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

Different strains of human immunodeficiency virus type 1 (HIV-1) vary in the ability to replicate in cells that bear the HIV-1 receptor, CD4. The mechanism responsible for these cell tropism differences is unknown. We examined different isolates of HIV-1 with regard to replication in specific tumor-derived CD4-positive T-cell lines and normal peripheral blood lymphocytes. To investigate early events in the virus life cycle at low multiplicities of infection, we used a modification of the polymerase chain reaction method. Use of a molecularly cloned primary HIV-1 isolate, HIV-1 JR-CSF, restricted for replication in T-cell lines, demonstrated that little or no viral DNA or RNA was synthesized in nonpermissive cells after infection. However, transfection of proviral DNA resulted in efficient transient virus production from these cells. Therefore, we conclude that at least one block to infection for HIV-1 strains in nonpermissive T cells occurs at a point in entry or uncoating before provirus formation.
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PMID:Human immunodeficiency virus type 1 T-cell tropism is determined by events prior to provirus formation. 239 28

A group of 23 pediatric patients seropositive for HIV antibody were studied by computed tomography and evaluated neurodevelopmentally. Significant neurodevelopmental delays were found in over 95% of the patients studied. CT findings in six patients were normal and thirteen of 23 (57%) had prominence of the CSF spaces. Less frequent findings included calcifications in the basal ganglia and white matter. Cerebral mass lesions included one case of lymphoma and one case of hemorrhage. The CT findings in the pediatric age group differs from the adult population in that contrast enhancing inflammatory mass lesions are uncommon.
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PMID:Pediatric AIDS. Neuroradiologic and neurodevelopmental findings. 246 Aug 18

To determine the effects of immunomodulatory agents upon HIV replication in macrophages, cultured monocyte-derived macrophages were treated with various substances and then infected with a macrophage-tropic strain of HIV-1. Pretreatment with rIFN-alpha, IFN-beta, and IFN-gamma, or bacterial LPS prevented viral replication in macrophages. In treated cultures, little or no infectious HIV or p24 core antigen was released into the supernatant, no virions were seen by electron microscopy, no viral RNA or DNA was detectable in the cell lysates, and no cytopathology (as determined by multinucleated giant cell formation) occurred. In contrast, pretreatment with a wide dose range of recombinant IL-1 beta, IL-2, IL-4, IL-6, M-CSF, TNF, or lymphotoxin failed to protect macrophages from productive infection by HIV. A consistent effect of granulocyte/macrophage-CSF on HIV replication in macrophages was not observed. In dose response studies, pretreatment with approximately 100 U/ml of IFN-alpha, approximately 10 U/ml of IFN-beta, or approximately 100 U/ml of IFN-gamma was sufficient to prevent virion release maximally and to prevent cytopathology completely. In kinetic studies, IFN-alpha, IFN-gamma, or LPS were added to the macrophage cultures either before or after infection with HIV. Even when added 3 d after infection with a multiplicity of 1 50% tissue-culture infectious dose per cell, all three treatments markedly reduced virion release, suggesting that these agents act at a point in the viral life cycle beyond the early events of virus binding, penetration, and uncoating. These data indicate that HIV replication in previously uninfected macrophages may be regulated by an inducible host cell mechanism. These findings may explain the restricted replication of HIV in macrophages in vivo and suggest an antiviral role for interferons in the therapy of HIV infection.
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PMID:Interferons and bacterial lipopolysaccharide protect macrophages from productive infection by human immunodeficiency virus in vitro. 246 37

We evaluated 130 consecutive HIV-infected neurologically asymptomatic individuals for intrathecal IgG production and myelin basic protein (MBP) levels. Although 56.7% of immunologically normal and 68.8% of immunocompromised patients had some CSF abnormality, no patient had an abnormal MBP level. The lack of MBP elevation in the CSF of these patients suggests that the production of intrathecal IgG is not related to active demyelination.
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PMID:Lack of cerebrospinal fluid myelin basic protein in HIV-infected asymptomatic individuals with intrathecal synthesis of IgG. 169 80

