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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prevention against the transmission of the HIV must be universal today, which means that it applies to all patients. Blood, tissues, the CSF are infected, but nasal secreta, tears and saliva are not contaminated unless they contain blood. The statistical risk of an HIV serological conversion when making an injection is an estimate of 0.1 to 0.3%, one hundred times less than with the hepatitis B virus. The best protection for maxillofacial surgeons, who are very exposed by the manipulation of objects (needle, wires) and by considerable projections of blood (rotary motor) is not a systematic HIV serological test for all patients, but goggles with side screens, a double pair of gloves and the use of an antiseptic acting on the HIV in case of staining.
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PMID:[The maxillofacial surgeon faced with the HIV-positive patient: risks and prevention]. 150 50

We described an 18 old homosexual man who after 5 days developed a neurologic picture associated with Human Immunodeficiency Viruses (HIV) seroconversion. The patient had developed a dissociative psychiatric disorder 6 months before, and after resolution of the acute neurologic disease a mild neuro-psychiatric disorder remained. After mononucleosis-like syndrome of three weeks, the patient developed a meningo-encephalitic process 48 h post admission. He evolved with tonic seizures and twilight state and was admitted into Intensive Care Unit because of epileptic status and deep coma. Evolution was favourable after 72 h of treatment with acyclovir and antiepileptic drugs. Laboratory data showed an inverted T4/T8 ratio and seroconversion to HIV-antibodies and p24-antigen both in serum and CSF. These observations confirm the existence of psychiatric as well neurological alterations in acute HIV infection, and also the significance of p24-antigen and Western-Blot in serum and CSF in showing the seroconversion profile.
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PMID:[Previous dissociative psychiatric disorder and status epilepticus in a case of acute HIV infection]. 150 7

We studied human megakaryocytes to determine if they both expressed and synthesized Fc gamma and CD4 membrane receptors. The strategy employed relied on demonstration of receptor protein and mRNA in megakaryocytes present in freshly made marrow smears, or in megakaryocytes isolated from aspirated normal bone marrow by counterflow centrifugal elutriation. Protein was detected immunochemically, whereas mRNA was detected either by in situ hybridization, or by reverse transcription, polymerase chain reaction (RT-PCR). Using these methods CD4 and Fc gamma RII protein and mRNA were detected in most megakaryocytes. Fc gamma RI and Fc gamma RIII protein was not detected in these cells. Megakaryocytes were also cultured with recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) to determine the effect of this growth factor on Fc gamma RII expression. As has been noted in cells of the monocyte-macrophage lineage, exposure to rhGM-CSF resulted in a significant increase in the level of megakaryocyte Fc gamma RII mRNA and protein. These observations are significant because they provide a physiologic basis for known viral trophism displayed by megakaryocytes. They are also of interest because they suggest that alternative portals exist for entry of human immunodeficiency virus (HIV-1) into megakaryocytes and that such infection may play a role in acquired immunodeficiency syndrome (AIDS)-related thrombocytopenia.
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PMID:Expression of Fc gamma RII and CD4 receptors by normal human megakaryocytes. 153 89

Neuro-cryptococcosis is a common opportunistic infection in AIDS or HIV infected patients. From a series of 10 neuro-cryptococcosis the four of them studied by magnetic resonance (MR) are reported. In AIDS patients a high suspicion of opportunistic infection of the CNS is needed as exemplified by two of the four patients who only presented cephalalgia. The other two patients suffered additional symptoms and signs of meningeal and CNS involvement, such as nuchal rigidity, cranial nerve palsies, papilloedema, gait ataxia and dismetria. Diagnosis was achieved (confirmed) by a positive culture, serology or indian ink test in CSF. CT scan did not contribute to the diagnosis and management of the patients. In contrast MR, showed in three of them a peculiar pattern of small, confluent, high-signal lesions, roughly symmetrically placed in the basal ganglia and the internal capsule. They probably correspond to the dilated Virchow-Robin spaces through which torulae migrate from the subarachnoid space.
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PMID:[Use of magnetic resonance in the diagnosis of neuro-cryptococcosis in the acquired immunodeficiency syndrome: study of 4 patients]. 155 79

Tumour necrosis factor (TNF-alpha) concentrations were determined in the CSF from 42 HIV-infected patients, with or without CNS involvement. In addition, 14 subjects with various neurological disorders but without HIV antibodies were included as controls. Raised CSF concentrations of TNF-alpha (greater than 40 ng/l) were detected both in patients with AIDS dementia complex (ADC) (6/9) and with CNS opportunistic infections (10/19) and, less commonly, in HIV infected subjects without CNS diseases (2/14) and in anti-HIV negative controls (1/14). The highest CSF concentrations of TNF-alpha (greater than 100 ng/l), however, were found in seven out of eight patients with cryptococcal meningitis. Although a role for TNF-alpha in demyelinating lesions associated with ADC has been suggested, our results indicate that a clear elevation of TNF-alpha in the CSF from HIV positive patients mostly occurs in acute inflammatory disorders, such as cryptococcal meningitis.
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PMID:Tumour necrosis factor (TNF-alpha) and neurological disorders in HIV infection. 156 86

