverse transcription failed to initiate efficiently in the simian cells. The block to reverse transcription was overridden at multiplicity of infection >1 or by preincubation of the nonhuman primate cells with virus, a feature reminiscent of the Friend virus resistance gene-1 (FV-1), restriction to murine leukemia virus replication in mouse cells. Heterokaryon analysis in which human and simian cells were fused demonstrated that the block was dominant. These findings suggested that the primate cells contain a dominant inhibitor that prevents
HIV
-1 reverse transcription.
...
PMID:A dominant block to HIV-1 replication at reverse transcription in simian cells. 1236 68
The fluorescence resonance energy transfer (FRET)-based
HIV
-1 virion fusion assay exploits the incorporation of
beta-lactamase
-Vpr chimeric proteins into
HIV
-1 virions and their subsequent delivery into the cytoplasm of target cells as a marker of fusion. This transfer can be monitored by the enzymatic cleavage of the CCF2-AM dye, a fluorescent substrate of
beta-lactamase
(BlaM), loaded into the target cells. BlaM cleavage of the beta-lactam ring in CCF2-AM prevents the FRET between the coumarin and fluorescein moieties of the dye. This cleavage changes the fluorescence emission spectrum of CCF2-AM from green (520 nm) to blue (447 nm), and thus permits detection of fusion by fluorescence microscopy, flow cytometry, or UV photometry. This assay is simple and rapid to perform, and exhibits high sensitivity and specificity. Importantly, it can be applied to study
HIV
-1 virion fusion in primary cells and can be combined with immunostaining for subset discrimination in heterogeneous target cell populations. Finally, the assay can also be adapted to study fusion mediated by the envelope proteins from other viruses through the construction of
HIV
-1 pseudotypes.
...
PMID:Fluorescence resonance energy transfer-based HIV-1 virion fusion assay. 1497 75
Chronic viral hepatitis is a common co-morbidity in Italian
HIV
-infected patients. It represents an important emergent associated risk of mortality in patients with
HIV infection
whose survival has increasingly improved by highly active antiretroviral therapy. In such patients further infectious predisposing factors, related to hepatic failure and esophageal haemorrhage, worsen the immunodeficiency due to
HIV infection
. Bacterial peritonitis has been reported in 3% of patients after esophageal endoscopic injection sclerotherapy emergency and in 0,5% of elective procedure. Combined antibiotic prophylaxis with aminopenicillins
beta-lactamase
inhibitor and fluoroquinolone should be regularly given to AIDS patients with decompensated liver cirrhosis who have esophageal variceal bleeding. A case of a pneumococcal bacterial peritonitis following emergency esophageal endoscopic sclerotherapy for variceal bleeding in patient with AIDS and liver cirrhosis with ascites is reported.
...
PMID:Pneumococcal bacterial peritonitis in an AIDS patient following esophageal endoscopic variceal sclerotherapy: case report and recommendations for antibiotic prophylaxis. 1532 31
A novel entry mechanism has been proposed for the avian sarcoma and leukosis virus (ASLV), whereby interaction with specific cell surface receptors activates or primes the viral envelope glycoprotein (Env), rendering it sensitive to subsequent low-pH-dependent fusion triggering in acidic intracellular organelles. However, ASLV fusion seems to proceed to a lipid mixing stage at neutral pH, leading to the suggestion that low pH might instead be required for a later stage of viral entry such as uncoating (L. J. Earp, S. E. Delos, R. C. Netter, P. Bates, and J. M. White. J. Virol. 77:3058-3066, 2003). To address this possibility, hybrid virus particles were generated with the core of human immunodeficiency virus type 1 (HIV-1), a known pH-independent virus, and with subgroups A or B ASLV Env proteins. Infection of cells by these pseudotyped virions was blocked by lysosomotropic agents, as judged by inhibition of
HIV
-1 DNA synthesis. Furthermore, by using
HIV
-1 cores that contain a Vpr-
beta-lactamase
fusion protein (Vpr-BlaM) to monitor viral penetration into the cytosol, we demonstrated that virions bearing ASLV Env, but not
HIV
-1 Env, enter the cytosol in a low-pH-dependent manner. This effect was independent of the presence of the cytoplasmic tail of ASLV Env. These studies provide strong support for the model, indicating that low pH is required for ASLV Env-dependent viral penetration into the cytosol and not for viral uncoating.
...
PMID:Low pH is required for avian sarcoma and leukosis virus Env-dependent viral penetration into the cytosol and not for viral uncoating. 1536 9
We recently described a sensitive and specific assay that detects the fusion of
HIV
-1 virions to a broad range of target cells, including primary CD4 cells. This assay involves the use of virions containing
beta-lactamase
-Vpr (BlaM-Vpr) and the loading of target cells with CCF2, a fluorogenic substrate of
beta-lactamase
. Since Vpr strongly associates with the viral core, uncoating of the viral particle might be required for effective cleavage of CCF2 by BlaM-Vpr. Here, we show that BlaM-Vpr within mature viral cores effectively cleaves CCF2, indicating that this assay measures virion fusion independently of uncoating. We also show that wildtype and Nef-deficient
HIV
-1 virions fuse with equivalent efficiency to HeLa-CD4 cells, SupT1 T cells, and primary CD4 T cells. Since Nef enhances cytoplasmic delivery of viral cores and increases viral infectivity, these findings indicate that Nef enhances an early post-fusion event in the multistep process of viral entry. Possible sites of Nef action include enlargement of the fusion pore, enhanced uncoating of viral particles, and more efficient passage of viral cores through the dense cortical actin network located immediately beneath the plasma membrane.
...