Although the control of retroviral disease in animal systems often involves antibody-dependent cell-mediated cytotoxicity (ADCC), the role of cytotoxic function in human retroviral disorders is uncertain. The ability of the neutrophil to kill HIV-infected targets directed by antiviral antibody was examined. Neutrophils from patients with AIDS killed HIV-infected MOLT-3A cells in a manner equivalent to neutrophils obtained from normal volunteers. Both granulocyte- and granulocyte-macrophage colony-stimulating factors (G-CSF and GM-CSF) markedly augmented the cytotoxic function. Studies done with fractionated human antisera revealed that ADCC to HIV-infected cells was mediated only by antibody to the env glycoprotein. ADCC in this system was not dependent on oxidative metabolism because neutrophils from patients with chronic granulomatous disease (CGD) were capable of CSF-augmented cytotoxicity. Although ADCC can be mediated by various classes of lymphocytes and mononuclear phagocytes, such cells may be infected by HIV. Because the neutrophil apparently is not productively infected by the virus, it is an ideal cell to focus on with regard to cytotoxic function in AIDS patients. The findings regarding neutrophil ADCC in AIDS are clinically relevant because the availability of CSFs now permits therapeutic regulation of neutrophils in AIDS patients, and presumably natural antibody may be useful in targeting HIV-infected cells for neutrophil cytotoxicity in vivo.
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PMID:Granulocyte- and granulocyte-macrophage colony-stimulating factors enhance neutrophil cytotoxicity toward HIV-infected cells. 247 84

Cryptococcus neoformans is an infrequent but important cause of severe disease in immunodepressed patients, especially in those with AIDS. We refer the case of a 45 year old patient with clinical, epidemiological and serological patterns of HIV-induced infection in the course of which the patient suffered a subacute neurologic syndrome with fatal evolution. The diagnosis was made by isolation of Cryptococcus neoformans in CSF and in palpable lymph nodes by fine-needle aspiration biopsy. Cryptococcal antigen titer of CSF was 1:2560. Treatment was standardized in the administration of amphotericin B (0.3 mg/kg/day) and 5-fluocytosine (150 mg/kg/day) for a period of six weeks. Factors that suggested poor prognosis were: a positive india ink preparation before treatment, a high initial CSF antigen titer, low CSF leukocyte count and the presence of Cryptococcus neoformans at an extraneural site. Since diagnosis of cryptococcosis was made when prominent localizing symptoms and signs were found, an intensive culture and serologic screening would be necessary in every patient with AIDS in order to establish an earlier diagnosis.
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PMID:[Cryptococcosis in acquired immunodeficiency syndrome (AIDS)]. 248 33

AIDS is no longer a rare disease affecting only a small segment of our population. It has now been observed throughout the United States and most other countries in the world. As the current data demonstrate, the effect of AIDS on the nervous system is profound and widespread. About 10% of all AIDS patients will first present with a neurological complaint. Evaluation of this complaint will then lead to the diagnosis of AIDS. Nearly 40% of all AIDS patients will develop major neurological symptoms during their lifetime; these symptoms may be related to primary HIV infection or secondarily to any of a number of opportunistic processes. At autopsy, 75% of AIDS patients will have neuropathological abnormalities. The AIDS-related central neurological syndromes are many and varied, as are their associated signs and symptoms. As with radiologic and serologic examination, the findings resulting from clinical examination of the AIDS patient with neurological illness are nonspecific. While there are clinical findings that are suggestive of one or another class of AIDS-related neurological illness, there is such overlap in their presentations as to make specific CNS diagnosis on the basis of clinical examination virtually impossible. The differential diagnosis of AIDS-related neurological illness is made even more difficult by the frequent observation of multiple CNS pathological processes in the same AIDS patient. Nearly one-third of all histologically examined AIDS cases had multiple intracranial pathologies. Multiple treatable pathological abnormalities have been identified both within the same intracranial lesion and within different lesions, and both simultaneously and sequentially. Thus, the evaluation and treatment of the AIDS patient with central neurological illness is a difficult challenge. Close attention must be paid to subtle neurological complaints, and careful neurological examination is warranted in all AIDS patients. Once the patient complains of neurological dysfunction or a neurological abnormality is identified on clinical examination, a careful workup including MRI or CT brain scanning and cerebrospinal fluid examination is indicated. Specific diagnosis must then be made on the basis of CSF findings, response to empiric therapy or biopsy. Therapy for AIDS-related CNS diseases in not unlike that for the same disease in other patient populations. (see Chapters 18 and 19). There is no cure for HIV encephalitis; azidothymidine (AZT) appears to cross the blood-brain barrier, and trials of AZT for the treatment of HIV encephalitis show early promise.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Central nervous system disorders in AIDS. 248 19