Neurosyphilis, a sexually transmitted disease that can cause neurologic damage, has become increasingly prevalent in the AIDS era. HIV carriers can contract neurosyphilis without the presence of other concurrent opportunistic infections. Because MR findings of neurosyphilis are seldom reported, we retrospectively reviewed and evaluated contrast-enhanced MR images of six young (average age, 33 years) HIV-positive men with high serum and CSF VDRL titers indicative of neurosyphilis. All six patients tested negative for concurrent opportunistic infections. Five patients had acute or subacute strokelike symptoms involving the basal ganglia or middle cerebral arteries; one had a parietal convexity mass mimicking meningioma with headache and ataxia. Contrast-enhanced MR images showed patchy enhancement involving the basal ganglia and middle cerebral artery territories in the first five patients and the convexity mass in the sixth patient. On the basis of brain biopsy, a convexity mass was diagnosed in the patient with syphilitic gumma. The imaging findings of the remaining five patients represented ischemic infarct caused by meningovascular syphilis. After penicillin treatment, serum and CSF VDRL titers decreased, and neurologic signs and symptoms improved in all six patients. A follow-up MR study in the patient with the gumma showed that the lesion resolved almost completely. In young HIV patients with stroke symptoms or a convexity mass, neurosyphilis should be considered. Contrast-enhanced MR can reveal the extent of involvement by neurosyphilis and should be used to facilitate diagnosis and proper treatment.
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PMID:Neurosyphilis in HIV carriers: MR findings in six patients. 159 Jan 35

Thuja polysaccharide g fraction (TPSg) was shown to be an inducer of the CD4+ fraction of the human peripheral blood T-cell subset (1,2). Furthermore, it could be demonstrated that TPSg is a potent inhibitor of the expression of HIV-1-specific antigens and of the HIV-1-specific reverse transcriptase (3). This report deals with the cytokine pattern induced by TPSg in human peripheral blood lymphocyte (PBL) and purified monocyte/macrophage cultures. In addition, a further characterization of the CD4+ T-cell fraction stimulated by TPSg was performed by FACS analysis. TPSg is induces IL-1 beta, IL-2, IL-3, IL-6, gamma-IFN, G-CSF, GM-CSF, and TNF-beta production in PBL cultures; and IL-1 beta and IL-6 in monocyte/macrophage cultures. Enzyme-linked immunosorbent assays (ELISAs) demonstrated that no IL-4 was produced by PBL cultures under TPSg influence.
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PMID:Mitogenic activity of high molecular polysaccharide fractions isolated from the cuppressaceae Thuja occidentalis L. enhanced cytokine-production by thyapolysaccharide, g-fraction (TPSg). 160 22

Chronically immunosuppressed individuals are susceptible to lymphoreticular tumors. Up to 15% of patients with congenital deficiencies such as ataxia=telangiectasia may develop malignancies, mainly high-grade B cell non=Hodgkin's lymphomas (NHLs). AIDS lymphomas are comprised of NHLs including Burkitt's lymphoma (BL) and primary cerebral lymphomas (PCLs). Almost 3% of all AIDS patients (2824 of 97,258 cases) developed NHL. Epstein-Barr virus (EBV) as a co-factor in AIDS lymphomagenesis has been studied: in 12 cases of 24 AIDS lymphomas EBV by DNA in situ hybridization was found. In an analysis of 6 primary cerebral lymphomas, .5 were positive for EBV DNA by Southern blotting. In Burkitt's lymphoma the characteristic genetic alteration affects the c-myc oncogene. In 1/3 of BL p53 mutations were found but none in the 43 NHLs suggesting that p53 mutations and c-myc activation act synergistically in the pathogenesis of these tumors. Cytotoxic agents dideoxyinosine, dideoxycytosine, and zidovudine may cause secondary neoplasia. 8 of 55 AIDS patients under zidovudine treatment developed high-grade lymphoma 23.8 months subsequently; recently doses were reduced. PCL was found in 21 of 90 patients. A 5.2 months survival was associated with combined treatment with cyclophosphamide, Oncovin (vincristine), methotrexate, etoposide, and cytosine arabinoside compared with 11.3 months with chemotherapy. Colony-stimulating factors (CSFs) alleviate drug-induced myelotoxicity and zidovudine-induced neutropenia, however, l8 of 11 patients receiving granulocyte-macrophage CSF developed hematological toxicity. Interleukine-2 produced by T-helper cells enhancing tumor cells cytotoxicity has been used in AIDS-associated cryptosporidial diarrhea and in 4 patients with AIDS lymphoma with modest response, but its stimulation of the HIV-infected substrate may increase viral proliferation.
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PMID:AIDS lymphomas. 161 63