PMID:HIV-1 virion fusion assay: uncoating not required and no effect of Nef on fusion. 1538 Mar 56
The Ebola filoviruses are aggressive pathogens that cause severe and often lethal hemorrhagic fever syndromes in humans and nonhuman primates. To date, no effective therapies have been identified. To analyze the entry and fusion properties of Ebola virus, we adapted a human immunodeficiency virus type 1 (HIV-1) virion-based fusion assay by substituting Ebola virus glycoprotein (GP) for the
HIV
-1 envelope. Fusion was detected by cleavage of the fluorogenic substrate CCF2 by
beta-lactamase
-Vpr incorporated into virions and released as a result of virion fusion. Entry and fusion induced by the Ebola virus GP occurred with much slower kinetics than with vesicular stomatitis virus G protein (VSV-G) and were blocked by depletion of membrane cholesterol and by inhibition of vesicular acidification with bafilomycin A1. These properties confirmed earlier studies and validated the assay for exploring other properties of Ebola virus GP-mediated entry and fusion. Entry and fusion of Ebola virus GP pseudotypes, but not VSV-G or
HIV
-1 Env pseudotypes, were impaired in the presence of the microtubule-disrupting agent nocodazole but were enhanced in the presence of the microtubule-stabilizing agent paclitaxel (Taxol). Agents that impaired microfilament function, including cytochalasin B, cytochalasin D, latrunculin A, and jasplakinolide, also inhibited Ebola virus GP-mediated entry and fusion. Together, these findings suggest that both microtubules and microfilaments may play a role in the effective trafficking of vesicles containing Ebola virions from the cell surface to the appropriate acidified vesicular compartment where fusion occurs. In terms of Ebola virus GP-mediated entry and fusion to various target cells, primary macrophages proved highly sensitive, while monocytes from the same donors displayed greatly reduced levels of entry and fusion. We further observed that tumor necrosis factor alpha, which is released by Ebola virus-infected monocytes/macrophages, enhanced Ebola virus GP-mediated entry and fusion to human umbilical vein endothelial cells. Thus, Ebola virus infection of one target cell may induce biological changes that facilitate infection of secondary target cells that play a key role in filovirus pathogenesis. Finally, these studies indicate that pseudotyping in the
HIV
-1 virion-based fusion assay may be a valuable approach to the study of entry and fusion properties mediated through the envelopes of other viral pathogens.
...
PMID:Studies of ebola virus glycoprotein-mediated entry and fusion by using pseudotyped human immunodeficiency virus type 1 virions: involvement of cytoskeletal proteins and enhancement by tumor necrosis factor alpha. 1561 20
Productive entry of human immunodeficiency virus (HIV) is believed to occur by direct fusion at the plasma membrane. Endocytic uptake of HIV particles has been observed in several studies but is considered to be nonproductive, leading to virus degradation in the lysosome. We show here that endocytosis contributes significantly to productive HIV entry in HeLa cells by using trans dominant-negative mutants of dynamin and Eps15. Inducible expression of a dominant-negative mutant of dynamin in a CD4-positive HeLa cell line reduced
HIV infection
by 40 to 80%. This effect was independent of the infectious dose and was observed for three different isolates. Analysis of reverse transcription products by real-time PCR and of virus entry by delivery of a virion-associated Vpr-
beta-lactamase
fusion protein revealed a similar reduction, indicating that the block occurred at the entry stage. A strong reduction of HIV entry was also observed upon transient transfection of a different trans dominant-negative variant of dynamin, and this reduction correlated with the relative inhibition of transferrin endocytosis. Expression of a dominant-negative variant of Eps15, which is specific for clathrin-dependent endocytosis, reduced HIV entry in HeLa cells by ca 95%, confirming the role of endocytosis for productive infection. In contrast, no effect was observed for a dominant-negative variant of caveolin. We conclude that dynamin-dependent, clathrin-mediated endocytosis can lead to productive entry of HIV in HeLa cells, suggesting this pathway as an alternative route of virus entry.
...
PMID:Involvement of clathrin-mediated endocytosis in human immunodeficiency virus type 1 entry. 1565 Jan 84
Incision and drainage combined with antibiotic therapies form the backbone of managing uncomplicated skin and skin structure infections (uSSSIs). An algorithm has been developed to guide the treatment of uSSSIs in the primary care setting in situations where initial empiric therapy is appropriate. This includes instances when a culture is taken, but it is deemed appropriate to begin an antibiotic empirically pending the results of the culture. The panel that developed the algorithm was chaired by Dr. Richard Scher of Columbia University and included thought leaders in the fields of clinical dermatology, dermatologic surgery, infectious disease, pediatric infectious disease, podiatry, and
HIV infection
. The panel acknowledged that the initial choice of antibiotic is generally determined by tolerability, ease of administration, cost, and efficacy. The usual choices for initial empiric therapy include cephalosporins,
penicillinase
-resistant penicillins, and beta-lactam/
beta-lactamase
inhibitor combinations. Currently marketed cephalosporins,
penicillinase
-resistant penicillins, and beta-lactam/
beta-lactamase
inhibitor combinations lack activity against methicillin-resistant Staphylococcus aureus (MRSA), and the increasing prevalence of community-acquired MRSA (CA-MRSA) was a major consideration when designing the treatment algorithm. Many CA-MRSA skin infections present as abscess, and drainage is the most important component of therapy in this setting. When the history and physical exam suggest CA-MRSA infection, and there is no fluctuant collection of purulent material to be drained, a sulfa drug or tetracycline is generally the best choice for initial empiric therapy.
...
PMID:Optimal antibacterial treatment of uncomplicated skin and skin structure infections: applying a novel treatment algorithm. 1630 Feb 25
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