CSF and serum of 80 HIV-seropositive patients in various stages of the disease were examined. Total as well as intrathecal IgG synthesis appeared to be frequently elevated in each diagnostic group. Abnormal CSF oligoclonal IgG fractions were significantly more frequent in asymptomatic patients. CSF pleocytosis was found with a lower percentage in neurological AIDS patients. In patients subdivided according to blood T helper cell count, the distribution of the abnormal CSF parameters confirms that the immunological response in the CNS is mediated by interaction with systemic immunity.
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PMID:[Intrathecal synthesis of IgG in HIV infections]. 252 91

We have investigated the influence of granulocyte-macrophage CSF (GM-CSF) on the replication of HIV-1 in cells of monocyte/macrophage (M/M) lineage, and its effect on the anti-HIV activity of several 2'3'-dideoxynucleoside congeners of thymidine in these cells in vitro. We found that replication of both HTLV-IIIBa-L (a monocytotropic strain of HIV-1) and HTLV-IIIB (a lymphocytotropic strain) is markedly enhanced in M/M, but not in lymphocytes exposed to GM-CSF in culture. Moreover, GM-CSF reduced the dose of HIV required to obtain productive infection in M/M. Even in the face of this increased infection, GM-CSF also enhanced the net anti-HIV activity of 3'-azido-2'3'-dideoxythymidine (AZT) and several related congeners: 2'3'-dideoxythymidine (ddT), 2'3'-dideoxy-2'3'-didehydrothymidine (D4T), and 3'-azido-2'3'-dideoxyuridine (AZddU). Inhibition of viral replication in GM-CSF-exposed M/M was achieved with concentrations of AZT and related drugs, which were 10-100 times lower than those inhibitory for HIV-1 in monocytes in the absence of GM-CSF. Other dideoxynucleosides not related to AZT showed unchanged or decreased anti-HIV activity in GM-CSF-exposed M/M. To investigate the possible biochemical basis for these effects, we evaluated the metabolism of several drugs in M/M exposed to GM-CSF. We observed in these cells markedly increased levels of both parent and mono-, di-, and triphosphate anabolites of AZT and D4T compared with M/M not exposed to GM-CSF. By contrast, only limited increases of endogenous competing 2'-deoxynucleoside-5'-triphosphate pools were observed after GM-CSF exposure. Thus, the ratio of AZT-5'-triphosphate/2'-deoxythymidine-5'-triphosphate and 2'3'-dideoxy-2'3'-didehydrothymidine-5'-triphosphate/2'-deoxythymi dine- 5'-triphosphate is several-fold higher in GM-CSF-exposed M/M, and this may account for the enhanced activity of such drugs in these cells. Taken together, these findings suggest that GM-CSF increases HIV-1 replication in M/M, while at the same time enhancing the anti-HIV activity of AZT and related congeners in these cells. These results may have implications in exploring new therapeutic strategies in patients with severe HIV infection.
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PMID:Replication of human immunodeficiency virus in monocytes. Granulocyte/macrophage colony-stimulating factor (GM-CSF) potentiates viral production yet enhances the antiviral effect mediated by 3'-azido-2'3'-dideoxythymidine (AZT) and other dideoxynucleoside congeners of thymidine. 253 49

A 26 year old male intravenous drug abuser presented with rapidly progressive paraplegia and total incontinence. CSF examination showed elevated protein level and pleocytosis. HIV testing was positive. Anti CMV titres were mildly elevated in serum and CSF. Death occurred 26 days after the onset of neurological signs. Necrotic and inflammatory lesions with numerous inclusion bodies characteristic of CMV were found in the roots of the cauda equina, conus terminalis and lumbar segments of the spinal cord. CMV subependymal encephalitis and HIV encephalitis were also present.
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PMID:Acute myeloradiculitis due to cytomegalovirus as the initial manifestation of AIDS. 253 37


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