Nonherpetic encephalitis outside the newborn period is usually a self-limited disease. The majority of patients will recover without significant sequelae, and require only supportive therapy during the acute illness. Though the underlying viral etiology frequently will escape detection, identification of the infecting agent has considerable prognostic value which can complement clinical measures of severity of disease. The most important initial task of the clinician faced with a case of presumptive viral encephalitis is to eliminate the possibility of a treatable illness. Once this has been done, the diagnosis of viral encephalitis can be supported by documenting the characteristic slow-wave background activity on EEG, and a mild lymphocellular pleocytosis in the CSF. Because viral encephalitis can be caused by such a large number of organisms, the search for an etiology can be daunting. Realizing that all the agents described above can, at times, cause encephalitis without any clue to their identity, one nevertheless may use several pieces of historical information to narrow the possibilities. Travel history, animal exposures, immunization history, and seasonality all may help to steer the search in a particular direction and, indeed, may point to a nonvirologic cause as well. In addition, detection of extraneurological signs and symptoms may strongly indicate a specific virologic diagnosis. Finally, knowledge of concurrent community epidemic patterns, and of surveillance data routinely collected by local and state health departments, can help to increase or decrease the likelihood of a given pathogen. The causative viral agent usually can be identified by serological testing and viral culture. Occasionally, single serological determinations are diagnostic: in rabies (when the patient has not received immune prophylaxis), eastern equine encephalitis, and HIV, since seropositivity is strongly associated with symptomatic illness; and in Epstein-Barr virus, if a panel of antibody determinations which can time the infection is available. In addition, high CSF: serum titers for antibody against any neurotropic agent is usually diagnostic, though the absence of a high central nervous system antibody titer does not eliminate any potential viral pathogen. With these few exceptions, a single serological determination for a given pathogen is almost always impossible to interpret; paired sera (one obtained upon diagnosis, and one obtained 10 to 14 days later, either just prior to hospital discharge or at a follow-up visit) are far more helpful. Many viruses that directly infect the central nervous system are difficult to recover from the CSF; therefore, viral isolation from the nasopharynx and stool also should be sought.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Viral encephalitis. 164 66

Viral genes capable of inducing vascular tumors in the skin of transgenic mice are the tat gene of HIV-1 and polyoma virus' middle T antigen gene. Instead of vascular tumors, the tat gene of HTLV-I causes thymic atrophy and mesenchymal tumors in transgenic mice. No proof exists that any of these genes contribute to the induction of KS but HIV-1 tat is a strong suspect. The gene product K-FGF of the oncogene K-fgf/hst (int) uses bFGF receptors, is homologous with bFGF and acts as a mitogen for fibroblasts, endothelial cells and melanocytes. The overexpression of the K-fgf gene in KS is not proven unequivocally; some doubts exist suggesting the activation of this gene during the laboratory procedure of transfection with KS cell heavy DNA. Growth factor(s) not well identified (IL-6?) are released from HTLV-I- or II, or HIV-1- or 2-infected T4 lymphocytes and in particular from HIV-1-infected macrophages. This growth factor(s) promote(s) the continuous proliferation of endothelial cells and KS cells. AIDS-KS cells release other growth factors identical with or closely related to basic FGF, a major inducer of angioneogenesis. In addition, acidic FGF, IL-1 alpha and -beta, GM-CSF, PDGF-B and TGF-beta are released from AIDS-KS cells. The release of GM-CSF is induced by IL-1. GM-CSF promotes granulocytic, monocytic and endothelial cell proliferation. TGF-beta is known to suppress lymphocyte-mediated cytotoxicity and may act as a local immunosuppressive factor together with interferon inactivators. We theorize that when TGF-beta production ceases, TNF-beta (lymphotoxin) production switches on leading to programmed cell death (apoptosis) of KS cells resulting in regression of these lesions. The newly discovered angiogenesis factors VEGF/VPF may emerge as protooncogene-oncogene products analogous to PDGF and c-sis activation. AIDS-KS heavy DNA transfects NIH3T3 cells. NIH3T3 cells carrying this gene induced angiosarcomas when implanted in mice. An as yet unidentified large virus (mycoplasma?) was derived from these cells during passages in culture. No causative relationship between this agent and Kaposi sarcoma has as yet been established. Even though IFN-alpha exerts antiretroviral effects in AIDS, we propose that the therapeutic effect of IFN-alpha in AIDS-KS is based on antiangiogenesis activity by suppressing protooncogenes-oncogenes of the FGF family.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Kaposi's sarcoma: its 'oncogenes' and growth factors. 165 29


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